134
TABLE OF CONTENTS Program at a Glance ................................................................................................................ 2 Office Bearers .......................................................................................................................... 5 Sponsors .................................................................................................................................. 6 Awards ..................................................................................................................................... 9 Invited Speakers .................................................................................................................... 10 Abstract Review Process and Presentation Formats .............................................................. 18 Program ................................................................................................................................. 19 2020 Accepted Abstracts ....................................................................................................... 39 Author Index........................................................................................................................ 118 Annual General Meeting: Agenda and Minutes 2019 ......................................................... 122 President’s Report ............................................................................................................... 125 TSANZ Membership List .................................................................................................... 129

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Page 1: tsanz.com.au€¦ · 13:15–17:00. Machine Perfusion Workshop : Upper Level City Room 1 : Sunday, 22 March 2020: 10:00–12:00 . National review of Paediatric kidney transplant recipients

TABLE OF CONTENTS

Program at a Glance ................................................................................................................ 2

Office Bearers .......................................................................................................................... 5

Sponsors .................................................................................................................................. 6

Awards ..................................................................................................................................... 9

Invited Speakers .................................................................................................................... 10

Abstract Review Process and Presentation Formats .............................................................. 18

Program ................................................................................................................................. 19

2020 Accepted Abstracts ....................................................................................................... 39

Author Index ........................................................................................................................ 118

Annual General Meeting: Agenda and Minutes 2019 ......................................................... 122

President’s Report ............................................................................................................... 125

TSANZ Membership List .................................................................................................... 129

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2

The Transplantation Society of Australia and New Zealand

Thirty-eighth Annual Scientific Meeting

PROGRAM AT A GLANCE

Friday, 20 March 2020

13:15–17:00 Machine Perfusion Workshop Upper Level City Room 1

Sunday, 22 March 2020

10:00–12:00 National review of Paediatric kidney transplant recipients - Work Shop Riverbank Room 1

12:30–13:30 Pancreas and Islet Transplant Advisory Committee (PITAC) City Suite 3/4

12:30–14:30 Liver and Intestinal Transplant Advisory Committee (LITAC) TBC

13:45–14:30 Vascular Composite Allograft Advisory Committee (VCAAC) City Suite 3/4

14:00–15:00 Registration Exhibition Hall M; Foyer

15:00–15:10 Official Opening: TSANZ President Exhibition Hall M

15:10–15:40 PLENARY 1: Astellas Symposium CAR-Tregs to Induce Transplantation Tolerance

Exhibition Hall M

15:45–16:45 CONCURRENT FREE COMMUNICATIONS SESSIONS Free Communications 1: I/R Injury, Organ Preservation Free Communications 2: Organ Donation and Allocation#1 Free Communications 3: Outcomes and complications#1

Exhibition Hall M City Room 1 City Room 2

16:45–17:00 Afternoon tea Exhibition Hall N

17:00–18:00 Astellas Josette Eris Lecture and Ian McKenzie Award Partnering With Patients to Address Patient-Important Outcomes in Transplantation

Exhibition Hall M

18:00–21:00 Welcome Reception: “Burden of Genius” Screening Mercury Cinema; 13 Morphett Street, Adelaide

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Program at a Glance

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Monday, 23 March 2020 06:15–07:15 Fun Run/Walk (4.8km) Sponsor: Transplant Australia Course Here

07:30–08:00 Breakfast with sponsors Exhibition Hall N

08:00–09:40 PLENARY 2: Joint TSANZ /OTA/ATCA Session Exhibition Hall M

09:40–10:40 CONCURRENT FREE COMMUNICATIONS SESSIONS Free Communications 4: Immunobiology Free Communications 5: Organ Donation and Allocation#2 Free Communications 6: Pancreas and Islet Transplantation

Exhibition Hall M City Room 1 City Room 2

10:40–11:10 Morning tea and Poster viewing Paediatric Transplant Advisory Committee (PTAC)

Exhibition Hall N City Suite 3/4

11:10–12:50 PLENARY 3: TSANZ/CareDx Symposium

Immunology

Exhibition Hall M

12:50–13:35 Lunch and Poster Viewing Xeno-Transplantation Working Group (XTWG)

Exhibition Hall N City Suite 3/4

13:35–15:35 President’s Prize Symposium Exhibition Hall M

15:35–16:00 Afternoon tea Exhibition Hall N

15:45–17:00 Lung Transplant Advisory Committee City Suite 3/4

16:00–17:00 CONCURRENT FREE COMMUNICATIONS SESSIONS Free Communications 7: CMV and Biomatrix Free Communications 8: Outcomes and Complications#2 Free Communications 9: Transplantation Surgery

Exhibition Hall M City Room 1 City Room 2

17:00–18:00 TSANZ Annual General Meeting Exhibition Hall M

19:00–23:00 TSANZ Annual Dinner Adelaide Town Hall

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Program at a Glance

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Tuesday, 24 March 2020

07:30–08:00 Coffee with sponsors Exhibition Hall N

08:00–09:30 Plenary 4: Joint TSANZ/Roche Symposium Indigenous Transplantation

Exhibition Hall M

09:30–10:30 CONCURRENT STATE OF THE ART SESSIONS STATE OF THE ART 1: Astellas Symposium Antibodies and Infections STATE OF THE ART 2: Joint TSANZ/Novartis Symposium Obesity and Nutrition

City Room 1 City Room 2

10:30–11:00 Morning tea Immunology and Tolerance Working Group (ITWG)

Exhibition Hall N City Suite 3/4

11:00–12:30 CONCURRENT STATE OF THE ART SESSIONS STATE OF THE ART 3: Astellas Symposium Transplantation Surgery STATE OF THE ART 4: Joint TSANZ/Novartis Symposium Innovations

City Room 1

City Room 2

12:30–13:30 Lunch Renal Transplant AC (RTAC) & Renal Allocation Working Group (RAWG)

Exhibition Hall N City Suite 3/4

13:30–15:00 Plenary 5: Joint TSANZ/Xvivo Symposium Perfusion and Donor Management

Exhibition Hall M

15:00–15:25 Afternoon tea Exhibition Hall N

15:25–16:00 The Great Debate: ‘Stem Cell Technology Will Make Organ Donation Redundant Within 10 Years’

Exhibition Hall M

16:00 ASM Concludes

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OFFICE BEARERS OF THE TRANSPLANTATION SOCIETY OF AUSTRALIA AND NEW ZEALAND

President

Professor Patrick (Toby) Coates President Elect & Chair, Advisory Committees/Working Groups Dr Helen Pilmore Honorary Secretary A/Professor Natasha Rogers Treasurer A/Professor Bronwyn Levvey Councillors Dr Nick Cross - EX-OFFICIO New Zealand Representative A/Professor Kelli MacDonald - Liaison with Scientific Societies Dr Christine Russell - Surgical Representative Dr Philip Clayton - RACP

A/Professor Kate Wyburn - AMDC Liaison Rep A/Prof Andrew Jabbour Dr Fiona Mackie Nigel Palk - ATCA Representative Scientific Program & Education Committee (SPEC) Dr Wai Lim (Co-Chair) Dr Lucy Sullivan (Co-Chair) Prof Henry Pleass A/Prof William Mulley Dr Darren Lee Dr Jeanette Villanueva Dr Philip Clayton (ASM) Dr Eu Ling Neo (ASM) A/Prof Chien-Li Holmes-Liew (PGC) Dr Andrea Viecelli (PGC) Dr Darling Rojas-Canales (Masterclass) Dr Sanda Stankovic (Masterclass) TSANZ Administrative Staff Mrs Nieves Piaggio Executive Officer Email: [email protected] Ms Kim Rawson Senior Project Officer Email: [email protected] Ms Roslyn Davies Administrative Officer Email: [email protected] Program and Abstract Book Ms Marina Katerelos Email: [email protected]

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SPONSORS

The Transplantation Society of Australia and New Zealand gratefully acknowledges the support of the following companies in providing sponsorship for the Annual Scientific Meeting.

Platinum Sponsor

Silver Sponsors

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Bronze Sponsors/ Exhibitors

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Award Sponsor

Mark Cocks Patient Forum

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AWARDS

The Transplantation Society of Australia and New Zealand gratefully acknowledges the support of the following companies for sponsoring awards presented at the Annual Scientific Meeting.

AWARDS

The President’s Prizes – Basic Science & Clinical (supported by TSANZ) Novartis/TSANZ Early Career Researcher Awards Kidney Health Australia Awards Lafferty Award (supported by TSANZ) Aviva Rosenfeld Award for Excellence in Patient Care in Transplantation (supported by TSANZ)

FINANCIAL STATEMENTS

The Transplantation Society of Australia and New Zealand (TSANZ) Financials for the Year Ended December 2019 are available on the easily accessible member password protected section of the TSANZ website www.tsanz.com.au.

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INVITED INTERNATIONAL SPEAKERS

Astellas Lecturer

Marina Berenguer Haym

Associate Professor of Medicine at the University of Valencia. Recognized in the field of Hepatology and Liver Transplantation with extensive research covering clinical, basic and translational works. Intellectual contributions in more than 400 publications in peer-reviewed journals (8844 citations; HIRSCH Index 47). Research Coordinator within a National Network Research Center in Hepatology, CIBER-EHD, leading one of the few CIBER groups in the Valencia region. Receipt of continuous grants both from public, private and competitive funds. Regular invited speaker in Hepatology forums as well as Consensus Conferences from which clinical practice guidelines are issued. Councilor in different Societies, such as ESOT (2011-14), ELITA (2017-20), ILTS (2013-17), AEEH (2009-10, 2013-14), SEPD (2004-08) or SET (2018-19). Associate editor in “Liver Transpl” and “J. Hepatol” from 2010 to 2014 and Deputy Editor in “Transplantation” (2015-2020) and J Hep Rep (2019-2022). Consultant/expert in National Grant Committees, such as "Agence National de la Recherche" (France) and "Instituto de Salud Carlos III" (Spain). Co-founder in 2016 of the Spanish Group of Women Hepatologists (GEMHEP) as well as first chair of the Women Committee within ILTS. Recipient of several Awards, including the Medical-Scientific Award from the LT Patient Association (2007), the Professional Career Acknowledgement granted by the Regional Government (2010) and the Mayo Clinic award (2014). International Liver Transplant Society-ILTS- President Elect in 2019.

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INVITED INTERNATIONAL SPEAKERS ______________________________________________________________

Sponsored by RACS Visitor Grant Program

Ina Jochmans

Qualified abdominal transplant surgeon with particular committed to ongoing research to improve outcome after liver and kidney transplantation by advancing dynamic organ preservation techniques and identification of modifiable factors influencing outcome through clinical trials, retrospective and registry studies, and translational studies. CURRENT POST 10/2019–present ASSOCIATE PROFESSOR, FACULTY OF MEDICINE KU Leuven, Leuven (Belgium) Department of Microbiology, Immunology, and Transplantation 08/2015–present CLINICAL RESEARCH MANDATE HOLDER (KOF-KOOR) University Hospitals Leuven, Leuven (Belgium) 2014–present DEPUTY CLINICAL DIRECTOR ABDOMINAL TRANSPLANTATION University Hospitals Leuven, Leuven (Belgium) 02/2013–present CONSULTANT ABDOMINAL TRANSPLANT SURGEON University Hospitals Leuven, Leuven, (Belgium) EXPERIENCE 10/2013–09/2019 ASSISTANT PROFESSOR, FACULTY OF MEDICINE KU Leuven, Leuven (Belgium) Department of Microbiology, Immunology and Transplantation 10/2016–04/2017 HONORARY CLINICAL FELLOW TRANSPLANT UNIT Addenbrookes Hospital, Cambridge (United Kingdom) 08/2008–07/2012 DOCTORAL TRAINING IN BIOMEDICAL SCIENCES (PhD) KU Leuven, Leuven (Belgium) Fellowship Research Foundation Flanders (FWO) 08/2005–01/2013 SURGICAL TRAINING AND FELLOWSHIP University Hospitals Leuven and collaborative Belgian hospitals

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INVITED INTERNATIONAL SPEAKERS ______________________________________________________________

Kiran Khush

Dr. Kiran K. Khush, MD, MAS is an Associate Professor of Cardiovascular Medicine at the Stanford University School of Medicine. Dr. Khush is an advanced heart failure transplant cardiologist who trained at Harvard Medical School and the University of California San Francisco. At Stanford, she leads a clinical and translational research program focusing on (1) donor evaluation and selection for heart transplantation, (2) non-invasive diagnosis of post-transplant complications, and (3) pathogenesis of cardiac allograft vasculopathy. She is Associate Director of the International Society for Heart and Lung Transplantation Thoracic Transplant Registry and is Program Director of the Advanced Heart Failure Transplant Cardiology fellowship program at Stanford. Dr. Khush’s research is funded by the National Institutes of Health, American Heart Association, Enduring Hearts Foundation, and other philanthropic sources.

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INVITED INTERNATIONAL SPEAKERS ______________________________________________________________

Megan Levings PhD Professor Department of Surgery and School of Biomedical Engineering Head

University of British Colombia

Dr. Megan Levings has been in the UBC Department of Surgery since 2003 when she was recruited back to Canada as a Canada Research Chair in Transplantation. In 2011 she joined the BC Children’s Hospital Research Institute where she now heads the Childhood Diseases Research Theme. Dr. Levings’ scientific career started with summer research positions in a fruit fly genetics lab at Simon Fraser University. She then did her graduate training in the genetics program with Dr. John Schrader at UBC, during which time she attended her first of many Canadian Society for Immunology meetings and developed a passion for immunology. In 1999 she joined Dr. Maria Grazia Roncarolo's lab in Milan, Italy, undertaking postdoctoral training in the emerging area of immune regulation. She was among the first groups to show that a special kind of white blood cell, known as a T regulatory cell, could be used as a therapy to stop harmful immune responses. She continues this line of research at UBC, and is now internationally recognized in the field of human immunology, chairs the Federation of Clinical Immunology Societies Centers' of Excellence and is a member of the NIH Immune Tolerance Network steering committee. Dr. Levings leads a vibrant group of trainees and staff who are researching how to use T regulatory cells to replace conventional immunosuppression in the context of transplantation and autoimmunity.

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INVITED INTERNATIONAL SPEAKERS ______________________________________________________________

Timucin Taner, MD, PhD Dr. Timucin Taner is the surgical director of liver transplantation at Mayo Clinic, Rochester. He has been a member of the Mayo Clinic transplant team since 2012, after having obtained a PhD in immunology from the University of Pittsburgh and completing surgical training at Mayo Clinic. His clinical practice involves living- and deceased-donor liver transplantation in both adult and paediatric patients. His research focuses on liver transplant immunobiology, specifically the mechanisms underlying the interplay between the liver allograft and the host immune responses. He is the Mayo Clinic Primary Investigator of two cellular therapy trials aiming at immunosuppression minimization after liver transplantation. He serves in numerous committees in national and international organizations, including the International Liver Transplantation Society (ILTS), American Association for the Study of Liver Diseases (AASLD) and American Society of Transplant Surgeons (ASTS).

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INVITED INTERNATIONAL SPEAKERS ______________________________________________________________

Chris Watson

Chris is a transplant surgeon from Cambridge where he is involved in liver, kidney and pancreas transplantation, and the occasional intestinal transplant. A previous president of the British Transplantation Society and former Associate Editor of the American Journal of Transplantation, for the last 6 years he chaired the Kidney Advisory Group of NHSBT, responsible for advising on allocation, governance, and all issues relating to renal transplantation. His term in that office culminated with the launch of the 2019 kidney allocation scheme, an evolution of the previous 2006 scheme and one hoped to produce more equitable access. Prior to that he chaired the Pancreas Advisory Group, and was responsible for securing funding for the national pancreas transplant programme and developing a pancreas allocation scheme that shared organs for whole organ and islet transplantation.

His research interests have been around increasing organ utilisation. Most recently has been focussing on optimising the results of livers from DCD donors, pioneering in situ normothermic regional perfusion in the UK, as well as developing a successful ex situ normothermic liver perfusion programme

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INVITED SPEAKERS

Professor Steve Alexander Nephrology Department, Children’s Hospital at Westmead, NSW

Ms Lucinda Barry

Chief Executive Officer Organ and Tissue Authority, ACT

Dr Samantha Bateman

Nephrologist, Central and Northern Adelaide Renal and Transplantation Service Royal Adelaide Hospital | SA Health

Dr Rob Carroll

Central & Northern Adelaide Renal Transplant Services (CNARTS) Royal Adelaide Hospital, SA

Jacob Chisholm

Consultant Surgeon, Flinders Medical Centre, SA

Jason Chuen Vascular, Endovascular and Transplant surgeon;

Director of Vascular Surgery Department, Austin Health, VIC

Professor Patrick (Toby) Coates Renal Unit, Royal Adelaide Hospital, SA

Eleanor Garrard

Executive Officer, National Indigenous Kidney Transplantation Taskforce SAHMRI Adelaide SA

Dr Bulang He

Head of Renal Transplant Surgery, Alfred Hospital,VIC

A/Professor Peter Hughes Royal Melbourne Hospital

Janina Kaczmarcyzk

Liver Transplant Surgery fellow, Flinders Medical Centre, SA

Anthony Meade Renal Dietitian of the Central Northern Adelaide Renal and Transplantation Services,

Royal Adelaide Hospital, SA

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INVITED SPEAKERS

Kelli Owen Transplant recipient and community representative

Indigenous Kidney Community Representative; NIKTT

Nigel Palk President - Australasian Transplant Coordinators Association (ATCA)

DonateLife SA

Dr Helen Pilmore Renal Unit, Auckland Hospital, NZ

Professor Henry Pleass

Professor of Surgery, Westmead Clinical School, NSW

Professor Greg Snell Medical Head of the Lung Transplant Service Alfred Hospital and Monash University, VIC

A/Professor Allison Tong

The University of Sydney School of Public Health Centre for Kidney Research, The Children’s Hospital at Westmead, NSW

Professor Angela Webster

Professor of Clinical Epidemiology, University of Sydney Senior Staff Specialist Transplantation and Renal Medicine, Westmead Hospital, NSW

A/Professor Alan Wigg

Hepatology and Liver Transplant Unit - Flinders Medical Centre, SA

Dr Melanie Wyld Department of Renal Medicine

Royal Prince Alfred Hospital, NSW

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ABSTRACT REVIEW PROCESS AND PRESENTATION FORMATS

A total of 97 abstracts were submitted this year. Abstracts were blinded for authors and institutions and were reviewed by four reviewers (see below) assigned by the Scientific Program and Education Committee (SPEC). Reviewers did not review abstracts if a conflict of interest was identified. Reviewers scored between 6 to 12 abstracts and in general there was a close agreement between scores. Two presentation formats will be used at the 2020 ASM. Free Communications session will have 5 oral presentations for Clinical abstracts (10 min presentation, 2 min questions) and 4 oral Presentations for Scientific abstracts (12 min presentation, 3 min questions). Abstracts will also be displayed as posters and the poster viewing sessions will be held during morning tea and lunch on Monday March 23. Presenters should be at their posters during the poster sessions to answer any questions from delegates. The President’s Prize (PP) will be awarded in two categories: Basic Science and Clinical. The highest-ranked abstracts from eligible applicants in both categories will be presented in a single PP session. The award in each category will be based on the quality of the abstract and the presentation on the day. The reviewers of the abstracts for the TSANZ 2020 meeting were: Stephen Alexander Richard Allen Leyla Aouad Michael Burke Scott Campbell Daniel Chambers Carolyn Clark Philip Clayton Michael Collins Peter Cowan Nick Cross Ian Dittmer Randall Faull Ross Francis Hilton Gock David Goodman David Gracey Ahmer Hameed Wayne Hancock

Munish Heer Peter Hopkins Frank Ierino Ashley Irish Nikky Isbel Andrew Jabbour Shilpanjali Jesudason Sean Kennedy Paul Lawton Darren Lee Wai Lim Grant Luxton Peter Macdonald Geoff McCaughan Solomon Menahem Bill Mulley Brian Nankivell Eu Ling Neo Kathy Nicholls

Philip O'Connell Kathy Paizis Helen Pilmore Henry Pleass Janske Reiling Veena Roberts Amanda Robertson Paul Robertson Christine Russell Alexandra Sharland Julian Singer Sebastian Stead Lucy Sullivan Andrew Sunderland Alison Tong Paul Trevillian Jeanette Villanueva Angela Webster Germaine Wong

The committee members thank these reviewers for their reviews and effort in supporting the meeting. Wai Lim and Lucy Sullivan Chairs of TSANZ Scientific Program & Education Committee (SPEC)

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The Transplantation Society of Australia and New Zealand

Thirty-eighth Annual Scientific Meeting

PROGRAM

Friday, 20 March 2020

13:15–17:00 Machine Perfusion Workshop Upper Level–City Room 1

Sunday, 22 March 2020

10:00–12:00 National Review of Paediatric Kidney Transplant Recipients - Work Shop

Riverbank Room 1

12:30–13:30 Pancreas & Islet Advisory Committee Meeting (PITAC)

City Suite 3/4

12:30–14:30 Liver and Intestinal Transplant Advisory Committee (LITAC)

TBC

13:45–14:30 Vascular Composite Allograft Advisory Committee (VCAAC)

City Suite 3/4

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TSANZ ASM Program

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Sunday, March 22, 2020

14:00–15:00 Registration Exhibition Hall M, Foyer

15:00–15:10 Official Opening: TSANZ President Prof Toby Coates

Exhibition Hall M

15:10–15:40 PLENARY 1: Astellas Symposium

Chair:

CAR-Tregs to Induce Transplantation Tolerance Prof Megan Levings

Exhibition Hall M

15:45–16:45

CONCURRENT FREE COMMUNICATIONS SESSIONS

Free Communications 1: Ischaemia Reperfusion Injury and Organ Preservation Chairs:

Exhibition Hall M

Abstract — Oral presentations —

1 15:45 EMPAGLIFLOZIN IMPROVES CARDIAC FUNCTIONAL RECOVERY OF DONOR HEARTS AFTER PROLONGED COLD ISCHAEMIA – AN ALTERNATIVE TO SODIUM-HYDROGEN EXCHANGE INHIBITION. VILLANUEVA JE, GAO L, SCHEUER SE, DOYLE A, JABBOUR A, HICKS M, MACDONALD PS

2 16:00 GASDERMIN-D MUTATION IS PROTECTIVE AGAINST RENAL ISCHEMIA REPERFUSION INJURY LI Jennifer, Alexander Stephen, ROGERS Natasha

3 16:15 A RAT MODEL OF CARDIAC DONATION AFTER CIRCULATORY DEATH (DCD) GAO Ling, DOYLE Aoife, VILLANUEVA Jeanette, SCHEUER Sarah, HICKS Mark, MACDONALD PS

4 16:30 A POINT MUTATION OF SHROOM3 PROMOTES CD206+ MACROPHAGE INFILTRATION AND KIDNEY FIBROSIS AFTER ISCHEMIA-REPERFUSION INJURY TANG Tianfeng, LU Bo, ROGERS Natasha, ZHENG Guoping , NICHOLSON Leigh, CAO Qi , MENON Madhav, MURPHY Barbara, ALEXANDER Stephen I, HU Min, O’CONNELL Philip J

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TSANZ ASM Program

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Sunday, March 22, 2020

15:45–16:45 Free Communications 2: Organ Donation and Allocation#1 Chairs:

City Room 1

Abstract — Oral presentations —

5 15:45 THE IMPACT OF DONOR TOBACCO AND MARIJUANA SMOKING HISTORY ON EARLY AND INTERMEDIATE-TERM LUNG TRANSPLANT OUTCOMES OKAHARA Shuji, LEVVEY Bronwyn, MCDONALD Mark, D'COSTA Rohit, OPDAM Helen, PILCHER David, SNELL Greg

6 15:57 PAEDAITRIC DECEASED DONOR KIDNEY TRANSPLANTATION IN AUSTRALIA: A 30 YEAR REVIEW. WHAT HAVE PAEDIATRIC BONUSES ACHIEVED AND WHERE TO FROM HERE? SYPEK Matthew P, DAVIES Chris, LE PAGE Amelia, CLAYTON Phil, HUGHES Peter, LARKINS Nicholas, WONG Germaine, KAUSMAN Joshua Y, MACKIE Fiona

7 16:09 FREQUENCY AND OUTCOMES OF KIDNEY DONATION FROM INTENSIVE CARE PATIENTS WITH ACUTE KIDNEY INJURY REQUIRING RENAL REPLACEMENT THERAPY OPDAM Helen, SANDERS Jo, FURNISS Hayley, HUGHES Peter, KANELLIS John, JONES Daryl

8 16:21 SUSPECTED VS. VERIFIED MELANOMA IN NSW DECEASED ORGAN DONOR REFERRALS: A DATA-LINKAGE COHORT STUDY, 2010-2015 ROSALES Brenda Maria, HEDLEY James, DE LA MATA Nicole, WALLER Karen, O'LEARY Michael, KELLY Patrick, WYBURN Kate, WEBSTER Angela

9 16:33 EVALUATION OF THE HALIFASTER FLOW CYTOMETRIC CROSSMATCH FOR THE DETECTION OF DONOR SPECIFIC ANTIBODIES. DE SANTIS Dianne, SUTANTO Michael, HOGAN Jesse, DOWNING Jonathan, MARTINEZ Patricia, D'ORSOGNA Lloyd

15:45–16:45 Free Communications 3: T-Regulatory Cells Chairs:

City Room 2

Abstract — Oral presentations —

10 15:45 CHOLECYSTITIS IN LUNG TRANSPLANTATION – A SINGLE CENTRE EXPERIENCE SLADDEN Timothy, CHANDRASEGARAM Manju, YERKOVICH Stephanie, CHAMBERS Daniel

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TSANZ ASM Program

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Sunday, March 22, 2020

11 15:57 IMPULSE OSCILLOMETRY HOLDS PROMISE IN BRONCHIOLITIS OBLITERANS SYNDROME

CROWHURST Thomas, BUSSELL Lauren, JOHNSTON Sonya, YEO Aeneas, YEUNG David, EDWARDS Suzanne, SNELL Gregory, HOLMES Mark, HOLMES-LIEW Chien-Li

12 16:09 IS TIMING REALLY EVERYTHING? WARM ISCHEMIC DEFINITIONS AND OUTCOMES FOR CARDIAC ALLOGRAFTS IN DCD WITHDRAWALS SCHEUER Sarah Elizabeth, CHEW Hong Chee, SOTO Claudio, HICKS Mark, GAO Ling, VILLANUEVA Jeanette , KAWANISHI Yujiro , WATSON Alasdair , CONNELLAN Mark, GRANGER Emily, JANSZ Paul , MACDONALD Peter

13 16:21 DUPLEX ULTRASOUND AS A SCREENING TOOL FOR TRANSPLANT RENAL ARTERY STENOSIS CORBETT Matthew, LAURENCE Jerome, ALLEN Richard, MEYBODI Farid

14 16:33 ANTIPLATELET AGENTS FOR CHRONIC KIDNEY DISEASE: AN UPDATED COCHRANE REVIEW NATALE Patrizia, PALMER Suetonia C, SAGLIMBENE Valeria M, RUOSPO Marinella, RAZAVIAN Mona , CRAIG Jonathan C, JARDINE Meg J, WEBSTER Angela C, STRIPPOLI Giovanni FM

16:45–17:00 Afternoon tea Exhibition Hall N

17:00–18:00 Astellas Josette Eris Lecture and Ian McKenzie Award Chairs:

17:00 Partnering With Patients to Address Patient Important Outcomes in Transplantation Prof Allison Tong

17:20 Josette Eris Lecture Prof Brenda Wilson AM

Exhibition Hall M

18:00–21:00 Welcome Reception: “Burden of Genius” Screening Mercury Cinema; 13 Morphett Street, Adelaide

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TSANZ ASM Program

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Monday, March 23, 2020

06:15–07:15 TSANZ Fun Run/Walk (4.8km) Sponsor: Transplant Australia River Torrens/Karrawirra Parri circuit

07:30–08:00 Breakfast with sponsors Exhibition Hall N

08:00–09:40 PLENARY 2: Organ and Tissue Authority Symposium

Joint TSANZ /OTA/ATCA Session Chairs:

08:00 New UK Kidney Allocation System Prof Chris Watson

08:30 Update From the Organ Transplant Authority Ms Lucinda Barry

08:50 Implementation of Flow Crossmatching for Organ Allocation in Australia Dr Rob Carroll

09:10 ANZKX Update Dr Peter Hughes

09:25 ATCA Update Mr Nigel Palk

Exhibition Hall M

09:40–10:40

CONCURRENT FREE COMMUNICATIONS SESSIONS

Free Communications 4: Immunobiology Chairs:

Exhibition Hall M

Abstract — Oral presentations —

15 09:40 GENERATION OF STABLE HUMAN INDUCED REGULATORY T-CELLS USING LOW-DOSE RAPAMYCIN KIM Juewan, HOPE Christopher, SCAFFIDI Jacqueline, CARROLL Robert, Barry Simon, COATES Toby

16 09:52 IDENTIFICATION OF A NOVEL SUBSET OF XENO-ANTIGEN SPECIFIC MEMORY CD4+FOXP3+TREGS IN ISLET-XENOTRANSPLANT TOLERANCE NICHOLSON Leigh, ZHAO Yuanfei, QIAN Yi Wen, TANG SooLing, CHEW Yi Vee, BURNS Heather, ZHANG Geoff, YI Shounan, ROGERS Natasha, HAWTHORNE Wayne, ALEXANDER Steve, O'CONNELL Philip, HU Min

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Monday, March 23, 2020

17 10:04 COMBINATIONAL THERAPY WITH POST-TRANSPLANT CYCLOPHOSPHAMIDE AND THE P2X7 ANTAGONIST BRILLIANT BLUE-G REDUCES LIVER DISEASE IN A HUMANISED MOUSE MODEL OF GRAFT-VERSUS-HOST DISEASE

CUTHBERTSON Peter, ADHIKARY Sam, SLUYTER Ronald, WATSON Debbie

18 10:16 PHOSPHOLIPASE A2 RECEPTOR CAR T CELLS LOCALISE TO THE KIDNEY SHAW Karli, WANG Yuan Min, HU Min, KARUNIA Jevin, ZHANG Geoff, CAO Qi, Lu Bo, MCCARTHY Hugh, HARRIS David, ALEXANDER Stephen

19 10:28 IL-4 REGULATES SECRETION OF THE IMMUNOMODULATORY CYTOKINE IL-10 BY HUMAN B CELLS PERKINS Griffith, HURTADO Plinio, COATES P. Toby

09:40–10:40 Free Communications 5: Organ Donation and Allocation#2 Chairs:

City Room 1

Abstract — Oral presentations —

20 09:40 COMMONLY USED CRITERIA TO INITIATE EX-VIVO LUNG PERFUSION (EVLP) HAVE NO SIGNIFICANT IMPACT ON EARLY POST LUNG TRANSPLANT (LTx) SURVIVAL OKAHARA Shuji, LEVVEY Bronwyn, MCDONALD Mark, D'COSTA Rohit, OPDAM Helen, PILCHER David, SNELL Greg

21 09:52 COUNTRY RANKING FOR DECEASED DONATION PERFORMANCE VARIES DRAMATICALLY DEPENDING ON THE METRIC USED OPDAM Helen, MCDONALD Mark, GOODWIN Melissa, BARRY Lucinda

22 10:04 INTERNATIONAL TRAVEL FOR OVERSEAS TRANSPLANTATION: A SURVEY OF AUSTRALIAN AND NEW ZEALAND CLINICIANS SMITH Georgia, GUJARI Diba, RUSSEL Oscar, PALMER Lyle, TOEWS Maeghan, WONG Germaine, LIM Wai, MCDONALD Stephen, CLAYTON Phillip, CROSS Nick, DITTMER Ian, Martin Dominique, COATES Patrick T

23 10:16 ACCESS TO DECEASED DONOR KIDNEY TRANSPLANTATION FOR SENSITIZED PATIENTS IN AUSTRALIA SYPEK Matthew, KAUSMAN Joshua, WYBURN Kate, HUGHES Peter, CLAYTON Phil

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Monday, March 23, 2020

24 10:28 FACTORS ASSOCIATED WITH DELAYED ACTIVE LISTING FOR DECEASED DONOR KIDNEY TRANSPLANTATION IN PATIENTS RECEIVING DIALYSIS IN AUSTRALIA – A SINGLE CENTRE PILOT STUDY

MCMICHAEL Lachlan, CLAYTON Philip

09:40–10:40 Free Communications 6: Pancreas and Islet Transplantation Chairs:

City Room 2

Abstract — Oral presentations —

25 09:40 20 YEARS OF ISLET ISOLATION OUTCOMES AT THE WESTMEAD ISLET TRANSPLANT PROGRAM HAWTHORNE Wayne, CHEW Yi Vee, WILLIAMS Lindy, ANDERSON Patricia, JIMENEZ Elvira, O'CONNELL Phil

26 09:52 PREGNANCY OUTCOMES FOR SIMULTANEOUS PANCREAS-KIDNEY TRANSPLANT RECIPIENTS VERSUS KIDNEY TRANSPLANT RECIPIENTS TANG Joanne, HEWAWASAM Erandi, GULYANI Aarti, MCDONALD Stephen, CLAYTON Phil, WEBSTER Angela, KANELLIS John, JESUDASEN Shilpanjali

27 10:04 PHENOTYPIC AND GENOTYPIC ANALYSIS OF HEREDITARY PANCREATITIS IN PATIENTS AND POTENTIAL CANDIDATES FOR TOTAL PANCREATECTOMY WITH ISLET AUTOTRANSPLANTATION (TP-IAT) WU Denghao, COATES PTH, PALMER Lyle, SCOTT Hamish, COUPER Richard, KASSAHN Karin, CHEN John

28 10:16 COMPARISON OF PANCREATA AND ISLET PREPARATIONS FROM HUMAN ORGAN DONORS - INFLUENCE OF FAMILY HISTORY OF DIABETES OR MARGINAL LEVELS OF HBA1C. MARIANA Lina, LOUDOVARIS Thomas, KOS Cameron, PAPAS Evan, SELCK Claudia, CATTERALL Tara, THOMAS Helen, KAY Thomas W H

29 10:28 TOTAL PANCREATECTOMY WITH AUTO ISLET CELL TRANSPLANTATION: A CASE SERIES BAMPTON Tristan, NEO Eu Ling, LOUDOVARIS Tom, RADFORD Toni, CHEN John, DROGEMULLER Chris, ETHERTON Colleen, KHURANA Sanjeev, Kirata Svjetlana, COUPER Richard, COATES P. Toby

10:40–11:10 Morning tea and Poster Viewing

Paediatric Transplant Advisory Committee (PTAC)

Exhibition Hall N

City Suite 3/4

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Monday, March 23, 2020

11:10–12:50 PLENARY 3: TSANZ/CareDx Symposium

Immunology Chairs:

11:10 Liver Transplant Immunology Prof Timucin Taner

11:40 Thymus-Derived Tregs as an Allogeneic Cell Therapy - Prof Megan Levings

12:10 The Secret Life of Donor Lungs: Passenger Cells and Molecules Transferred With Transplant Prof Greg Snell

12:30 Donor-Derived Cell-Free DNA for non-Invasive Diagnosis of Post-Transplant Complications A/Prof Kiran Khush

Exhibition Hall M

12:50–13:35 Lunch and Poster Viewing

Xeno-Transplantation Working Group (XTWG)

Exhibition Hall N

City Suite 3/4

13:33–15:35 President’s Prize Symposium Chair: TSANZ President, Prof Toby Coates

Exhibition Hall M

— Oral presentations —

30 13:35 THE EFFECT OF AGEING ON MYOCARDIAL SUSCEPTIBILITY TO ISCHAEMIA IN A RODENT MODEL OF DONATION AFTER CIRCULATORY DEATH. VILLANUEVA JE, CHEW HC, GAO L, SCHEUER SE, DOYLE A, JABBOUR A, HICKS M, MACDONALD PS

31 13:50 TRENDS IN CAUSES OF DEATH IN AUSTRALIAN AND NEW ZEALAND KIDNEY TRANSPLANT RECIPIENTS: A REGISTRY ANALYSES BY ERA AND TIME POST-TRANSPLANT YING Tracey, SHI Bree, Kelly Patrick, Clayton Philip, CHADBAN Steve

32 14:05 AN INFLAMMATORY INDEPENDENT ROLE FOR P65 (RELA) IN INSULIN HOMEOSTASIS ZAMMIT Nathan W, WALTERS Stacey N, MCDOWELL Joseph, GREY Shane, T.

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Monday, March 23, 2020

33 14:20 BRIEF NORMOTHERMIC MACHINE PERFUSION FOR THE ASSESSMENT AND REVIVAL OF DISCARDED HUMAN KIDNEYS

HAMEED Ahmer M, LU David B, ELLIS Patrick, XU Bo, HU Min, CHEW Yi Vee, KEUNG Karen , P’NG Chow H, GASPI Renan , ZHANG Chris , ROBERTSON Paul , ALEXANDER Stephen , THOMAS Gordon , LAURENCE Jerome , DE ROO Ronald , WONG Germaine , MIRAZIZ Ray , O’GRADY Greg, YUEN Lawrence , HAWTHORNE Wayne J. , ROGERS Natasha M. , PLEASS Henry C.

34 14:35 CO-AXIAL PRINTING OF MURINE ISLETS WITH HUMAN REGULATORY T-CELLS PREVENTS XENORESPONSE IN VITRO KIM Juewan, HOPE Christopher, PERKINS Griffith, YUE Zhilian, LIU Xiao, GANTUMUR Narangerel, DROGEMULLER Christopher, CARROLL Robert, BARRY Simon, WALLACE Gordon, COATES Toby

35 14:50 PERCEIVED VS. VERIFIED RISK OF CANCER TRANSMISSION FROM DECEASED ORGAN DONORS – A NSW COHORT STUDY 2010-2015 USING DATA LINKAGE HEDLEY James, DE LA MATA Nicole, ROSALES Brenda, WALLER Karen, O'LEARY Michael, CAVAZZONI Elena, KELLY Patrick, WYBURN Kate, WEBSTER Angela

36 15:05 DISCOVERY OF PMHC EPITOPES FOR DIRECTLY ALLOREACTIVE T CELLS. SON Eric Taeyoung, PAUL-HENG Moumita, LEONG Mario, FARIDI Pouya, DUDEK Nadine, ALEXANDER Ian, BERTOLINO Patrick, PURCELL Anthony, BOWEN David, MIFSUD Nicole, SHARLAND Alexandra

37 15:20 NEW BLOOD BORNE VIRUS INFECTIONS AMONG ORGAN TRANSPLANT RECIPIENTS: A DATA-LINKED COHORT STUDY EXAMINING TRANSMISSION AND DE NOVO HEPATITIS B, C AND HIV INFECTIONS WALLER Karen, DE LA MATA Nicole, HEDLEY James, ROSALES Brenda, O'LEARY Michael, CAVAZZONI Elena, RAMACHANDRAN Vidiya, RAWLINSON William, KELLY Patrick, WYBURN Kate, WEBSTER Angela

15:35–16:00 Afternoon tea Exhibition Hall N

15:45–17:00 Lung Transplant Advisory Committee (LTAC)

City Suite 3/4

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Monday, March 23, 2020

16:00–17:00

CONCURRENT FREE COMMUNICATIONS SESSIONS

Free Communications 7: CMV and Biomatrix Chairs:

Exhibition Hall M

Abstract — Oral presentations —

38 16:00 THE DETECTION OF CMV IN SALIVA CAN MARK A SYSTEMIC INFECTION WITH CMV IN RENAL TRANSPLANT RECIPIENTS WATERS Shelley, LEE Silvia, LLOYD Megan, IRISH Ashley, PRICE Patricia

39 16:15 VARIATIONS IN THE CYTOMEGALOVIRUS GENE US28 MAY ALTER IMMUNE RESPONSES IN IMMUNOCOMPRIMISED PATIENTS WATERS Shelley, LEE Silvia, MUNYARD Kylie, ARIYANTO Ibnu, KRESOJE Nina, GAUDIERI Silvana, LEARY Shay, IRISH Ashley, PRICE Patricia, ALLCOCK Richard

40 16:30 CYTOMEGALOVIRUS (CMV) BURDEN ASSOCIATES WITH MEASURES OF CARDIOVASCULAR HEALTH IN RENAL TRANSPLANT RECIPIENTS AND HEALTHY ADULTS AFFANDI Jacquita, LEE Silvia, CHIH HuiJun, WATERS Shelley, PRICE Patricia, IRISH Ashley

41 16:45 INNATE IMMUNE SENSING AND TISSUE REMODELLING OF A BIODEGRADABLE TEMPERING MATRIX SUPPORTED ISLET GRAFT. WALTERS Stacey N, BAILEY Jacqueline, CULTRONE Daniele, ROJAS-CANALES Darling, DROGEMULLER Chris, PENKO Danielle, LOUDOVARIS Thomas, KAY Thomas, KORBUTT Gregory, GREENWOOD John E, COATES Toby , GREY Shane T

16:00–17:00 Free Communications 8: Outcomes and Complications#2 Chairs:

City Room 1

Abstract — Oral presentations —

42 16:00 METFORMIN REDUCES CALCINEURIN INHIBITOR NEPHROTOXICITY FERNANDO Mangalee, TAYLOR Kylie, AU Amy, HERATH Sanjeeva, ERLICH Jonathan, ENDRE Zoltan

43 16:12 RAPID DETECTION OF KIDNEY TRANSPLANT INJURY BY QUANTIFYING DONOR-DERIVED CELL-FREE DEOXYRIBONUCLEIC ACID VIA MASSIVELY MULTIPLEX POLYMERASE CHAIN REACTION MCKANNA Trudy, SIGDEL Tara K., ACOSTA Felipe, NAVARRO Samantha, ZIMMERMANN Bernhard, DEMKO Zachary P., MOSHKEVICH Solomon, BILLINGS Paul R. , SARWAL Minnie M.

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Monday, March 23, 2020

44 16:24 RELATIVE SURVIVAL IN KIDNEY TRANSPLANT RECIPIENTS WITH DE-NOVO CANCERS VS NON-TRANSPLANT CANCER PATIENTS: A POPULATION STUDY 1980-2016

DE LA MATA Nicole, ROSALES Brenda, KELLY Patrick, WEBSTER Angela

45 16:36 GRAFT SURVIVAL AND VISUAL ACUITY FOLLOWING SURGICAL VARIATIONS OF CORNEAL TRANSPLANTATION IN EYES WITH FUCHS ENDOTHELIAL DYSTROPHY KEANE MC, MILLS RAD, COFFEY NE, JONES VJ, COSTER DJ, WILLIAMS KA

46 16:48 EVALUATION OF GRAFT FUNCTION AFTER KIDNEY RE-TRANSPLANTATION IN A SINGLE CENTRE IN VIETNAM DANG Ngoc Tuan Anh, HOANG Nu Ngoc Nhung, PHAM Nhu Hiep

16:00–17:00 Free Communications 9: Transplantation Surgery Chairs:

City Room 2

Abstract — Oral presentations —

47 16:00 TRANSPLANTATION OF KIDNEYS FROM PAEDIATRIC DONORS AGED 1 YEAR AND UNDER: AN ANALYSIS OF THE AUSTRALIAN AND NEW ZEALAND DIALYSIS AND TRANSPLANT (ANZDATA) REGISTRY FROM 1963 TO 2018 YAO Jinna, CLAYTON Philip, WYBURN Kate, TOVMASSIAN David, CHOKSI Harsham, LEE Taina, LAU Howard, ALLEN Richard, YUEN Lawrence, LAURENCE Jerome, PLEASS Henry

48 16:12 DUAL KIDNEY TRANSPLANTATION: TWO GOOD OR DOUBLE TROUBLE? HANNA Thomas, TAYLOR Sam, O'MAHONY Kate, DITTMER Ian, LANGLANDS Janice, MANLEY Paul, MUTHUKUMARASWAMY Carl

49 16:24 THE EFFECT OF SURGICAL CLOSURE OF HEMODIALYSIS ARTERIOVENOUS FISTULA AFTER SUCCESSFUL KIDNEY TRANSPLANTATION MARUI Yuhji, YOZA Naoto, MATSUMURA Kaori, USUBA Wataru, AOKI Naoto, NISHI Tomohiro, KATSUOKA Yuichi, NAKAZAWA Ryuto, SASAKI Hideo, KIKUCHI Eiji

50 16:36 TOTAL PANCREATECTOMY WITH ISLET AUTOTRANSPLANTATION FOR CHRONIC PANCREATITIS: AN AUSTRALIAN PERSPECTIVE TOVMASSIAN David, YOON Peter, YAO Jinna, HAWTHORNE Wayne, YUEN Lawrence, ALLEN Richard, LAURENCE Jerome, O'CONNELL Philip, ROGERS Natasha, PLEASS Henry

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Monday, March 23, 2020

51 16:48 THE USE OF DECEASED DONOR VESSELS IN KIDNEY TRANSPLANTATION

LEE Taina, VERRAN Deborah, LAURENCE Jerome, PULITANO Carlo

17:00–18:00 TSANZ Annual General Meeting Exhibition Hall M

19:00–23:00 TSANZ Annual Dinner Adelaide Town Hall

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Tuesday, March 24, 2020

07:30–08:00 Coffee with sponsors Exhibition Hall N

08:00–09:30 PLENARY 4: Joint TSANZ/Roche Symposium

Indigenous Transplantation Chairs:

08:00 National Indigenous Kidney Transplant Taskforce Progress Ms Eleanor Garrard

08:30 Consumer Engagement in Indigenous Transplantation Research (provisional) Dr Samantha Bateman / Ms Kelli Owen

09:00 Liver Transplantation in Indigenous Australians Prof Alan Wigg

Exhibition Hall M

09:30–10:30 CONCURRENT STATE OF THE ART SESSIONS

STATE OF THE ART 1: Astellas Symposium

Antibodies and Infections Chairs:

09:30 Viral Hepatitis Infections in Organ Transplantation A/Prof Marina Berenguer

09:50 TB Risk Assessment Prof Alan Wigg

10:10 Utilisation of Increased Viral Risk Donors Prof Angela Webster

City Room 1

09:30–10:30 STATE OF THE ART 2: Joint TSANZ/Novartis Symposium

Obesity and Nutrition Chairs:

09:30 Liver Transplantation in Obese Recipients Prof Timucin Taner

09:50 Non-Surgical Weight Loss Strategies in Obese Renal Transplant Candidates Mr Anthony Meade

10:10 The Role of Bariatric Surgery in NASH and Liver Transplantation Dr Jacob Chisholm

City Room 2

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Tuesday, March 24, 2020

10:30–11:00 Morning tea

Immunology and Tolerance Working Group (ITWG)

Exhibition Hall N

City Suite 3/4

11:00–12:30 CONCURRENT STATE OF THE ART SESSIONS

STATE OF THE ART 3: Astellas Symposium

Transplantation Surgery Chairs:

11:00 Liver Transplantation in Cholangiocarcinoma Prof Timucin Taner

11:30 Robotic Surgery: The Role in Kidney Transplantation A/Prof Bulang He

11:50 Effects of Donor Hepatectomy and Nephrectomy Times on Transplant Outcomes A/Prof Ina Jochmans

12:10 Update on Pancreas Transplantation Prof Henry Pleass

City Room 1

11:00–12:30 STATE OF THE ART 4: Joint TSANZ/Novartis Symposium

Innovations Chairs:

11:00 Donor Selection for Heart Transplantation: Changing Perceptions and Practices A/Prof Kiran Khush

11:30 3D Printing and Transplantation – Separating Fact From Fantasy Dr Jason Chuen

12:00 Intracutaneous Islet Cell Transplantation Prof Toby Coates

City Room 2

12:30–13:30 Lunch

Renal Transplant AC (RTAC) & Renal Allocation Working Group (RAWG)

Exhibition Hall N

City Suite 3/4

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Tuesday, March 24, 2020

13:30–15:00 PLENARY 5: Joint TSANZ/Xvivo Symposium

Perfusion and Donor Management Chairs:

13:30 Normothermic Machine Perfusion and Liver Machine Perfusion Prof Chris Watson

14:00 Kidney Machine Perfusion A/Prof Ina Jochmans

14:30 The Spanish Miracle in Organ Donation: Myth or Reality? A/Prof Marina Berenguer

Exhibition Hall M

15:00–15:25 Afternoon tea Exhibition Hall N

15:25–16:00 The Great Debate: Stem Cell Technology Will Make Organ Donation Redundant Within 10 Years Moderator:

Pro team: Prof Megan Levings and Dr Janina Kaczmarczyk

Con team: Prof Steve Alexander and Dr Melanie Wyld

Pro Team, speaker 1

Con Team, speaker 1

Pro Team, speaker 2

Con Team, speaker 2

Pro Team rebuttal (if required)

Con Team rebuttal (if required)

Exhibition Hall M

16:00 ASM Concludes

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TSANZ ASM, Adelaide March 22-24, 2020 Posters

Abstract — Poster — Exhibition Hall N

52 OPTIMISING A MOUSE MODEL OF RENAL ISCHEMIA REPERFUSION INJURY PEFANIS Aspasia, MCRAE Jennifer M, BONGONI Anjan K, IERINO Frank L, COWAN Peter J

53 COMPARISON OF IN VITRO SUPPRESSION OF CD4+CD25-T EFFECTOR CELL PROLIFERATION BY TH2-LIKE TREG AND NAIVE TREG USING A REFINED FLOW CYTOMETRY BASED ASSAY RAKESH Prateek, VERMA Nirupama, BEDI Sukhandeep, TRAN Giang, ROBINSON Catherine, HODGKINSON Suzanne, HALL Bruce

54 IN VIVO IDENTIFICATION OF GENES ASSOCIATED WITH KIDNEY GRAFT FIBROSIS MA Xiaoqian, LU Bo, CAO Qi, ZHAO Yuanfei, HU Min, YI Shounan, O'CONNELL Philip

55 ASSESSING CYTOMEGALOVIRUS IMMUNITY IN POST LUNG TRANSPLANT RECIPIENTS LI Jenny, GARDINER Brad, OATES Clare, LIN Jie, JALALI Sedigheh, CRISTIANO Yvonne, LEVVEY Bronwyn, BROOKS AG, SNELL GI, WESTALL GP, SULLIVAN LC

56 RENAL TRANSPLANT SCREENING FOR ADVANCED COLORECTAL NEOPLASIA IN THE WELLNESS CLINIC TAN Rachel Yi Ping, VAN DER JEUGD Jane , JUNEJA Rajiv, BARBARA Jeffrey

57 EFFECT OF DIET ON HUMAN ISLET FUNCTION CHEUNG Charmaine, Burns Heather, STOKES Rebecca, GUNTON Jenny

58 THE USE OF FREESTYLE LIBRE FLASH GLUCOSE MONITORING SYSTEM TO MONITOR BLOOD GLUCOSE LEVELS IN A DIABETIC PORCINE MODEL PENKO Daniella, NITSCHKE Jodie, JOHNSTON Julie, MATHEWS Loren, JOHNS Daniel, MUIRHEAD Robb, PULLAN Caitlin, DROGEMULLER Christopher, TORPY David, KUCHEL Timothy, COATES P. Toby H

59 IN VITRO ACTIVATION OF HUMAN CD4+CD25+CD127LO TREG SUBPOPULATIONS VERMA NIRUPAMA D, Al-Atiyah Ranje, TRAN GIANG, HODGKINSON SUZANNE J, HALL BRUCE M

60 CHARACTERISATION OF DONOR-DERIVED LYMPHOCYTES IN THE CIRCULATION OF LUNG-TRANSPLANT RECIPIENTS STANKOVIC Sanda, CHRISTIANO Yvonne, WESTALL Glen, LEVVEY Bronwyn, BROOKS Andrew, SNELL Gregory, SULLIVAN Lucy

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TSANZ ASM, Adelaide March 22-24, 2020 Posters

Abstract — Poster — Exhibition Hall N

61 USE OF HLA EPITOPES IN A VIRTUAL CROSSMATCH (VXM) TO BETTER ASSESS LUNG TRANSPLANT (LTX) COMPATIBILITY HIHO Steven, SULLIVAN Lucy, WESTALL Glen, SNELL Greg

62 EARLY CESSATION OF PATIENT CONTROLLED ANALGESIA (PCA) LAPAROSCOPIC DONOR NEPHRECTOMY KEOGH Kandice, LAWSON Malcolm , PRESTON John, Wood Simon, GRIFFIN Anthony, RHEE Handoo

63 DOES DONOR TERMINAL, ADMISSION OR BEST ESTIMATE GLOMERULAR FILTRATION RATE PREDICT KIDNEY TRANSPLANTATION OUTCOMES? IRISH Georgina Laura, COATES Toby, CLAYTON P A

64 INVESTIGATION OF FALSE POSITIVE LUMINEX RESULTS USING SURROGATE FLOW CROSSMATCHING DOWNING Jonathan, VUKOVIC Irena, SUTANTO Michael, WONG Zo-Ee, LE Cindy, DEY Jacqueline, HOGAN Jessie, DE SANTIS Dianne, MARTINEZ Patricia

65 UNDERSTANDING AND ATTITUDES TOWARD ACCEPTING AN INCREASED VIRAL RISK DONOR IN PATIENTS ACTIVE ON THE KIDNEY TRANSPLANT WAITING LIST KANSAL Arushi , DENDLE Claire, KANELLIS John, MULLEY William

66 T-CELL ADOPTIVE IMMUNOTHERAPY FOR BK NEPHROPATHY JAHAN Sadia, SCUDERI Carla, FRANCIS Leo, KHANNA Rajiv, JOHN George

67 TREATMENT OF SAPOVIRUS INFECTION IN A RENAL TRANSPLANT PATIENT JAHAN Sadia, SCUDERI Carla, FRANCIS Leo, KHANNA Rajiv, JOHN George

68 THE SURGICAL MANAGEMENT OF URETERIC COMPLICATIONS IN RENAL TRANSPLANTATION: A 10-YEAR REVIEW OF OUTCOMES AT A TERTIARY CENTRE. MYAT Lin Lin, MAY Stephen

69 SERIOUS INFECTIONS ARE COMMON AMONG HIV-INFECTED KIDNEY TRANSPLANT RECIPIENTS: A SINGLE-CENTRE EXPERIENCE HERON JE, GILLIN A, LEE F, JARDINE MJ, CHADBAN SJ, WYBURN K, GRACEY DM

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TSANZ ASM, Adelaide March 22-24, 2020 Posters

Abstract — Poster — Exhibition Hall N

70 MALAKOPLAKIA CAUSING DIARRHOEA AND WEIGHT LOSS IN A RENAL TRANSPLANT RECIPIENT ELLIOTT Rachel, MAJONI William, CAMPBELL Kirsty, KHAN Afaq

71 PREVALENCE OF AT1R ANTIBODY AMONG MALAYSIAN MULTI-ETHNIC KIDNEY TRANSPLANT RECIPIENTS JALALONMUHALI Maisarah, CAROLL Robert, DEAYTON Sue, EMERY Tim, HUMFREYS Ian, LIM Sue Jin, NG Kok Peng, LIM Soo Kun, COATES Toby

72 WITHDRAWN

73 BONE MINERAL DENSITY IN PAEDIATRIC KIDNEY TRANSPLANT RECIPIENTS HAWTHORNE Madeline, CRAIG Elizabeth, KENNEDY Sean

74 RENAL ALLOGRAFT TORSION AND PSEUDOANEURYSMS OF THE PANCREATIC ARTERY FOLLOWING SIMULTANEOUS PANCREAS-KIDNEY TRANSPLANTATION: A CASE REPORT TAN Sarah, TAN Rachel, CEHIC Gabrielle, WU Michael, KANELLIS John, BARBARA Jeffrey

75 COMPARISON OF THE EFFECT OF SINGLE VS DUAL ANTIPLATELET AGENTS ON POST-OPERATIVE HAEMORRHAGE AFTER RENAL TRANSPLANTATION: A SYSTEMATIC REVIEW AND META-ANALYSIS AGOSTINHO Nelson, LEE Taina, D'SOUZA Kenneth, YAO Jinna, LAM Susanna, HAMEED Ahmer, PULITANO Carlo, YUEN LAWRENCE, JOSEPH David Morris, QASABIAN Raffi, SANDROUSSI Charbel, CHADBAN Steven, YING Tracey, CELERMAJER David, PLEASS Henry, LAURENCE Jerome Martin

76 UTILISATION OF PERIOPERATIVE INTRAVENOUS FLUIDS IN DECEASED DONOR KIDNEY TRANSPLANTATION IN AUSTRALIA AND NEW ZEALAND: A CROSS-SECTIONAL SURVEY COLLINS Michael, REIDLINGER Donna, FAHIM Magid, HAWLEY Carmel, CHADBAN Steven

77 PARVOVIRUS B19 INDUCED DIABETES MELLITUS IN A RENAL TRANSPLANT RECIPIENT PARK Yeung Ae, CHOW Kevin V, MASTERSON Rosemary

78 MANAGING TUBERCULOSIS TRANSMISSION RISK TO EXPOSED KIDNEY TRANSPLANT RECIPIENTS LI Jennifer, GILROY Nicky, CHO Jin Gun, BAG S, ROGERS Natasha, CHAPMAN Jeremy Robert

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TSANZ ASM, Adelaide March 22-24, 2020 Posters

Abstract — Poster — Exhibition Hall N

79 ASSOCIATION BETWEEN SOCIOECONOMIC STATUS, PRE-EMPTIVE REPEAT TRANSPLANTATION AND MORTALITY POST KIDNEY ALLOGRAFT FAILURE WONG Yun Hui Sheryl, WONG Germaine, MCDONALD Stephen, CLAYTON Philip, JOHNSON David, HAWLEY Carmel, VIECELLI Andrea, PILMORE Helen, WALKER Rachael, ROBERTS Matthew, LOK Charmaine, POLKINGHORNE Kevan, BOUDVILLE Neil, LIM Wai Hon

80 INCIDENCE AND RISK FACTORS OF POLYOMAVIRUS (BK) INFECTION IN KIDNEY AND KIDNEY PANCREAS (SPK) TRANSPLANT RECIPIENTS ALLAN Lachlan, YAO Jinna, AMARATUNGA Rajith, PLEASS Henry, WONG Germaine

81 “HYPERACUTE” T CELL MEDIATED REJECTION (TCMR) OF A STABLE RENAL ALLOGRAFT FOLLOWING PD1 BLOCKADE FOR RECURRENT HEAD AND NECK SQUAMOUS CELL CARCINOMA (HNSCC) ROWLANDSON Matthew, TREVILLIAN Paul, MALLESARA Girish, FORMBY Mark, HARDSTAFF Ruth

82 VALIDATION OF PARENTHOOD EVENTS REPORTED TO AUSTRALIA AND NEW ZEALAND DIALYSIS AND TRANSPLANT (ANZDATA) REGISTRY WITH THE MULTI-JURISDICTIONAL PERINATAL DATA COLLECTIONS. HEWAWASAM Erandi, DAVIES Christopher, GULYANI Aarti, MCDONALD Stephen, CLAYTON Philip, JESUDASON Shilpanjali

83 MANAGEMENT OF TRANSPLANT KIDNEY AUTOLOGOUS SAPHENOUS VEIN GRAFT ANEURYSM HANLON Lucy, AGOSTINHO Nelson , HEWA-GEEGANAGE Shanika, LEE Taina, GILLIN Adrian, VERRAN Deborah, LAURENCE Jerome Martin

84 LIVE KIDNEY DONOR ALLOGRAFT LITHIASIS: A SYSTEMATIC REVIEW OF STONE RELATED MORBIDITY IN DONORS YAO Jinna, TOVMASSIAN David, LAU Howard, LEE Taina, ALLEN Richard, YUEN Lawrence, LAURENCE Jerome, PLEASS Henry

85 IMPACT OF KIDNEY TRANSPLANT TRAINING ON SECOND WARM ISCHAEMIA TIME AMARATUNGA RA, ALLAN L, YAO J, ROBERTSON P, KABLE K, ROGERS N, WONG G, ALLEN R, RYAN B, YUEN L, PLEASS H

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TSANZ ASM Program

38

TSANZ ASM, Adelaide March 22-24, 2020 Posters

Abstract — Poster — Exhibition Hall N

86 ANALYSING THE EFFECT OF A CLOSED INCISION NEGATIVE PRESSURE WOUND THERAPY (CINPWT) SYSTEM ON SURGICAL SITE INFECTIONS AND WOUND COMPLICATIONS IN KIDNEY TRANSPLANT RECIPIENTS. A PROPENSITY SCORE MATCHED ANALYSIS LAM Susanna, HUYNH Annie, LAURENCE Jerome

87 SELECTIVE URETERIC STENT INSERTION IN RENAL TRANSPLANT PATIENTS RANA Abdul Ahad, OLAKKENGIL Santosh, BHATTACHARJYA Shanthanu, RUSSELL Christine, DIAS Brendan

88 SPONTANEOUS RENAL ALLOGRAFT RUPTURE IN A PAIR OF DECEASED DONOR KIDNEYS: A CASE REPORT TOVMASSIAN David, YOON Peter, YAO Jinna, YUEN Lawrence, ALLEN Richard, LAURENCE Jerome, PLEASS Henry

89 OPTIMAL SURGICAL MANAGEMENT OF RENAL HYPERPARATHYROIDISM KRIGE AJ, BOCHNER MA, KOLLIAS J, WHITFIELD RJ, BINGHAM JMM

90 PRE-TRANSPLANTATION NATIVE NEPHRECTOMY IN POLYCYSTIC KIDNEY DISEASE: AN OVERVIEW OF INDICATIONS AND CASE REPORT. PERERA Dinushi, YAO Jinna, ALLAN Lachlan, PLEASS Henry

91 IMPACT OF PROLONGED COLD ISCHAEMIC TIME IN AN OVINE MODEL OF RENAL TRANSPLANTATION KRIGE AJ, JOHNSON JK, RUSSELL CH, PALMER LJ, COATES PTH

92 A BIOETHICAL ARGUMENT FOR INCREASING ABORIGINAL LIVING KIDNEY DONATION WEIGHTMAN Alison

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39

2020 ASM ACCEPTED ABSTRACTS

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SUNDAY, 22 March Free Communications1 RI and Organ Preservation

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IRI and Organ Preservation Abstract No. 1 EMPAGLIFLOZIN IMPROVES CARDIAC FUNCTIONAL RECOVERY OF DONOR HEARTS AFTER PROLONGED COLD ISCHAEMIA – AN ALTERNATIVE TO SODIUM-HYDROGEN EXCHANGE INHIBITION. VILLANUEVA JE1, GAO L1, SCHEUER SE1, DOYLE A1, JABBOUR A1,2, HICKS M1,3, MACDONALD PS1,2 1Transplantation Laboratory, Victor Chang Cardiac Research Institute, Sydney, 2Heart and Lung Clinic, St Vincent's Hospital, Sydney, 3Clinical Pharmacology, St Vincent's Hospital, Sydney Background: Donor heart scarcity has forced consideration of “marginal” donor hearts that have undergone prolonged cold ischaemia during transportation, despite increased susceptibility to ischaemia-reperfusion injury. Pre-clinical studies using sodium-hydrogen exchange inhibitors (NHEI) to supplement cardiac preservation solutions improves functional recovery but are not clinically used following neurotoxicity in clinical trials. One promising alternative is the sodium-glucose cotransporter 2 inhibitor Empagliflozin (Empa) - the first anti-diabetic drug with positive cardiovascular outcomes. Aim: To elucidate the cardioprotective potential of Empa-supplementation during cold preservation of donor hearts. Methods: Wistar rat (320-420g; n=5-7) hearts were perfused ex-vivo and baseline aortic flow (AF) and cardiac output (CO) measured. Hearts were arrested, stored in Celsior±0.3–10µM Empa, zoniporide (1µM) (6h, 4°C) then reperfused (37°C, Langendorff 15min, working 30min). Post-reperfusion AF and CO were expressed as percentage of baseline. Coronary effluent was assessed for lactate dehydrogenase (LDH) release. Results: Empa-supplemented donor hearts showed dose-dependent improved functional recovery. Compared to unsupplemented hearts, 10µM Empa-supplementation significantly improved AF (54±11% vs 10±7%, p=0.006) and CO (55±12 vs 16±8, p=0.03) recovery. Hearts supplemented with the NHEI zoniporide showed significantly improved AF (63±7%, p=0.002 vs control) and CO (65±9%, p=0.01) recovery. A trend for reduced LDH efflux was observed in hearts supplemented with 1-10µM Empa or zoniporide compared to controls. Conclusion: Cardiac supplementation with 10µM Empa during cold storage yields significantly improved functional recovery, with similar cardioprotective efficacy to zoniporide. Since Empa is approved for clinical use, this study highlights its potential as a suitable alternative for NHEI in donor heart preservation.

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SUNDAY, 22 March Free Communications1 RI and Organ Preservation

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Abstract No. 2 GASDERMIN-D MUTATION IS PROTECTIVE AGAINST RENAL ISCHEMIA REPERFUSION INJURY LI Jennifer1,2, ALEXANDER Stephen3, ROGERS Natasha1,4,5 1Centre for Transplant and Renal Research, Westmead Institute for Medical Research, Westmead, Sydney, 2School of Medicine, University of Sydney, 3Centre for Kidney Research, The Children's Hospital at Westmead, Sydney, 4Department of Renal Medicine, Westmead Hospital, Sydney, 5Department of Medicine, University of Sydney Background: Pyroptosis, a pro-inflammatory form of cell death, is dependent on membrane pore formation through the assembly of cleaved Gasdermin-D molecules. We hypothesized that this is important in the pathophysiology of ischemia-reperfusion injury (IRI). Aims: Examine the effects of Gasdermin-D mutation on inflammation in acute kidney injury. Methods: Male C57BL/6 mice were exposed to ethyl-N-nitrosourea mutagenesis, leading to an isoleucine to asparagine mutation (I105N) in the GasderminD gene. Chimeric mice were generated by whole body irradiation, followed by infusion of syngeneic donor bone marrow cells. Age- and gender-matched littermate control wild-type, heterozygous and homozygous GasderminDI105N mice and chimeric mice were subjected to bilateral renal IRI (36°C, 22mins). Mice were analyzed 24-hours post-reperfusion for renal function, histology and biomolecular phenotyping. Results: Homozygote and heterozygote GasderminDI105N mice were protected from renal IRI in a gene dose-dependent manner when compared to wild-type, demonstrating lower mean serum creatinine (15.7, 48.1 and 85.5µmol/L respectively, p<0.001), less histological tubular injury and cell death (1.8, 3.6 and 5.1 TUNEL+ cells/hpf, p<0.01) and decreased expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, RANTES). Chimer mice were checked for engraftment after 8 weeks. The susceptibility of GasderminDI105N chimeric mice (receiving wild-type donor bone marrow) to IRI was similar to that of wild-type controls, indicating that hematopoietic cells rather than parenchymal cells, are key drivers of injury. Conclusion: GasderminDI105N mice were protected from IRI and demonstrates the importance of the pyroptosis pathway on acute kidney injury. Manipulation of GasderminD is an attractive target to mitigate inflammation and cellular death following injury.

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SUNDAY, 22 March Free Communications1 RI and Organ Preservation

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Abstract No. 3 A RAT MODEL OF CARDIAC DONATION AFTER CIRCULATORY DEATH (DCD) GAO Ling1, DOYLE Aoife1, VILLANUEVA Jeanette1,2, SCHEUER Sarah1,2, HICKS Mark3,4, MACDONALD PS1,2,5 1Transplantation Laboratory, Victor Chang Cardiac Research Institute, Sydney, 2School of Medicine, University of New South Wales, Sydney, 3Department of Pharmacy, St Vincent's Hospital, Sydney, 4School of Medicine & Pharmacology, University of New South Wales, Sydney, 5Department of Cardiology, St Vincent's Hospital, Sydney Background: Organ donation after circulatory death (DCD) has increased over the last decade however concerns on the use of DCD hearts remain due to exposure to warm ischemic injury during stand-off period after withdrawal of life support (WLS). Aim: To develop a preclinical DCD rat model to investigate: 1) ischaemic damage to DCD hearts; and 2) cardioprotective effects of pharmacological conditioning strategies to improve DCD heart quality. Methods: Wistar rats (male, 340-420g, n=3-5) were anaesthetised and monitored continuously for pulse oximetry, ECG and blood pressure. WLS was initiated by tracheal ligation after i.v administration of heparin (500IU). Once pressure trace was absent, stand-off times of 10-, 15- and 20-min were observed. Hearts were retrieved, flushed with ice-cold Celsior (100ml) via aortic cannulation, and reperfused ex vivo for 1hr (Krebs-Heinsleit buffer, 37oC). Control sham hearts were retrieved without tracheal ligation and stand-off. The cardiac functional recovery during reperfusion was measured by cardiac output (CO), coronary flow (CF), heart rate (HR) and pulse pressure (PP). Coronary effluent was assessed for lactate dehydrogenase (LDH) release. Results: Compared to sham controls, all DCD hearts had significantly reduced cardiac functional recoveries (Table 1), closely correlated to increased stand-off time from 10 to 20min (p < 0.01). LDH release was significantly increased in DCD15 and DCD20 hearts (p < 0.05 vs sham and DCD10). Conclusions: This preclinical DCD model has established a platform for further investigation into ischaemia-reperfusion injury of DCD hearts and testing strategies to improve DCD heart quality to increase the donor heart pool. Group CO (M ± SE)

ml/min CF (M ± SE) ml/min

HR (M ± SE) bpm

PP (M ± SE) mmHg

Sham 63 ± 4.4** 20 ± 0.3* 238 ± 4# 45 ± 3.0** DCD10 39 ± 4.3* 18 ± 2.4* 223 ± 11# 34 ± 3.5* DCD15 19 ± 7.7 7.4 ± 2.4 172 ± 26 20 ± 3.6 DCD20 5.3 ± 2.0 3.9 ± 1.4 122 ± 30 16 ± 2.2 **P 0.05 vs others. * p < 0.05 vs DCD15 and DCD20. # p < 0.05 vs DCD20

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SUNDAY, 22 March Free Communications1 RI and Organ Preservation

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Abstract No. 4 A POINT MUTATION OF SHROOM3 PROMOTES CD206+ MACROPHAGE INFILTRATION AND KIDNEY FIBROSIS AFTER ISCHEMIA-REPERFUSION INJURY TANG Tianfeng1, LU Bo1, ROGERS Natasha1, ZHENG Guoping1, NICHOLSON Leigh1, CAO Qi1, MENON Madhav2, MURPHY Barbara2, ALEXANDER Stephen I3, HU Min1,3, O’CONNELL Philip J4 1Centre for Transplant and Renal Research, University of Sydney, 2Division of Nephrology, Mount Sinai School of Medicine, New York, 3Centre for Kidney Research, The Children's Hospital at Westmead, Sydney, 4Centre for Kidney Research, University of Sydney Introduction: A donor SHROOM3 SNP variant was identified with Kidney-transplant fibrosis in humans. Aim: Investigate the impact of a point mutation of SHROOM3 in kidney-injury and fibrosis in mouse IRI model. Methods: Both renal-pedicles were occluded for 25 mins at 36.5°C on C57BL/6-mice that were homozygous (C/C), heterozygous (T/C) or WT (T/T) at position 92,951,065 of SHROOM. Samples were assessed after 24h/4wks after IRI. Results and Discussion: After 24h-IRI, in male-mice, significantly higher serum-creatinine (SCr) and renal-injury grades were observed in all three-genotypes compared to shams (p<0.05). mRNA expression of SHROOM3/TNF-α/IL-6/IL-1β/Cxcl2/Ccl2 was increased in kidneys of CC-mice compared to shams and/or the other two-genotypes (p<0.05). In female-mice, SCr in three-genotypes was not significantly higher than shams suggesting female-mice were more resistant to ischemic-AKI than male-mice. Injury-grades of CT and CC-female-mice were higher than WT/shams (p<0.05). Increased SHROOM3/TNF-α/IL-6 mRNA levels were observed in CC-kidneys compared to shams (p<0.05). After 4wks, the kidneys of CC-mice in both sexes, had an increased infiltrate of F4/80+CD206+ macrophages and worse renal-fibrosis compared to Sham and/or WT-mice (p<0.05). The SCr had improved in both male/female mice. Whilst the SCr in all male-mice had returned to baseline, the SCr in CC female-mice remained higher than shams (p<0.05). Moreover, worse renal-fibrosis was also observed in CT -female-mice. Neutrophils (Ly6G+) and CD3+ cells were increased at 24h and 4wks in all-groups with no differences among three-genotypes. Conclusion: A point mutation of SHROOM3 is a risk genotype for renal fibrosis and this mutation appears to have greater effect in female mice. CD206+ macrophages play an important role on the process of fibrosis.

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SUNDAY, 22 March Free Communications 2 Organ Donation and Allocation#1

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Organ Donation and Allocation#1 Abstract No. 5 THE IMPACT OF DONOR TOBACCO AND MARIJUANA SMOKING HISTORY ON EARLY AND INTERMEDIATE-TERM LUNG TRANSPLANT OUTCOMES OKAHARA Shuji1,2, LEVVEY Bronwyn2,3, MCDONALD Mark4, D'COSTA Rohit5, OPDAM Helen6, PILCHER David1,7, SNELL Greg2,8 1Department of Epidemiology and Preventative Medicine, Monash University, Melbourne, 2Lung Transplant Service, Alfred Hospital, Melbourne, 3Faculty of Medicine, Nursing & Health Sciences, Monash University, Melbourne, 4Analytics and Technology, Organ and Tissue Authority, 5DonateLife Victoria, 6Organ and Tissue Authority, 7Department of Intensive Care, Alfred Hospital, Melbourne, 8Faculty of Medicine, Monash University, Melbourne Purpose: Donor tobacco and marijuana smoking are common in the lung donor pool, with both known to adversely affect post-lung transplant (LTx) outcomes. The intermediate survival outcomes and extent of the interactions of these smoking histories has not been described. Methods: DonateLife records and clinical databases were combined, with univariate and multivariate analyses undertaken to clarify the relation between donor tobacco and/or marijuana history and LTx outcomes. Results: Between 2014-2018, 304 LTx were performed from 296 donors, including: A) 140 (46%) never smokers; B) 114 (38%) tobacco-light smokers (=<20 pk years) ± marijuana-light smoker (=intermittent use < 5yrs); C) 16 (5.3%) tobacco-heavy smokers (>20pk years) ± marijuana-light smokers; D) 20 (6.6%) marijuana-heavy smokers (= daily use or > 5 yrs) + tobacco-light or heavy smokers (n=6 light marijuana only & n= 8 no data resulted not included) (Table 1). Donor smoking type, history and extent varied with donor age & gender. Smoking category adversely impacted 24hrPF ratio. Never smoker A) vs Combination D) were the only categories to show 3yr survival rate difference [P=0.02 by Logrank (Figure 1), Hazard Ratio: 3.00 (95%CI: 1.17-7.69), P=0.02 by Cox Regression, adjusted for LTx type, diagnosis, and extended donor]. Conclusion: A donor smoking history generally has only a small effect on early and later outcomes. Despite a significantly younger donor age, a combined heavy marijuana and tobacco usage history may have long term consequences that need to be balanced against the risk of no-transplant for an individual waiting list potential recipient. Table 1. Donor Tobacco & Marijuana Category & Recipient outcomes

Never (n = 140)

Tobacco-light ± Marijuana-light (n = 114)

Tobacco-heavy ± Marijuana-light (n = 16)

Tobacco-light/heavy + Marijuana-heavy (n = 20)

P-value

Donor characteristic

Age a (yrs) 45 45 52 33 <0.01

Gender; Male (%) 46 58 50 70 0.09

Recipient outcomes

PaO2/FIO2 ratio (T24) a 344 315 311 294 0.02

PGD grade 3 (%) 8 11 13 10 0.86

Mechanical ventilation b (hrs) 24 24 50 23 0.21

ICU stay b (days) 4.6 4.8 5.6 4.1 0.56

90-day mortality (%) 4 3 0 0 0.71

3-yr survival rate (95% CI)

0.92 (0.87-0.97)

0.81 (0.73-0.90)

0.85 (0.68-1.00)

0.57 (0.36-0.91) 0.04

a Mean value, b Median value

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SUNDAY, 22 March Free Communications 2 Organ Donation and Allocation#1

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Abstract No. 5 (cont) Figure 1. 3-yr survival curve by smoking category

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SUNDAY, 22 March Free Communications 2 Organ Donation and Allocation#1

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Abstract No. 6 PAEDAITRIC DECEASED DONOR KIDNEY TRANSPLANTATION IN AUSTRALIA: A 30 YEAR REVIEW. WHAT HAVE PAEDIATRIC BONUSES ACHIEVED AND WHERE TO FROM HERE? SYPEK Matthew P1,2,3,4, DAVIES Chris5, LE PAGE Amelia6, CLAYTON Phil7,3, HUGHES Peter1, LARKINS Nicholas8, WONG Germaine9,10, KAUSMAN Joshua Y2, MACKIE Fiona11 1Nephrology and Renal Transplant, Royal Melbourne Hospital, 2Nephrology and Renal Transplant, Royal Children's Hospital, Melbourne, 3ANZDATA, 4Department of Medicine, University of Melbourne, 5Statistics, ANZDATA, 6Nephrology and Renal Transplant, Monash Children's Hospital, 7Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 8Nephrology and Renal Transplant, Perth Children’s Hospital, 9Nephrology and Renal Transplant, Westmead Hospital, Sydney, 10Centre for Kidney Research, University of Sydney, 11National Transplantation Services, Sydney Children's Hospital AIMS: To review the trends in deceased donor transplantation for paediatric recipients, assess the impact of paediatric bonuses and identify outstanding areas of need for this population. METHODS: A registry-based study of all deceased donor kidney only transplants to recipients under the age of 18 years in Australia between 1989 and 2018 conducted using de-identified data. Six areas are reported on including: incidence and prevalence, transplant activity, access, donor characteristics, HLA matching, and patient and graft survival. Analysis was predominantly descriptive with summary statistics and transplant characteristics presented graphically to assess trends. Patient and graft survival across eras were assessed using the Kaplan Meier method. RESULTS: There have been an average of 20 deceased donor kidney transplants to paediatric recipients performed annually with a gradual increase in the last decade, reaching 27 in 2017. Paediatric candidates had consistently higher rates of transplantation and shorter time from dialysis initiation to transplantation compared with adult candidates. No disadvantage to adult recipients was seen following introduction of paediatric bonuses. Donors to paediatric recipients have more favourable characteristics that have improved in recent years, despite changes in the donor pool. HLA matching is poorer for paediatric recipients compared to adult recipients. Both patient and graft survival have improved for paediatric recipients in the most recent era CONCLUSIONS: The current allocation system provides rapid access to high quality deceased donors for paediatric recipients. Interventions at the level of organ allocation are required to improve immunological matching for this population group, while balancing the trade-off between wait-time and organ quality for young patients.

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SUNDAY, 22 March Free Communications 2 Organ Donation and Allocation#1

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Abstract No. 7 FREQUENCY AND OUTCOMES OF KIDNEY DONATION FROM INTENSIVE CARE PATIENTS WITH ACUTE KIDNEY INJURY REQUIRING RENAL REPLACEMENT THERAPY OPDAM Helen1,2, SANDERS Jo3, FURNISS Hayley3, HUGHES Peter4,5, KANELLIS John6,7, JONES Daryl2,8,9 1Organ and Tissue Authority, 2Department of Intensive Care, Austin Hospital, Melbourne, 3DonateLife Victoria, 4Department of Nephrology, Royal Melbourne Hospital, 5Department of Medicine, Royal Melbourne Hospital, 6Department of Nephrology, Monash Medical Centre, Melbourne, 7Department of Medicine, Monash Medical Centre, Melbourne, 8School of Public Health, Monash University, Melbourne, 9Department of Surgery, University of Melbourne BACKGROUND: Donor organ shortages limit access to kidney transplantation and there is a need to increase the donor pool. The presence of acute kidney injury (AKI) in deceased donors has traditionally been a relative contraindicate on to renal transplantation, even though renal recovery may be favourable in the absence of chronic renal disease. METHODS: We undertook an 8 years retrospective observational study of potential deceased organ donors with AKI requiring renal replacement therapy (RRT). We evaluated the rate of successful transplantation as well as short term and outcomes at a median of 19.5 (13.0-52.7) months after donation. RESULTS: Amongst 1058 consented potential organ donors, 39 patients had AKI requiring RRT, of which 19 became donors (13 not medically suitable, 7 did not proceed to donation). The median (interquartile range (IQR)) donor age was 41 (34-50) years. From the 38 donated kidneys 34 were transplanted. The median (IQR) age of recipients was 53 (42.8-58.5) years and they were dialysis free in a median (IQR) of 5.5 (2.3-10.8) days. Only minor abnormalities were found at 3 and 6 months renal biopsies, and two patients experienced graft failure in the first 12 months. CONCLUSIONS: Amongst deceased donors with AKI receiving RRT outcomes of renal transplantation seems acceptable in the absence of pre-existing renal failure and other donor co-morbidity. Such patients may be an important additional source of kidney donation.

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SUNDAY, 22 March Free Communications 2 Organ Donation and Allocation#1

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Abstract No. 8 SUSPECTED VS. VERIFIED MELANOMA IN NSW DECEASED ORGAN DONOR REFERRALS: A DATA-LINKAGE COHORT STUDY, 2010-2015 ROSALES Brenda Maria1,2,3, HEDLEY James1,2, DE LA MATA Nicole1,2, WALLER Karen1,2, O'LEARY Michael4, KELLY Patrick1,2, WYBURN Kate5,3, WEBSTER Angela1,2,6 1Centre for Organ Donor Evidence, University of Sydney, 2School of Public Health, University of Sydney, 3Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, 4NSW Organ and Tissue Donation Service, 5School of Medicine, University of Sydney, 6Centre for Transplant and Renal Research, Westmead Hospital, Sydney Introduction: Donor assessment is time-sensitive and medical history often relies on imperfect information by proxy. Misclassification of skin cancers at referral may lead to missed opportunities in organ donation. Aims: We sought to compare melanoma history suspected at referral with cancer registry records. Methods: We linked NSW deceased-donor referrals 2010-2015 from Organ and Tissue Donation Service (OTDS) with cancers reported in NSW Central Cancer Registry (CCR) 1976-2013, including in-situ cancers. We compared suspected melanoma in OTDS referrals and melanoma (C43), and unspecified malignant skin cancers (C44) in CCR, using ICD-10-AM, and estimated the sensitivity and specificity of referral logs. We cross tabulated against donation outcomes. Results: Of 2, 974 referrals, 25(31%) were suspected of melanoma. Of these, 8(32%) were verified as in situ melanoma (C43), but 17(68%) suspected melanoma had no matching CCR record. Twelve were declined for melanoma risk alone but could have safely donated. Additionally,13 referrals had verified melanomas not known by OTDS. Of these, 2 with in-situ superficial spreading melanoma donated at least one solid organ. (Figure 1) OTDS referral logs had poor sensitivity (38%) and positive predictive value (32%) for melanoma but high specificity and negative predictive value (99%). Conclusions: Cancer typology and histology results at time of donor referral would improve the cancer risk classification and potentially identify more opportunities for donation.

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SUNDAY, 22 March Free Communications 2 Organ Donation and Allocation#1

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Abstract No. 8 (cont) Figure 1: Organ donor referrals suspected and verified of melanoma in NSW 2010-2015 with donation outcomes.

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SUNDAY, 22 March Free Communications 2 Organ Donation and Allocation#1

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Abstract No. 9 EVALUATION OF THE HALIFASTER FLOW CYTOMETRIC CROSSMATCH FOR THE DETECTION OF DONOR SPECIFIC ANTIBODIES. DE SANTIS Dianne, SUTANTO Michael, HOGAN Jesse, DOWNING Jonathan, MARTINEZ Patricia, D'ORSOGNA Lloyd Department of Clinical Immunology, PathWest, Fiona Stanley Hospital The complement-dependent cytotoxicity crossmatch (CDCXM) is currently used in the donor allocation process. However, it lacks the ability to detect the presence of donor-specific antibodies that may be associated with graft outcomes. In this study, we evaluate the Halifaster FCXM method described by Liwski et al which is reported to reduce flow crossmatch time by ≥ 60%, conserve reagents and reduce the overall cost of flow crossmatching, all without compromising quality or sensitivity. A total of 291 T and B cell flow crossmatches were performed and assessed against the presence of donor specific antibodies detected at >2000 MFI for all loci using the LabScreen Single Antigen Bead assay (SAB). 45/291 (15.5%) T cell negative FCXM crossmatches observed in the absence of Class I DSA and 78/291 (26.8%) B cell negative FCXM crossmatches observed in the absence of Class I and/or II DSA. 213/291 (73.2%) T cell positive FCXM crossmatches observed in the presence of Class I DSA and 175/291 (60.1%) B cell positive FCXM crossmatches observed in the presence of Class I and/or II DSA. The remaining FCXM crossmatches were either false positive (FCXM positive, DSA negative) or false negative (FCXM negative, DSA positive). These results could be contributed to either antibodies directed to low expressing loci such as HLA-C, DQB1 or DPB1 or the incorrect assignment of DSA due to false positive reactions caused by denatured antigen on the beads. The results in this study confirmed that the FCXM provided better sensitivity to that of the current CDCXM.

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SUNDAY, 22 March Free Communications 3 Outcomes and Complications#1

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Outcomes and Complications#1 Abstract No. 10 CHOLECYSTITIS IN LUNG TRANSPLANTATION – A SINGLE CENTRE EXPERIENCE SLADDEN Timothy1,2,3, CHANDRASEGARAM Manju3, YERKOVICH Stephanie1, CHAMBERS Daniel1,2 1Queensland Centre for Pulmonary Transplantation and Vascular Disease, Prince Charles Hospital, Brisbane, 2School of Medicine, University of Queensland, Brisbane, 3Department of Surgery, Prince Charles Hospital, Brisbane Aims: Lung transplantation entails significant insult to the transplant recipient including ischaemic organ injury, cardio-pulmonary by-pass and immune suppression. Many of these processes have been demonstrated to predispose to the development of cholecystitis. Cholecystitis, especially acalculous cholecystitis, is associated with increased mortality and morbidity in ICU patients and is challenging to diagnose. We aimed to quantify the incidence and identify associations with various factors known to predispose to cholecystitis in the lung transplant population. Methods: From 2003 to 2018 all patients who underwent a lung transplant at The Prince Charles Hospital, Brisbane, were included in this study. Recipient clinical records were used to identify cases and collect demographic and clinical data along with histology results. Results: 415 Recipients underwent lung transplant over this period with recipients who previously underwent cholecystectomy (n=40) or underwent a combined liver, heart and lung transplant (n=7) excluded from analysis. 20 (5.4%) recipients developed acute cholecystitis post-transplant (see table). The incidence of cholecystitis was highest in the first 3 months post-transplant (n=9, 45%). In subgroup analysis of recipients with acute cholecystitis, first 3 months post-transplant compared to >3 months, recipeints were older (55.2 vs 46.8yrs; p=0.007) and had an increase incidence of gangrenous, perforated or ulcerated gall bladders on histology (56% vs 9%; p=0.049). Conclusions: Cholecystitis is a relatively common complication post-transplant and histologically more severe in the early post-transplant period. Clinicians should be aware of the possibility of occult cholecystitis in the transplant patient with undifferentiated sepsis or abdominal pain. Acute Cholecystitis (n=20) No Cholecystitis (n=368) P value Age (median, IQR) 52.6 (38.8 – 58.1) 47.5 (32.4 – 57.4) 0.55 Male Sex, n (%) 16 (80) 181 (54) 0.035 Reason for Tx, n (%) CF COPD IPF other

6 (33) 6 (33) 5 (28) 1 (6)

90 (34) 77 (30) 49 (19) 45 (17)

Onset post Tx (days)(median, IQR)

364 (60.5-1236) n/a

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SUNDAY, 22 March Free Communications 3 Outcomes and Complications#1

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Abstract No. 11 IMPULSE OSCILLOMETRY HOLDS PROMISE IN BRONCHIOLITIS OBLITERANS SYNDROME CROWHURST Thomas1,2,3, BUSSELL Lauren2, JOHNSTON Sonya2, YEO Aeneas1,2,3, YEUNG David3,4, EDWARDS Suzanne5, SNELL Gregory6, HOLMES Mark1,2,3, HOLMES-LIEW Chien-Li1,2,3 1SA Lung Transplant Service, Royal Adelaide Hospital, 2Department of Thoracic Medicine, Royal Adelaide Hospital, 3Discipline of Medicine, University of Adelaide, 4Department of Haematology, Royal Adelaide Hospital, 5Adelaide Health Technology Assessment, University of Adelaide, 6Lung Transplant Service, Alfred Hospital, Melbourne Introduction: Bronchiolitis obliterans syndrome (BOS) is a major limitation in lung transplantation and is characterised by fibrotic obstruction of small airways. Spirometry is used to monitor for BOS. Impulse oscillometry (IOS) may add value given its sensitivity for small airway obstruction. We hypothesised (a) BOS will cause predictable abnormalities in IOS and (b) IOS will identify BOS before spirometry. Methods: We performed a prospective longitudinal diagnostic study on a consecutive sample of adult bilateral lung transplant recipients. Patients with non-BOS causes of allograft dysfunction were excluded. Linear mixed-effects models and Pearson correlation coefficients were used to test associations between spirometric and IOS parameters. Univariate binary logistic regression models were used to assess the value of IOS parameters in predicting the development or worsening of BOS, with spirometry as the comparator. Ethics approval and prospective registration were completed. Results: This interim analysis includes 232 tests on 62 patients, with new or worsened BOS observed on 15 occasions. Linear mixed-effects models showed IOS parameters (resistance at 5 Hz [R5] and reactance at 5 Hz [X5]) were associated with FEV1, both as static and dynamic values (p<0.05). Pearson correlation coefficients demonstrated moderately strong statistically significant associations between R5 and FEV1 (r=-0.54) and X5 and FEV1 (r=0.70). Neither IOS nor spirometry demonstrated predictive value in foretelling the development or worsening of BOS. Conclusion: IOS correlates closely with spirometry in BOS. This interim analysis is underpowered to assess the value of IOS in predicting new or worsening BOS. Data collection is continuing to address this.

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SUNDAY, 22 March Free Communications 3 Outcomes and Complications#1

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Abstract No. 12 IS TIMING REALLY EVERYTHING? WARM ISCHEMIC DEFINITIONS AND OUTCOMES FOR CARDIAC ALLOGRAFTS IN DCD WITHDRAWALS SCHEUER Sarah Elizabeth1,2, CHEW Hong Chee1, SOTO Claudio1, HICKS Mark3, GAO Ling2, VILLANUEVA Jeanette2, KAWANISHI Yujiro1, WATSON Alasdair1, CONNELLAN Mark1, GRANGER Emily1, JANSZ Paul1, MACDONALD Peter1,2 1Department of Heart and Lung Transplantation, St Vincent's Hospital, Sydney, 2Transplantation Laboratory, Victor Chang Cardiac Research Institute, Sydney, 3Department of Pharmacology, St Vincent's Hospital, Sydney Aims. DCD heart transplantation is now established with >130 performed worldwide, and excellent early and mid-term results. However, definitions of functional warm ischemic time (WIT) remain contentious and variable. This study investigated the relationship between these various definitions and cutoffs and early graft function in a high volume single-center cohort. Methods. Thirty-five heart transplants from DCD donors were performed at a single-center (July 2014-October 2019), and 13 DCD allografts instrumented onto the ex-situ perfusion device but not implanted due to poor recovery. Forty of the 48 donor files from the local database contained complete end-of-life withdrawal data, and were utilized for analysis. Transplanted donors were grouped into those that did (n=9) or did not (n=21) require peri-operative ECMO support, indicative of severe primary graft dysfunction (sPGD). Results. Despite concerns regarding the WIT DCD allografts are exposed to during withdrawal of life support (WLS), a longer WIT according to any of the current or proposed definitions (see Table 1) was not associated with sPGD or the decline of the organ in our cohort. A longer duration from WLS to circulatory arrest (CAr), systolic <90mmHg to CAr, and O2 saturations <70% to CAr was associated with a significantly lower rate of sPGD (see Table 1). Only a prolonged period between CAr and delivery of preservation flush, asystolic WIT (aWIT) was associated with increased risk for sPGD (see Table 1). Conclusions. These findings should provoke renewed discussions regarding current WIT definitions, and an increased focus on minimization of aWIT during DCD allograft retrievals. Table 1: Relationship between proposed significant periods during WLS, early graft function and utilization of cardiac allografts.

Time period (min) sPGD No sPGD Non-utilized WLS – CAr 7.9 ± 2.1 12.3 ± 4.7** 13.9 ± 6.2** BP < 90 – CAr 2.8 ± 2.3 6.3 ± 3.9** 6.7 ± 3.8** O2 Sats < 70% – CAr 6.0 ± 1.7 9.6 ± 4.2** 10.8 ± 6.1* aWIT 14.8 ± 2.8 11.9 ± 2.3** 12.2 ± 2.6*

*p<0.05, versus allografts where there was sPGD in the recipient; **p<0.01, versus allografts where there was sPGD in the recipient. Significance determined using paired t-tests.

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SUNDAY, 22 March Free Communications 3 Outcomes and Complications#1

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Abstract No. 13 DUPLEX ULTRASOUND AS A SCREENING TOOL FOR TRANSPLANT RENAL ARTERY STENOSIS CORBETT Matthew1, LAURENCE Jerome2,1,3, ALLEN Richard2, MEYBODI Farid2 1University of Sydney, 2Westmead Hospital, Sydney, 3Royal Prince Alfred Hospital, Sydney Aims – Duplex ultrasound (DUS) is often used as a screening tool for transplant renal artery stenosis (TRAS). However, the DUS diagnostic criteria for TRAS are not well validated against long-term clinical outcomes. There is no reliable diagnostic gold standard for this scenario. Methods – A retrospective analysis of consecutive renal transplant recipients at RPA from 2003-2009 was performed, including analysis of routine post-transplant DUS, performed at approximately 6 weeks post transplant. Long-term outcome data was extracted from ANZDATA in December 2015. Results – Based on a peak systolic velocity (PSV) >260cm/s, TRAS was identified in 22% (94/419) of recipients. The median follow-up was 3261 days. Intervention was performed in 4%(17/419) of recipients on clinical grounds. There was no difference in graft survival between the TRAS and non-TRAS groups (Hazard Ratio =0.781 95%CI 0.51-1.21 p = 0.27). Creatinine was measured up to 10 years post transplant (Figure 1) and there was no difference between the TRAS and non TRAS groups at any time point (p = >0.359). Conclusions – TRAS diagnosed by routine DUS using these diagnostic criteria does not identify a group of patients at greater risk of graft loss or inferior graft function. The utility of screening for TRAS is low, but may provide a valuable baseline. It may be reasonable to use DUS directed only by clinical findings suggestive of TRAS, which might indicate intervention if TRAS were diagnosed. Abstract No. 14 ANTIPLATELET AGENTS FOR CHRONIC KIDNEY DISEASE: AN UPDATED COCHRANE REVIEW NATALE Patrizia1,2,3, PALMER Suetonia C4,5, SAGLIMBENE Valeria M1,3, RUOSPO Marinella1,3, RAZAVIAN Mona6, CRAIG Jonathan C7, JARDINE Meg J6, WEBSTER Angela C1,8, STRIPPOLI Giovanni FM1,9,3 1School of Public Health, University of Sydney, 2Centre for Kidney Research, Westmead Millennium Institute, Westmead Hospital, Sydney, 3Department of Emergency and Organ Transplantation, University of Bari, 4Department of Medicine, University of Otago, 5University of Otago,, 6Renal and Metabolic Division, George Institute for Global Health, Camperdown, 7College of Medicine and Public Health, Flinders University, Adelaide, 8Cochrane Renal Group, Westmead Millennium Institute, Westmead Hospital, Sydney, 9Cohrane Kidney and Transplant, Westmead Hospital, Sydney Background: Antiplatelet agents are widely used to prevent cardiovascular events. The risks and benefits of antiplatelet treatment may be different in people with chronic kidney disease (CKD) for whom occlusive atherosclerotic events are less prevalent, and bleeding hazards might be increased. As several recent trials have reported, we updated the Cochrane review evaluating the effects of antiplatelet treatment for the prevention of cardiovascular and adverse kidney outcomes in individuals with CKD. Methods: We selected randomised controlled trials of any antiplatelet treatment versus placebo or no treatment, or direct head-to-head antiplatelet agent studies in people with CKD. Treatment effects were estimated by random-effects meta-analysis. Evidence certainty was adjudicated using GRADE methodology. Results: 110 studies (52424 participants) were included. Risk of bias was generally high or unclear. Antiplatelet agents probably reduce the risk of myocardial infarction (RR 0.87, 95% CI 0.76 to 0.99; moderate certainty evidence) and increase major bleeding (RR 1.35, 95% CI 1.10 to 1.65; moderate certainty evidence), and may increase the risk of minor bleeding in CKD and haemodialysis patients (RR 1.55, 95% CI 1.27 to 1.90; low certainty evidence). Limited data were available for direct head-to-head comparisons of antiplatelet drugs. Conclusions: Antiplatelet agents probably reduce myocardial infarction and increase major bleeding, and may increase minor bleeding in CKD and haemodialysis patients. The treatment effect of direct head-to-head comparisons of antiplatelet drugs is very uncertain an rarely reported.

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MONDAY, 23 March Free Communications 4 Immunobiology

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Immunobiology Abstract No. 15 GENERATION OF STABLE HUMAN INDUCED REGULATORY T-CELLS USING LOW-DOSE RAPAMYCIN KIM Juewan1, HOPE Christopher2,3, SCAFFIDI Jacqueline1, CARROLL Robert4,5, BARRY Simon2,3, COATES Toby4,5 1Department of Molecular and Biomedical Science, University of Adelaide, 2Department of Gastroenterology, Women's and Children's Hospital,Adelaide, 3Molecular Immunology Group, University of Adelaide, 4Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 5Discipline of Medicine, University of Adelaide Introduction: Induced Tregs (iTregs) provide an attractive avenue for Treg therapy in transplantation. It has recently been shown mTOR-regulated glycolysis is important for iTreg-differentiation. In previously published protocols, generation of stable iTregs has not been achieved and high-dose rapamycin was utilised. Here, for the first time, we optimised an iTreg-differentiation protocol using low-dose rapamycin to generate stable human iTregs. Method: Using varied concentrations of rapamycin (1-100 ng/mL) for iTreg-differentiation, glycolytic activity was assessed by measuring ECAR (extracellular acidification rate) and CD25 and FOXP3 expression were evaluated. The stability of iTregs differentiated with 1ng/mL rapamycin, TGF-β and retinoic acid was further assessed by measuring CD25 and FOXP3 expression without IL-2, with Th17-polarizing cytokines and upon re-stimulation. Moreover, expression of Th17-signature genes was assessed, and function of iTregs was evaluated by suppression assay. Results: With 10 and 100 ng/mL rapamycin, ECAR measurements of iTregs were significantly reduced compared with nTregs, whereas with 1 ng/mL, iTregs showed intermediate ECAR readings between nTregs and iTregs differentiated with 10 and 100 ng/mL rapamycin. iTregs differentiated with 1 ng/mL rapamycin displayed higher CD25 and FOXP3 MFI than with 10 and 100 ng/mL rapamycin. iTregs differentiated with 1 ng/mL rapamycin remained >98% CD25+FOXP3+ without IL-2 and with Th17-polarizing cytokines, with no up-regulation of Th17-signature genes, RORC and IL17A. Furthermore, these iTregs remained >98% CD25+FOXP3+ and highly suppressive upon re-stimulation. Conclusion: We showed that 1 ng/mL rapamycin partially inhibits glycolysis and produces iTregs which are phenotypically and functionally stable, demonstrating therapeutic potentials of iTregs generated with low-dose rapamycin.

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MONDAY, 23 March Free Communications 4 Immunobiology

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Abstract No. 16 IDENTIFICATION OF A NOVEL SUBSET OF XENO-ANTIGEN SPECIFIC MEMORY CD4+FOXP3+TREGS IN ISLET-XENOTRANSPLANT TOLERANCE NICHOLSON Leigh1, ZHAO Yuanfei1, QIAN Yi Wen1, TANG SooLing1, CHEW Yi Vee1, BURNS Heather1, ZHANG Geoff2, YI Shounan1, ROGERS Natasha1, HAWTHORNE Wayne1, ALEXANDER Steve2, O'CONNELL Philip1, HU Min1 1Centre for Transplant and Renal Research, Westmead Institute for Medical Research, 2Centre for Kidney Research, The Children's Hospital at Westmead, Sydney Background: Blockade of the B7-CD28 and CD40-CD154 pathways induces tolerance towards porcine-islet-cell-cluster (NICC) xenografts in mice. Aims: 1) Investigate CD4+Foxp3+Tregs in mouse-model of NICC xenograft-tolerance, 2) identify in situ immune-cell subtypes using imaging mass cytometry (IMC) and 3) assess the function of these Foxp3+Tregs Methods: C57BL/6-DEREG-mice with diphtheria-toxin(DT)-receptor/GFP attached to Foxp3-gene were transplanted with NICC under renal-capsule. Recipient-mice received CTLA-4-Fc and MR-1 mAb. Foxp3+Tregs were depleted by DT from day 3-17 (induction-phase), or 80-100 days post-transplantation (maintenance-phase). NICC-xenograft function determined by insulin/glucagon staining and serum porcine-c-peptide concentration. A 28-antibody panel for IMC was used to identify in situ cells and a bioinformatics pipeline was created for data analysis. Results: More CD4+Foxp3+Tregs were seen in NICC-xenografts of treated mice on day-8 and 100 than day-20. Foxp3+ cells increased significantly in the draining-lymph-nodes of treated mice on day-8 (P=0.0010) and 100 (P=0.0128) when compared to the untreated/rejecting groups. CD4+Foxp3+Treg depletion during induction- or maintenance-phase led to rapid xenograft rejection. CD4+Foxp3+Tregs from lymphoid-organs of graft-tolerant DEREG-mice showed a significant increase in CD127, downregulated CD25, and reduced CD27 and CD62L expression compared to naïve/rejecting xenografts. IMC successfully quantified in situ immune-cell subsets (Fig.1), showing increased CD4+CD25-Foxp3+Tregs in tolerant compared to rejecting grafts, and localized within grafts at day-20. CD127+hiCD25+/lowCD44+hiCD62L-CD27-CD4+Foxp3+Tregs were transferred to NICC-transplanted Rag-\- mice and had a greater suppressive capacity than naïve-Tregs. Conclusion: Foxp3+Tregs are essential for NICC-xenograft survival in this model. Importantly, CD127+hiCD44+hiCD62L-CD27-CD25+/lowCD4+Foxp3+Tregs were a subpopulation of Tregs that showed features of antigen-specific memory.

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Abstract No. 17 COMBINATIONAL THERAPY WITH POST-TRANSPLANT CYCLOPHOSPHAMIDE AND THE P2X7 ANTAGONIST BRILLIANT BLUE-G REDUCES LIVER DISEASE IN A HUMANISED MOUSE MODEL OF GRAFT-VERSUS-HOST DISEASE CUTHBERTSON Peter1,2, ADHIKARY Sam1,2, SLUYTER Ronald1,2, WATSON Debbie1,2 1Illawarra Health and Medical Research Institute, University of Wollongong, 2Molecular Horizons and School of Chemistry and Molecular Bioscience, University of Wollongong Background: Graft-versus-host disease (GVHD) is a severe and often lethal complication arising following allogenic haematopoietic stem cell transplantation. We have previously shown that treatment with post-transplant cyclophosphamide (PTCy) significantly reduces clinical signs of GVHD and extends survival in humanised mice. However, this treatment reduces regulatory T cells (Tregs). We have also demonstrated that the P2X7 antagonist Brilliant Blue G (BBG) preserves Tregs and reduces clinical disease in humanised mice. Aim: To investigate the combination treatment of PTCy with BBG in a humanised NOD-scid IL2Rγnull (NSG) mouse model of GVHD. Methods: NSG mice were injected i.p. with 20 x 106 hPBMC (day 0). Mice were injected (i.p.) with BBG (50 mg/kg) or saline (day 0-10) and cyclophosphamide (33 mg/kg) (day 3/4). Mice were monitored for clinical GVHD for 3 or 10 weeks. Human cell engraftment was examined by flow cytometry, and tissue damage via histology. Results: Combination treatment with PTCy/BBG did not impact engraftment of human immune cells in NSG mice. Humanised mice treated with PTCy/BBG show slightly prolonged survival, decreased weight loss and clinical score, compared to PTCy alone. Treatment with BBG/PTCy shows increased Tregs compared to PTCy alone at day 21 (P=0.08), however there was no difference in Tregs at endpoint (P=0.75). Finally, combination treatment with PTCy/BBG significantly reduced histological disease in the liver and skin at endpoint. Conclusion: This study shows combination treatment with BBG/PTCy reduces disease severity in the liver and skin; however this did not significantly improve survival in this model, compared to PTCy alone. Abstract No. 18 PHOSPHOLIPASE A2 RECEPTOR CAR T CELLS LOCALISE TO THE KIDNEY SHAW Karli1, WANG Yuan Min1, HU Min2, KARUNIA Jevin1, ZHANG Geoff1, CAO Qi2, LU Bo2, MCCARTHY Hugh1, HARRIS David2, ALEXANDER Stephen1 1Centre for Kidney Research, The Children's Hospital at Westmead, Sydney, 2Centre for Transplant and Renal Research, Westmead Millennium Institute, Westmead Hospital, Sydney Background: Idiopathic Membranous nephropathy is a leading cause of autoimmune renal disease driven in many cases by the cognate antigen M-type phospholipase A2 receptor (PLA2R) expressed on podocytes. Chimeric antigen receptors (CAR) T cells use antibody fragments to direct T cells to specific antigens, and have achieved clinical success in cancer. The strategy can be translated to use PLA2R targeting to direct Tregs to the kidney. Aims: We aim to develop CAR T cells directed towards PLA2R using a PLA2R-specific monoclonal antibody which targets human, mouse and rat kidneys. Method: Mice were immunized with PLA2R peptides to produce monoclonal antibodies (mAb) against PLA2R. Hybridomas were established, screened, and sequenced for use in making the single-chain variable fragment (ScFv). The PLA2R-CAR plasmid was transformed in competent E. coli cells for DNA extraction, and transformed in GP2-293 cell line. CD4+ T cells from mice spleen were stimulated then transduced with packaged PLA2R-CAR cells, sorted and injected into mice. Results: Human expression of the M-type PLA2R in podocytes was confirmed in vitro and identified in anti-PLA2R mAb mouse sera of immunized mice, and sequenced for the mAb hybridoma. PLA2R-CAR plasmid and CD4+ CAR-T cells were successfully generated and injected into mice. PLA2R CAR-T cells were confirmed in circulation by flow cytometry and in kidneys by immunofluorescent staining. We identified more PLA2R CAR-T cells infiltrating kidney than control CAR-T cells. Conclusion: We have developed PLA2R-CAR-T cells against a podocyte target antigen in membranous nephritis. CD4 T cells expressing a CAR construct containing a scFv targeted at PLA2R preferentially targeting kidney has been demonstrated.

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Abstract No. 19 IL-4 REGULATES SECRETION OF THE IMMUNOMODULATORY CYTOKINE IL-10 BY HUMAN B CELLS PERKINS Griffith1, HURTADO Plinio2,3, COATES P. Toby2,3 1School of Biological Sciences, University of Adelaide, 2Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 3School of Medicine, University of Adelaide Background: B-cells can secrete IL-10, and in humans, they do so predominantly in response to unmethylated CpGB DNA and CD40 ligation. The physiological function of this response is unclear. However, it is highly predictive of kidney transplant outcome suggesting a suppressive role in immune homeostasis, as has been demonstrated in mice. Aim: To identify and investigate conditions which regulate B-cell IL-10 secretion in response to CpGB and CD40L. Methods: Purified human B-cells (>97%) were cultured with CpGB and rhCD40L-expressing NIH3T3 cells to stimulate IL-10 production, and the effect of twenty known immunomodulatory factors on IL-10 secretion was assessed by ELISpot and ELISA. IL-4 was further investigated as a regulator of the B-cell IL-10 response by cytokine bead array, intracellular flow cytometry, and using a B-cell-derived NF-kB reporter cell line (Ramos Blue). Results: Seven factors were identified as putative regulators of IL-10 secretion in response to CpGB and CD40L. Amongst these, IL-4 decreased IL-10 concentrations in supernatant by >80% (p<0.05) after 24 hours. This effect was selective for IL-10; TNFα and IL-6 concentrations increased, and no decrease was observed in CpGB-induced NF-kB activity, nor induction of activation markers CD40, CD69, CD80, and CD86. Production of IL-10 protein was unaffected. Conclusion: IL-4 has been studied for its effects on B-cells since its discovery as ‘B-cell growth factor-1’ in 1982. We show for the first time that IL-4 alters the inflammatory profile of human B-cells by inhibiting IL-10 secretion in response to CpGB and CD40L. Implications for the anti-graft response will be discussed.

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MONDAY, 23 March Free Communications 5 Organ Donation and Allocation#2

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Organ Donation and Allocation#2 Abstract No. 20 COMMONLY USED CRITERIA TO INITIATE EX-VIVO LUNG PERFUSION (EVLP) HAVE NO SIGNIFICANT IMPACT ON EARLY POST LUNG TRANSPLANT (LTX) SURVIVAL OKAHARA Shuji1,2, LEVVEY Bronwyn2,3, MCDONALD Mark4, D'COSTA Rohit5, OPDAM Helen6, PILCHER David1,7, SNELL Greg2,8 1Department of Epidemiology and Preventative Medicine, Monash University, Melbourne, 2Lung Transplant Service, Alfred Hospital, Melbourne, 3Faculty of Medicine, Nursing & Health Sciences, Monash University, Melbourne, 4Analytics and Technology, Organ and Tissue Authority, 5DonateLife Victoria, 6Organ and Tissue Authority, 7Department of Intensive Care, Alfred Hospital, Melbourne, 8Faculty of Medicine, Monash University, Melbourne Purpose: Ex-vivo lung perfusion (EVLP) is a complex, expensive assessment tool suggested to predict successful early graft function and therefore which ‘extended’ lungs should be used. Theoretic ‘graft at-risk’ criteria for EVLP initiation used in EVLP trials include: donor age>55yrs, PaO2/FIO2 (PF) <300, abnormal chest X ray, aspiration, >10 units transfusion, DCD, expected graft ischemia time (GIT) >6hrs. Our centre routinely uses extended donor lungs without EVLP. Methods: DonateLife records and clinical databases were combined. Univariate and multivariate analyses were undertaken to clarify the relationship between EVLP initiation criteria and lung-transplant (LTx) outcomes. Results: 304 LTx were performed 2014 to 2018 from 704 donor referrals (=42% conversion rate, =11.3 LTx per million population, cf US = 7.0 LTx PMP). 69% of LTx used donor lungs with >1 criterion for EVLP assessment (25% = 2, 5.2% = >3 criteria). Table 1 outlines the incidence and effect of these criteria. A PF <300 and GIT >6hrs had small effects on outcomes <90dys. Multivariate analyses noted no donor criteria association with PGD3. Mechanical ventilation hours are associated with type of LTx and recipient’s diagnosis (Table 2). Conclusion: At least 1 recommended criterion for EVLP initiation was present in the majority of LTx donors. These did not predict early outcomes- with very acceptable results overall. However, the relevance of combination or extreme criteria in donor lungs not used is unknown. Based on this study, the true utility of EVLP to enhance LTx acceptability and success rates, beyond good clinical management alone, requires an RCT. Table 1. EVLP criteria & Recipient early outcomes Donor characteristics N PaO2/FIO2

ratio (T24) a PGD grade 3 (%)

Mechanical ventilation b (hrs)

ICU stay b (days)

90-day mortality (%)

Age < 55-yr-old 208 331 8 24 4.6 2.4 ≥ 55-yr-old 96 320 11 27 4.9 4.2

Last PaO2/FIO2 ≥ 300 281 331 9 24 4.6 2.1 < 300 23 284 * 13 25 7.4 13.0 †

Chest radiograph findings

Clear 189 329 9 22 4.6 2.4 Abnormal 115 326 11 28 5.6 * 4.3

History of aspiration - 207 322 9 24 4.8 4.3 + 97 340 9 24 4.5 0 *

Multiple blood transfusion

≤ 10unit 266 330 10 26 4.7 3.4 > 10unit 38 311 5 21 4.6 0

DBD or DCD DBD 205 332 9 24 4.7 2.9 DCD 99 319 9 24 4.8 3.0

Extended ischemia time ≤ 6hrs 260 331 9 24 4.6 1.9 > 6hrs 44 309 11 33 5.6 9.1 †

Typical EVLP criteria 1) PaO2/FIO2, 2) CXR, 3) Transfusion, 4) DCD, 5) Ischemia time

None 94 343 7 21 3.9 1.1

≥ 1 210 321 10 26 5.0 † 3.8

a Mean value, b Median value * p<0.05, † p<0.01

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MONDAY, 23 March Free Communications 5 Organ Donation and Allocation#2

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Table 2. Multivariate analysis of freedom from mechanical ventilation Hazard ratio 95%CI P value

Donor variables

Age ≥ 55-yr-old 0.96 0.73-1.27 0.97

Last P/F ratio < 300 0.68 0.41-1.13 0.14

CXR; Abnormal 0.81 0.64-1.02 0.08

History of aspiration 0.90 0.70-1.16 0.42

Blood transfusion >10U 1.23 0.88-1.71 0.23

DCD 0.96 0.73-1.28 0.79

Ischemia Time > 6hr 0.73 0.50-1.06 0.10

Sex; M 1.13 0.86-1.47 0.39

Donor smoking >20 pack*year 0.85 0.52-1.39 0.51

Recipient

Age (per 1-yr-old) 1.00 0.99-1.01 0.55

Sex; M 1.21 0.91-1.59 0.18

Diagnosis; Pulmonary hypertension or Chronic lung allograft dysfunction

0.40 0.28-0.57 <0.001

Operation

Procedure; Single lung transplant 1.79 1.25-2.57 <0.01 By the proportional subdistribution hazards regression model

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Abstract No. 21 COUNTRY RANKING FOR DECEASED DONATION PERFORMANCE VARIES DRAMATICALLY DEPENDING ON THE METRIC USED OPDAM Helen1,2, MCDONALD Mark1, GOODWIN Melissa1, BARRY Lucinda1 1Organ and Tissue Authority, 2Department of Intensive Care, Austin Hospital, Melbourne BACKGROUND: Deceased donation performance by country is commonly reported internationally as deceased donors per million living population (pmp). This metric has acceptance due to its long history of use but is limited for reasons including inconsistent donor definitions between countries, some countries having a high proportion of ‘donors’ from whom no organs are transplanted, and that living population is not well related to the deceased donor pool. METHODS: Measures for deceased donation performance were identified through a review of the literature and by accessing publicly available reports and websites of donation and transplantation organizations. These measures included deceased donors pmp, transplants from deceased donors pmp and number of deceased donors per 10,000 deaths. Data for these elements were obtained from publicly available sources and rates deduced, including for the number of transplants from deceased donors per 10,000 deaths. Countries were ranked according to each of these metrics. RESULTS: Using data available from 2017 and 2018, Australia ranked variably depending on the metric used, from 15th place internationally using the metric of deceased donors pmp to 3rd place when using organ transplants from deceased donors per 10000 deaths. In addition, the proportionate difference between Australia and top performing countries was less when using deaths as a denominator as compared with living population. CONCLUSIONS: The ranking of countries and magnitude of difference in performance varies according to the metric used. Australia ranks highly in metrics using deaths rather than living population in the denominator. Figure. Country ranking according for 4 different metrics for deceased donation and transplantation

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MONDAY, 23 March Free Communications 5 Organ Donation and Allocation#2

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Abstract No. 22 INTERNATIONAL TRAVEL FOR OVERSEAS TRANSPLANTATION: A SURVEY OF AUSTRALIAN AND NEW ZEALAND CLINICIANS SMITH Georgia1, GUJARI Diba2, RUSSELL Oscar1, PALMER Lyle2, TOEWS Maeghan3, WONG Germaine4, LIM Wai5, MCDONALD Stephen2, CLAYTON Phillip1,6, CROSS Nick7,8, DITTMER Ian9, MARTIN Dominique10, COATES Patrick T1,2 1Royal Adelaide Hospital, 2University of Adelaide, University of Adelaide, 3Adelaide Law School, 4Westmead Hospital, Sydney, 5Sir Charles Gairdner Hospital, Perth, 6ANZDATA, 7Chistchurch Hospital, 8Otago University, 9Aukland District Health Board, 10Deakin University Aims To obtain information from Australian and New Zealand clinicians involved in the care of individuals that have travelled internationally for organ transplantation (ITOT). Methods: Descriptive survey distributed to all registered (n=540) Australian and New Zealand nephrologists, transplant physicians and surgeons via the Transplantation Society of Australia and New Zealand (TSANZ) and the Australia and New Zealand Society of Nephrology (ANZSN). The primary outcome was information provided by clinicians regarding individuals who had considered or engaged in ITOT. Secondary outcomes included descriptive details of the characteristics and the complications of Australians and New Zealanders involved in ITOT and a comparison of our data with data derived from the ANZDATA registry. This data includes New Zealand physicians, building on data published in 2019 where the survey was completed by Australian physicians only. Results: The response rate was 41.1%. A majority (67%, n=133) of responding practitioners reported having discussed ITOT with at least one patient, and 52.2% (n=129) practitioners reported having cared for at least one patient following ITOT. 129 cases were reported by Australian respondents and 26 by New Zealand respondents between 1980 and 2018, with China (31%) the most frequent destination reported from both countries. Most recipients were born in countries other than Australia or New Zealand (92.2%). Complications following ITOT were frequent occurring in 38.7% of patients. Conclusion: Responding transplant practitioners were likely to have discussed ITOT with patients and had frequently been involved with clinical care of these individuals. Strategies to educate patients around the risks and consequences of ITOT are needed.

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MONDAY, 23 March Free Communications 5 Organ Donation and Allocation#2

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Abstract No. 23 ACCESS TO DECEASED DONOR KIDNEY TRANSPLANTATION FOR SENSITIZED PATIENTS IN AUSTRALIA SYPEK Matthew1,2,3,4, KAUSMAN Joshua2, WYBURN Kate5, HUGHES Peter1, CLAYTON Phil6,3 1Nephrology and Renal Transplant, Royal Melbourne Hospital, 2Nephrology and Renal Transplant, Royal Children's Hospital, Melbourne, 3ANZDATA, 4Department of Medicine, University of Melbourne, 5Nephrology and Renal Transplant, Royal Prince Alfred Hospital, Sydney, 6Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital Aims: In March 2016 Australia’s deceased donor (DD) kidney allocation system transitioned from the use of cell based cytotoxic panel reactive antibody (PRA) assays to calculated PRA (cPRA) based on solid phase assay antibody detection for defining transplant candidate sensitization. We aimed to assess the impact of this on the distribution of sensitization of patients on the deceased donor kidney waiting list and examine transplant rates by cPRA in the contemporary era. Methods: A historical record of changes in PRA/cPRA was reconstructed for all wait-listed patients between 01/02/2013 and 31/12/2018. Transplantation rate by cPRA was calculated per 100 active waiting years. Multivariate Poisson regression was used to examine the association between degree of sensitization and transplant rate in the contemporary era (01/03/2016-31/12/2018). Results: The introduction of cPRA resulted in major changes in the distribution of sensitization on the DD waiting list with a 75% increase in patients with cPRA 80-95% and a 5-fold increase in patients with cPRA ≥99%, for example (Figure 1). Any degree of sensitization ≥50% was associated with a reduced transplant rate compared to non-sensitized patients, however, patients with a cPRA of ≥99% had a dramatic reduction compared to other groups: aIRR 0.10 (95% CI 0.08-0.13) compared to aIRR 0.38 (95% CI 0.30-0.48) for cPRA 95-98%, and aIRR 0.76 (95% CI 0.64-0.90) for cPRA 80-94%, for example. Conclusions: Introduction of cPRA dramatically changed how patients on the DD waiting list are classified in terms of sensitization. Under the current allocation system HLA sensitization, particularly cPRA ≥99%, is associated with decreased rate of transplantation.

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Abstract No. 24 FACTORS ASSOCIATED WITH DELAYED ACTIVE LISTING FOR DECEASED DONOR KIDNEY TRANSPLANTATION IN PATIENTS RECEIVING DIALYSIS IN AUSTRALIA – A SINGLE CENTRE PILOT STUDY MCMICHAEL Lachlan1,2, CLAYTON Philip1,3,2 1Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 2School of Medicine, University of Adelaide, 3ANZDATA Background: Patients with end-stage kidney disease have multiple treatment options including renal transplantation which offers superior survival and quality of life compared to dialysis with less financial burden. A recent analysis has identified only 12.1% of patients in Australia being actively listed for renal transplantation within 12 months of commencing dialysis with significant variations between state jurisdictions. We present a pilot study assessing, at the centre level, factors associated with delayed active listing for kidney transplantation in Australia. Methods: Data from NOMS and ANZDATA were used to identify patients between the ages of 18-75 with an estimated post-transplant survival of greater than 90% in receipt of haemodialysis for more than 12 months. Individual semi-structured surveys were forwarded to patient’s treating consultants. Results: 92 patients were identified for inclusion with 64 surveys completed. The average age of patients was 45 years, 50% female patients, 83% of Caucasian ethnicity and an average of 4.09 years on dialysis. 48% of patients were obese or morbidly obese and 54% of patients were current or former cigarette smokers. Secondary medical factors were identified as the primary cause for delayed listing. 25% of patients had obesity identified as a surgical impediment to transplantation and 15% of patients had uncorrected cardiovascular disease affecting listing. Limited engagement with renal services, compliance and rural location were also identified in 10.9%, 9%, 7.8% of patients. Conclusions: Clinical, psychological and geographical factors may represent factors associated with delays to transplant listing. Further analysis is required to determine centre-based trends within Australia.

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MONDAY, 23 March Free Communications 6 Pancreas and Islet Transplantation

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Pancreas and Islet Transplantation Abstract No. 25 20 YEARS OF ISLET ISOLATION OUTCOMES AT THE WESTMEAD ISLET TRANSPLANT PROGRAM HAWTHORNE Wayne1,2, CHEW Yi Vee2, WILLIAMS Lindy2, ANDERSON Patricia3, JIMENEZ Elvira2, O'CONNELL Phil2 1Department of Surgery, University of Sydney, 2Centre for Transplant and Renal Research, The Westmead Institute of Medical Research, 3Department of Renal Medicine, Westmead Hospital, Sydney Aims: Islet cell transplantation for type 1 diabetes relies heavily on successful isolation outcomes to ensure successful transplantation. As such we aimed to evaluate our islet isolation outcomes and identify factors during donor selection, organ procurement and islet isolation influencing the preparation leading to a transplant. Methods: Islets were isolated from pancreata of heart beating deceased donors using collagenase and NP (SERVA). Donor characteristics, pancreas procurement data, isolation yield and outcomes were collected and compared to determine correlation between each variable. Isolations were also divided into Transplanted (Tx) VS Non-transplanted preparations (Non-Tx) to identify variables significantly influencing isolation outcomes. Results: Data from 256 islet isolations collected between July 2000 and November 2019 were evaluated. On average, 32% of islet preparations were transplanted, with 71% of isolations in 2018-2019 reaching release criteria. Transplantable yields (defined as 300,000 IEQ; 4,000 IEQ/kg for a 75kg recipient) were obtained from donors aged between 20-60 years, with BMI >20kg/m2, and weight >55kg. Compared to non-tx (n=180), Tx (n=76) had significantly higher total IEQ (566,048±239,140 VS 322,873±194,275 IEQ) and IEQ/g pancreas (6,862±3,184 VS 5,043±3,626 IEQ/g). Higher donor BMI, donor weight, pancreas weight, and lower CIT, were significantly correlated (p<0.001) to Tx. Tx also exhibited significantly higher viability, purity, and beta cell viability and stimulation indices compared to Non-tx. Conclusions: We found that increased donor BMI/weight and lower CIT all have significant effects on outcomes. In particular these influence which islet isolations resulted in transplantable yields/outcomes.

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Abstract No. 26 PREGNANCY OUTCOMES FOR SIMULTANEOUS PANCREAS-KIDNEY TRANSPLANT RECIPIENTS VERSUS KIDNEY TRANSPLANT RECIPIENTS TANG Joanne1, HEWAWASAM Erandi2,3, GULYANI Aarti3, MCDONALD Stephen1,3,4, CLAYTON Phil1,3,4, WEBSTER Angela5,6, KANELLIS John7, JESUDASEN Shilpanjali1,3,4 1Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 2Faculty of Health Sciences, University of Adelaide, 3ANZDATA, 4University of Adelaide, 5University of New South Wales, Sydney, 6Centre for Transplant and Renal Research, Westmead Hospital, Sydney, 7Department of Nephrology, Monash Medical Centre, Melbourne Aim: Data about pregnancy outcomes for Simultaneous Pancreas-Kidney Transplant Recipients (SPKR) are limited. We aim to compare pregnancy outcomes in SPKR to Kidney Transplant Recipients (KTR). Methods: Maternal parameters, transplant, pregnancy and fetal outcomes reported to the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry from 2001-17 were summarized and compared. Results: A total of 19 pregnancies to 15 SPKR mothers, and 348 pregnancies (including 10 twins) to 235 KTR mothers were reported. Maternal ages were similar (SPKR 33.9 years, SD 3.9; KTR 32.3 years, SD 4.8, p=0.10), however SPKR had a shorter transplant-to-first-pregnancy interval compared to KTR (SPKR 3.3 years, IQR(1.7, 4.1); KTR 5 years, IQR(2.6, 8.7), p=0.02). SPKR had more peripheral vascular disease (26% vs. 1%, p<0.05) and coronary artery disease (21% vs. 3%, p<0.05). Median creatinine at 3 months post-partum remained similar between groups (KTR -3 umol/L, IQR(-15, 6), SPKR -3, IQR(-11, 3), p=0.86). There were no observed differences in maternal, foetal or kidney transplant outcomes (Table 1), and >20 week live birth rates were comparable (SPKR 93.8% vs. KTR 96.8%, p=0.06). Twenty-four KTR had Diabetes (6 (25%) Type 1 diabetes, 18 (75%) Type 2 diabetes) and comparison to SPKR showed no difference in outcomes. Conclusions: SPKR did not appear to have an increased risk of maternal, fetal or kidney transplant complications compared to KTR. However, the number of SPKR pregnancies are low so interpretation is cautious. Table 1: Maternal, Kidney Transplant and Fetal Outcomes in KTR and SPKR pregnancies KTR

348 parenthood events SPKR 19 parenthood events

p-value

N N Maternal complications, n (%)

Pre-eclampsia 299 98 (32.8%) 16 5 (31.3%) 0.901

Gestational diabetes 214 13 (6.1%) 11 0 (0.0%) 0.401

Years of transplant function post pregnancy, median (IQR)

343 6.3 (3.0, 10.5) 19 4.9 (2.2, 9.0) 0.322

358 babies 19 babies p-value N N Pregnancy outcome, n (%) 358 19 0.383

Live delivery 300 (83.8%) 15 (78.9%) Spontaneous abortion

(<20 weeks) 40 (11.2%) 2 (10.5%)

Stillbirth >20 weeks 10 (2.8%) 1 (5.3%) Surgical termination 8 (2.2%) 1 (5.3%) Fetal morphology, n (%) 308 15 1.003

Abnormal 6 (1.9%) 0 (0.00%) Normal 276 (89.6%) 14 (93.3%) Unknown 26 (8.4%) 1 (6.7%) Birth weight in grams, median (IQR)

265 2500 (2080, 3090)

15

2469 (1869, 3130)

0.692

Gestational age in weeks, median (IQR)

344 34.5 (30.0, 38.0)

18 33.5 (27.0, 36.0)

0.172

1Compared using chi-squared test; 2Compared using Wilcoxon rank-sum; 3Compared using Fisher Exact test

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MONDAY, 23 March Free Communications 6 Pancreas and Islet Transplantation

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Abstract No. 27 PHENOTYPIC AND GENOTYPIC ANALYSIS OF HEREDITARY PANCREATITIS IN PATIENTS AND POTENTIAL CANDIDATES FOR TOTAL PANCREATECTOMY WITH ISLET AUTOTRANSPLANTATION (TP-IAT) WU Denghao1, COATES PTH2,3, PALMER Lyle4, SCOTT Hamish5, COUPER Richard6, KASSAHN Karin5, CHEN John7 1School of Medicine, Faculty of Health Sciences, University of Adelaide, 2Renal Transplant Unit, Royal Adelaide Hospital, 3School of Medicine, University of Adelaide, 4School of Public Health, University of Adelaide, 5Department of Pathology, Centre for Cancer Biology, Hanson Institute, SA Pathology, 6Department of Gastroenterology, Adelaide Women's and Children's Hospital, 7Department of Liver Transplantation, Royal Adelaide Hospital Introduction: Hereditary Pancreatitis (HP) is caused by inheritance of genetic mutations in PRSS1/2, SPINK1, CFTR and CTRC gene regions. HP frequently results in inflammation of the pancreas from a young age, chronic abdominal pain, and dependency upon opioids. Total Pancreatectomy with Islet Autotransplantation (TP-IAT) effectively treats patients of HP and prevents diabetes and risk of pancreatic cancer later in life. This project aims to identify HP cases and assess the correlation between phenotypic disease outcome and genotypic mutation variant. Methods: Patients with HP were identified from hospital records and interviewed for phenotype. Criteria include: personal and family medical history, pain management, medical prescriptions, previous surgery, smoking and alcohol history, and quality of life. Salivary biosamples were obtained to be whole-exome-sequenced (WES). Results: 4 families of 42 individuals, plus 33 additional familial probands of HP had been identified thus far. All 4 families possess the mutation PRSS1, albeit different allelic variants (3 with R122H, 1 with A86T). One PRSS1 R122H mutation variant family also possessed SPINK1 N34S mutation, a known HP disease modifier mutation. In these well-phenotyped families, 23 PRSS1 and 5 SPINK1 genetic mutation carriers were identified from our study cohort. 13 of whom suffered from phenotypic symptoms of HP. Interestingly, 12 of the 33 probands have been genotyped and showed no known HP-associated mutation. Conclusion: Phenotypic disparity in mutation carriers suggests possible existence of unknown modifier genes for HP. Disease phenotype in probands with no known mutation also suggest possible existence of novel HP-associated mutations. WES and bioinformatic analysis study required for further investigation.

Figure 1: genetic pedigrees of four hereditary pancreatitis families (A, B, C, and D). Showing PRSS1, SPINK1 mutation carriers and individuals phenotypic for hereditary pancreatitis.

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MONDAY, 23 March Free Communications 6 Pancreas and Islet Transplantation

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Abstract No. 28 COMPARISON OF PANCREATA AND ISLET PREPARATIONS FROM HUMAN ORGAN DONORS - INFLUENCE OF FAMILY HISTORY OF DIABETES OR MARGINAL LEVELS OF HBA1C. MARIANA Lina, LOUDOVARIS Thomas, KOS Cameron, PAPAS Evan, SELCK Claudia, CATTERALL Tara, THOMAS Helen, KAY Thomas W H Immunology & Diabetes, St Vincent's Institute, Melbourne Background: Many believe diabetes is due to a combination of genetic and environmental factors, but the importance of family history of diabetes (FHD) or levels of Glycated hemoglobin (HbA1c) in pancreatic islet quantity has never been determined. HbA1c is an important indicator of long-term glycemic control and reflects the cumulative glycemic history of the preceding two to three months. Here we compare the islet yields from organ donors who were diabetic or non-diabetic, with or without FHD, as well as the possible implication of HbA1c level. Methods: Islets were isolated based on the Ricordi Method. A HbA1c level of ≥6.5% was considered as diabetic, a marginal level was 5.7-6.4% and ≤5.7% as non-diabetic. An islet equivalent (IEQ) is a 150µm cell sphere. Results: Pancreata from non-diabetic organ donors with FHD (n=46), T1Diabetic (n=13) and T2Diabetic (n=24) donors had significantly less islets, with means of 298,996 IEQ, 14,657IEQ and 168,834IEQ respectively than non-diabetic donors with no FHD (n=146), 382,423IEQ. Islet yields per gram pancreas from non-diabetic donors (n=34, HbA1c < 5.7%, 5,103IEQ/gm pancreas) were significantly higher, p=0.034, than marginal/prediabetic donors (n=19, HbA1c 5.7-6.4%, 4,211IEQ/gm pancreas). Conclusion: Our data confirms previously published results that diabetic donors are deficient in islet numbers, further validating their exclusion as an islet transplant donor. The new finding of less islets in pancreata from non-diabetic donors with a diabetic family member or with a marginal HbA1C supports the involvement of genetic predisposition in T2D and may need to be taken into consideration when accepting donors for transplant.

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MONDAY, 23 March Free Communications 6 Pancreas and Islet Transplantation

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Abstract No. 29 TOTAL PANCREATECTOMY WITH AUTO ISLET CELL TRANSPLANTATION: A CASE SERIES BAMPTON Tristan1, NEO Eu Ling2, LOUDOVARIS Tom3, RADFORD Toni4, CHEN John2, DROGEMULLER Chris1, ETHERTON Colleen4, KHURANA Sanjeev5, KIRATA Svjetlana1, COUPER Richard6, COATES P. Toby4 1University of Adelaide, 2Flinders Medical Centre, Adelaide, 3St Vincent's Institute, Melbourne, 4Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 5Paediatric Surgery, Women's and Children's Hospital, 6Gastroenterology and Hepatology, Women's and Children's Hospital Aims: The aim for this case series is to describe the South Australian (SA) experience of Total Pancreatectomy with Auto Islet Cell Transplantation (TP-IAT). Methods: Patients were carefully selected for TP-IAT surgery according to the Minnesota Criteria, with eligible patients requiring a confirmed diagnosis of chronic pancreatitis or hereditary pancreatitis, chronic narcotic dependence unresponsive to maximal medical therapy and adequate islet cell function. Patient ages ranged from 7 to 51, with four of these under 18. The pancreatectomy was performed in SA, the removed pancreas flown to Melbourne for islet cell isolation, and then returned to Adelaide on the same day for islet infusion. Results: Consisting of 10 patients, this series is the largest in Australia to date. Pancreas weight, total islet equivalent (IEQ) and IEQ per kilogram are displayed in figure one. One patient died day 3 after TP-IAT from a STEMI due to anaemia related to non-transfusion as a Jehovah’s Witness. Of the nine other patients, all remain C-peptide positive. Six became insulin independent, with the other three achieving stable glycaemic control on low insulin dosage. All patients demonstrated drastic improvement in pain management, with all nine improving from chronic narcotic dependence to being free of any long-term analgesia. Conclusion: TP-IAT has demonstrated remarkable success thus far, with initial results demonstrating stable glycaemic control, significant insulin independence and almost total relief from chronic pain.

Figure 1: Operative details of the SA based TP-IAT patients. HP = Hereditary pancreatitis, CP = Chronic pancreatitis *Patient 2 deceased

Patient State of origin

Date of surgery

Age (years)

Diagnosis Pancreas weight (grams)

Total IEQ

IEQ/Kg Insulin Independent

1 SA 7/2015 7 HP (PRSS1) 21 28,565 1,146 No 2* SA 6/2016 51 CP 181 158,210 2,181 No 3 SA 4/2017 17 HP (PRSS1) 83 489,000 7,300 Yes 4 QLD 7/2017 31 CP 45 284,000 3,500 No 5 SA 8/2018 17 HP (PRSS1) 42 653,000 11,600 Yes 6 SA 9/2018 41 CP 43.8 122,054 1,805 Yes 7 NSW 11/2018 27 HP

(SPINK-1) 55.1 150,268 2,613 No

8 SA 4/2019 40 HP (PRSS1) 98.5 617,874 5,999 Yes 9 WA 7/2019 8 HP (PRSS1) 45.4 302,4581 11,457 Yes 10 SA 11/2019 36 CP 65.1 229,056 4,250 Yes

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MONDAY, 23 March President’s Prize Symposium

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President’s Prize Symposium Abstract No. 30 THE EFFECT OF AGEING ON MYOCARDIAL SUSCEPTIBILITY TO ISCHAEMIA IN A RODENT MODEL OF DONATION AFTER CIRCULATORY DEATH. VILLANUEVA JE1, CHEW HC1, GAO L1, SCHEUER SE1, DOYLE A1, JABBOUR A1,2, HICKS M1,3, MACDONALD PS1,2 1Transplantation Laboratory, Victor Chang Cardiac Research Institute, Sydney, 2Heart and Lung Clinic, St Vincent's Hospital, Sydney, 3Clinical Pharmacology, St Vincent's Hospital, Sydney Background: An ageing population and advances in heart failure management contributes to the scarcity of quality donor hearts. Hearts from older donors or those procured via donation after circulatory death(DCD) can alleviate transplant wait-lists. DCD hearts are particularly vulnerable to warm ischemic times(WIT) inherent to the donation pathway however little is known of the effects of age and DCD on cardiac functional recovery. Aims: Test ageing effects on (1) ischaemic tolerance and cardiac functional recovery in a rodent DCD model; (2) cardiac recovery after supplementation with glyceryl trinitrate(GTN), erythropoietin(EPO) and zoniporide(Z); (3) mitochondrial respiratory capacity. Methods: Wistar rats (12-, 18-, 24-mo, corresponding to 30-, 45-, 60- human years) were subjected to DCD (20-min fixed WIT). Hearts were procured, instrumented onto a Langendorff perfusion circuit, and flushed with Celsior preservation solution±GTN/EPO/Z. Hearts were perfused (Langendorff 30-min, working 30-min) and functional recovery measured via aortic flow(AF). Native heart tissue (3-, 12-, 24-mo) was collected for oxidative phosphorylation assessment (Oroboros-O2k oxygraph). Results: Compared to unsupplemented 12-mo hearts, unsupplemented 18- and 24-mo hearts showed a 6-fold decrease in AF recovery. GTN/EPO/Z supplementation significantly increased AF recovery of 18-mo hearts to supplemented 12-mo levels however GTN/EPO/Z did not improve AF recovery in 24-mo hearts. Compared to 12-mo heart tissue, 24-mo hearts exhibited significantly impaired mitochondrial oxygen flux at complex I, II, and uncoupled maximal respiration stage. Conclusion: Ischaemic tolerance after DCD declines with age. Pharmacological supplementation improves ischaemic tolerance however benefits are lost in older hearts, which may be attributed to impaired mitochondrial respiratory capacity.

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MONDAY, 23 March President’s Prize Symposium

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Abstract No. 31 TRENDS IN CAUSES OF DEATH IN AUSTRALIAN AND NEW ZEALAND KIDNEY TRANSPLANT RECIPIENTS: A REGISTRY ANALYSES BY ERA AND TIME POST-TRANSPLANT YING Tracey1,2, SHI Bree2, KELLY Patrick3, CLAYTON Philip4, CHADBAN Steve1,2 1Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, 2School of Medicine, University of Sydney, 3School of Public Health, University of Sydney, 4Department of Renal Medicine, Royal Adelaide Hospital Background: Donor and recipient characteristics in kidney transplantation(KT) have changed dramatically since the 1980s. Along with an increase in marginal donors and older recipients, incremental improvements have ensued in immunosuppression, surgical techniques and cardiovascular(CV) disease management. A contemporary assessment of the risks and determinants of deaths in KT recipients is required to inform our patients. Methods: We included all kidney-only transplant recipients from ANZDATA between 1980- 2017. We censored patients at graft loss or last follow-up. We calculated crude death rates by dividing the number of deaths by the total patient-years at risk. Adjusted death rates per 5-year intervals were compared using a piecewise exponential model, stratified by time post-transplant. Results: 22,078 incident recipients accumulated 183,964 person-years follow-up. The adjusted all-cause death rate was 2% per-annum, stable since 2005. Compared with 1995- 1999, recipients in 2015-2017 were older (mean age 47 vs.41) and had more comorbidities (CVD 25% vs.13%, diabetes 24% vs.10%). Since 1980, there has been a significant reduction in CV and infection-deaths at all periods post-transplant. Recipients in the current era had a 56% reduction in CV deaths (adjHR=0.44, 95%CI 0.36-0.52) and 53% reduction in infection- deaths (adjHR=0.47, 95%CI 0.36-0.61), compared with recipients in 2000-2004. Short-term cancer-deaths have remained stable over time, with a marginal fall in long-term cancer- deaths since 2005. Conclusion: The risk of death after KT has reduced significantly since 1980, driven by a reduction in CV deaths at all timepoints and a decline in infection-deaths. Contrary to previous studies, cancer-deaths have remained stable over time after adjusting for time post-transplant.

0 2

4 6

8

0 2

4 6

8

0 2

4 6

8

0 2

4 6

8

0 2

4 6

8

1980 1985 1990 1995 2000 2005 2010 2015 1980 1985 1990 1995 2000 2005 2010 2015 1980 1985 1990 1995 2000 2005 2010 2015

1980 1985 1990 1995 2000 2005 2010 2015 1980 1985 1990 1995 2000 2005 2010 2015

0-3m 1-5yr

5-10yr 10yr+

CV death Cancer death Infection-related death Other death

Calender time

Adjusted death rate per 100 patient-years By time period post-transplant

3-12m

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MONDAY, 23 March President’s Prize Symposium

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Abstract No. 32 AN INFLAMMATORY INDEPENDENT ROLE FOR P65 (RELA) IN INSULIN HOMEOSTASIS ZAMMIT Nathan, W.1, WALTERS Stacey, N.2, MCDOWELL Joseph2, GREY Shane, T.2 1Immunology Department, 2Immunology Department, Garvan Institute of Medical Research, Sydney Isolated islets express NF-κB dependent inflammatory factors that impair transplant outcomes. Strategies to block intra-islet NF-κB activation via the overexpression of its constitutive inhibitor, IκBα, have failed to significantly prolong graft survival. Here we test whether deletion of the NF-κB transcription factor could improve upon these findings. Mice with beta-cell specific deletion of RELA (bP65KO), a core component of the NF-κB transcription factor complex, prevented NF-κB activation in TNF-stimulated islets, and reduced the expression of pro-inflammatory genes. bP65KO mice exhibited normal blood glucose levels and beta-cell mass, but exhibited marked glucose intolerance when challenged with a glucose bolus, due to a lack of blood insulin. The observed defect was beta-cell intrinsic, as when transplanted to diabetic wild-type syngeneic recipients pP65KO islets failed to restore euglycemia. To test whether loss of beta-cell homeostasis was specific to P65 deletion or to a general loss of NF-κB signalling, we impaired NF-κB signalling by gene targeting two upstream NF-κB signalling components; a beta cell specific deletion of NEMO, an essential component for NF-κB activation (bNEMOKO); or a beta-cell specific knock-in of the NF-κB inhibitor Tnfaip3 (aka A20; bA20Tg). Both bNEMOKO and bA20Tg islets had reduced induction of NF-κB and inflammatory mRNAs. But in contrast to bp65KO mice, bNEMOKO and bA20Tg mice were glucose tolerant. These data provide evidence that the NF-κB transcription factor RELA/p65 plays a key role in maintaining beta-cell homeostasis independent of its known biology to regulate inflammatory gene expression, and has implications for approaches to target NF-κB signalling for islet transplantation.

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Abstract No. 33 BRIEF NORMOTHERMIC MACHINE PERFUSION FOR THE ASSESSMENT AND REVIVAL OF DISCARDED HUMAN KIDNEYS HAMEED Ahmer M1,2,3, LU David B2,4, ELLIS Patrick2, XU Bo5, HU Min2, CHEW Yi Vee2, KEUNG Karen2,6, P’NG Chow H7, GASPI Renan4, ZHANG Chris4, ROBERTSON Paul4, ALEXANDER Stephen6,8, THOMAS Gordon6,9, LAURENCE Jerome6,10, DE ROO Ronald11, WONG Germaine2,6,12, MIRAZIZ Ray13, O’GRADY Greg14, YUEN Lawrence11,6, HAWTHORNE Wayne J.11,2,3, ROGERS Natasha M.2,6,12, PLEASS Henry C.11,6,10 1Surgery, Westmead Hospital, Sydney, 2Westmead Institute for Medical Research, 3Sydney Medical School, 4Transplant Unit, Westmead Hospital, Sydney, 5Thermo Fisher Scientific, Victoria, Australia, 6Sydney Medical School, University of Sydney, 7Institute for Clinical Pathology and Medical Research, Westmead Hospital, Sydney, 8Department of Nephrology, The Children’s Hospital at Westmead, 9Department of Surgery, The Children’s Hospital at Westmead, 10Department of Surgery, Royal Prince Alfred Hospital, Sydney, 11Department of Surgery, Westmead Hospital, Sydney, 12Department of Nephrology, Westmead Hospital, Sydney, 13Department of Anaesthesia, Westmead Hospital, Sydney, 14Auckland Bioengineering Institute, University of Auckland Aims: Using a series of discarded and/or non-utilized human kidneys, we aimed to investigate the mechanistic basis and translational potential of normothermic machine perfusion (NMP) as a viable and superior preservation strategy to the current gold standard of cold static storage (CS). Methods: Discarded deceased donor kidneys (n = 15) underwent brief (one hour) NMP after a period of CS during transportation. Renal perfusion, biochemical, and histologic parameters were analyzed. Leukocyte efflux was measured in selected grafts (i.e. passenger leukocyte load). In the event that paired kidneys were available, NMP was directly compared to CS alone using simulated transplantation with whole allogeneic blood, followed by assessment of perfusion and functional parameters, markers of ischemia-reperfusion injury (IRI), and RNA sequencing. Results: All kidneys were successfully perfused, with demonstration of improving renal blood flows and resistance (median 260 ml/min and 0.29 mmHg/ml/min, respectively), and urine output (median 21 ml), in all but one kidney during NMP. NMP completely resolved non-perfused regions in discarded DCD kidneys, deeming them transplantable. In paired kidneys, transcriptomic analyses showed induction of stress and inflammatory genes in NMP kidneys, with upregulation of pathways promoting cell survival and proliferation. Furthermore, in comparison to CS kidneys, their corresponding NMP pairs had significantly better renal perfusion and functional parameters, and reduced cell death, oxidative stress, and complement activation. Conclusions: NMP allowed for the rejuvenation of marginal kidneys, ameliorating ischaemia-reperfusion injury and allowing more objective graft assessment than CS alone. NMP can increase the utilization of marginal kidneys whilst simultaneously enhanching transplant outcomes.

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Abstract No. 34 CO-AXIAL PRINTING OF MURINE ISLETS WITH HUMAN REGULATORY T-CELLS PREVENTS XENORESPONSE IN VITRO KIM Juewan1, HOPE Christopher2, PERKINS Griffith3, YUE Zhilian4, LIU Xiao4, GANTUMUR Narangerel4, DROGEMULLER Christopher5, CARROLL Robert5, BARRY Simon2,6, WALLACE Gordon4, COATES Toby5,7 1Department of Molecular and Biomedical Science, 2Department of Gastroenterology, Women's and Children's Hospital, 3Department of Molecular and Biomedical Science, University of Adelaide, 4Intelligent Polymer Research Institute, University of Wollongong, 5Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 6 Faculty of Health and Medical Sciences, University of Adelaide, 7Department of Medicine, University of Adelaide Introduction: 3D-bioprinting facilitates the fabrication of complex 3D-architectures. 3D-bioprinting of regulatory T-cells (Tregs) with islets may overcome the immunosuppressive shortcomings inherent in islet transplantation. This project aims to characterise 3D-bioprinted human Tregs using alginate-GelMA bioink and evaluate the efficacy of co-axial printing of islets with Tregs. Method: Natural Tregs were FACS sorted from peripheral blood, whereas induced Tregs were induced from naïve CD4+ T-cells using TGF-β, all-trans retinoic acid and rapamycin. Tregs were suspended in media (‘non-printed’) or printed in a photo- and chemically-crosslinked alginate-GelMA bioink. Tregs were analyzed by flow cytometry for viability (propidium iodide), phenotype (CD25 and FOXP3) and functionality (TGF-β, CD69, CD39 and CTLA-4). CD154 suppression assay evaluated Treg function. Trans-well migration assays were performed to evaluate the bioprinted Treg migration. Furthermore, murine islets were co-axially printed with or without human Tregs. Printed structures were co-cultured with human PBMCs. Results: 3D-bioprinted Tregs retained viability above 80% with no significant decreases compared to non-printed cells, up to 3 days post-bioprinting. 3D-bioprinting maintained expression of Treg phenotypic and functionality markers and suppressive capacity. 3D-bioprinting was also shown to significantly reduce migration of Tregs in response to CCL1. Furthermore, murine islets co-axially printed with human Tregs were highly viable up to 3 days post-printing, while islets printed alone displayed substantial cell death. Conclusion: 3D-bioprinting had a minimal impact on viability, phenotype and function of Tregs. Furthermore, we demonstrated printing prevents Treg migration from the 3D-bioprinted structures. Lastly, co-axial printing of murine islets with human Tregs prevented xenoresponse in vitro.

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Abstract No. 35 PERCEIVED VS. VERIFIED RISK OF CANCER TRANSMISSION FROM DECEASED ORGAN DONORS – A NSW COHORT STUDY 2010-2015 USING DATA LINKAGE HEDLEY James1, DE LA MATA Nicole1, ROSALES Brenda1, WALLER Karen1, O'LEARY Michael2, CAVAZZONI Elena2, KELLY Patrick1, WYBURN Kate1,3, WEBSTER Angela1,4 1Centre for Organ Donation Evidence (CODE), University of Sydney, 2NSW Organ and Tissue Donation Service, 3Renal Unit, Royal Prince Alfred Hospital, Sydney, 4Centre for Transplant and Renal Research, Westmead Hospital, Sydney Introduction: Donor suitability assessment is often time-sensitive, with imperfect information available at referral. Opportunities for donation may be missed if donors are rejected based on inaccurate information. Aims: We sought to compare assessment of cancer transmission risk based on information available at referral (perceived) versus subsequently obtained (verified) detailed medical history, and to identify any missed opportunities for donation. Methods: Cohort study of deceased organ donor referrals in NSW 2010-2015 from the NSW Biovigilance Register. Referrals from NSW who had consent and were otherwise suitable for donation (except for perceived or verified tumour) were analysed. Perceived tumour details were obtained from Organ and Tissue Donation Service referral logs, while verified details were based on the Central Cancer Registry and Admitted Patient Data Collection. Cancer transmission risk was graded using Transplantation Society of Australia and New Zealand guidelines. Results: Among 772 referrals otherwise suitable for donation, 601 (78%) had accurately classified cancer transmission risk (κ=0.59). Overall, 53 suitable referrals were rejected due to cancer transmission risk (missed opportunities), including 49 (92%) with overestimated risk (perceived high, verified low/none), and 4 (8%) due to excessive risk aversion (perceived and verified low risk). Missed opportunities had overestimated transmission risk for tumours including leukaemia (8, 16%), lung (8, 16%), melanoma (7, 14%), brain (6, 12%), and breast (6, 12%). Conclusions: Despite time pressure and limited information availability, there is moderate agreement between perceived and verified cancer transmission risk. Nevertheless, improved information availability (e.g. via data linkage) could meaningfully increase the number of actual donors. Table 1: Perceived vs. verified cancer transmission risk in otherwise suitable organ donor referrals

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Abstract No. 36 DISCOVERY OF PMHC EPITOPES FOR DIRECTLY ALLOREACTIVE T CELLS. SON Eric Taeyoung1, PAUL-HENG Moumita1, LEONG Mario1, FARIDI Pouya2, DUDEK Nadine2, ALEXANDER Ian3, BERTOLINO Patrick4, PURCELL Anthony2, BOWEN David4, MIFSUD Nicole2, SHARLAND Alexandra1 1Central Clinical School, University of Sydney, 2Department of Biochemistry and Molecular Biology, Monash University, Melbourne, 3Gene Therapy Research Unit, Children's Medical Research Institute Australia, 4Central Clinical School, Centenary Institute Australia

Introduction and Aims: Direct allorecognition of intact donor MHC-I molecules is required for tolerance induction. Few pMHC epitopes recognised by alloreactive CD8+ T cells are known. We determined the role of the self-immunopeptidome in direct allorecognition and tolerance induction, and identified the pMHC targets of allospecific T cells. Methods: We excluded donor MHC-I presentation of endogenous peptides by expressing a single chain trimer comprising donor heavy chain, β2m and peptide. A global alteration in the bound peptide repertoire was introduced using MHC-I molecules which are stable in the presence of low-affinity peptides or even when empty. Mice were challenged with donor skin grafts. H-2Kb peptide repertoire was determined using immunoaffinity purification and tandem mass spectrometry, and Kb-reactive CD8+ T cells were screened using pMHC tetramers. Results: Skin graft tolerance in recipient mice with a polyclonal repertoire of responding T cells was only achieved when donor MHC-I was able to present the normal repertoire of self-peptides. 332 unique Kb-bound peptides were shared by multiple tissues. Of 88 peptides screened, 18 bound >5% of alloreactive T cells from male B10.BR (H-2k). pMHC epitopes recognised by male B10.BR mice were also recognised by female B10.BR (R=0.80, p<0.0001) and male BALB/c (H-2d) (R=0.64, p<0.0001). Combining pMHC tetramers yielded a cumulative increase in alloreactive T cell detection compared to a single strongly-recognised tetramer (45.4±1.2% versus 14.1±1.7%, p=0.0001). Conclusion: Direct recognition of epitopes comprising donor MHC-I and self-peptides is required for tolerance induction. Epitopes for directly-alloreactive CD8+ T cells can be identified using pMHC multimer staining.

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Abstract No. 37 NEW BLOOD BORNE VIRUS INFECTIONS AMONG ORGAN TRANSPLANT RECIPIENTS: A DATA-LINKED COHORT STUDY EXAMINING TRANSMISSION AND DE NOVO HEPATITIS B, C AND HIV INFECTIONS WALLER Karen1, DE LA MATA Nicole1, HEDLEY James1, ROSALES Brenda1, O'LEARY Michael2, CAVAZZONI Elena2, RAMACHANDRAN Vidiya3, RAWLINSON William3, KELLY Patrick1, WYBURN Kate4,5, WEBSTER Angela1,6 1School of Public Health, University of Sydney, 2NSW Organ and Tissue Donation Service, 3Serology and Virology Division, NSW Health Pathology Randwick, Prince of Wales Hospital, Sydney, 4School of Medicine, University of Sydney, 5Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, 6Centre for Transplant and Renal Research, Westmead Hospital, Sydney Introduction: Blood borne virus (BBV) infections can complicate organ transplantation. Systematic monitoring to distinguish donor-transmitted infection from de novo post-transplant infection is challenging. Additional information can be obtained through linkage of administrative health data. Aims: We aimed to identify donor-transmitted and de novo BBV infections among organ transplant recipients. Methods: Cohort study of all solid organ donor-recipient pairs in NSW, 2000-2015. Donor and recipient BBV infections were identified from transplant registries and administrative health data. Proven/probable donor-transmissions were identified among new recipient infections within 12 months of transplant, classified according to an international algorithm. All other new BBV infections were de novo infections. Results: Of 2,120 organ donors, 73 donors had BBV infection (11 active, 62 past). Donors with BBV donated to 176 recipients, of whom 24 had the same BBV as their donor, and 152 did not; these 152 recipients were at risk of donor-transmission. Among those at risk, there were 3 proven/probable BBV transmissions (1 hepatitis C [HCV], 2 hepatitis B [HBV]) and 149 recipients with non-transmissions. All donor-transmissions were previously recognised by donation services, and were from donors with known BBV. There were no deaths from transmissions. There were 70 recipients with de novo BBV, of whom two died from new HBV. Conclusion: This work confirms the safety of Australian organ donation, with no unrecognised BBV transmissions and many non-transmissions from donors with BBV. This may support increased use of BBV donors. However, de novo BBV infections were substantial and preventable. Data-linkage can assist biovigilance systems. Figure 1: Flowchart proven/probable donor-transmissions and de novo post-transplant infections

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MONDAY, 23 March Free Communications 7 CMV and Biomatrix

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CMV and Biomatrix Abstract No. 38 THE DETECTION OF CMV IN SALIVA CAN MARK A SYSTEMIC INFECTION WITH CMV IN RENAL TRANSPLANT RECIPIENTS WATERS Shelley1, LEE Silvia1,2, LLOYD Megan3,4, IRISH Ashley5,6, PRICE Patricia1 1School of Pharmacy & Biomedical Science, Curtin Health Innovation Research Institute, Curtin University, 2Department of Microbiology, Pathwest Laboratory Medicine, 3School of Medical and Health Sciences, Edith Cowan University, 4School of Biomedical Sciences, University of Western Australia, 5Renal Unit, Fiona Stanley Hospital, 6School of Medicine and Pharmacology, University of Western Australia Background: Human cytomegalovirus (CMV) is often transmitted through saliva. The salivary gland is a site of CMV replication and saliva can be used to diagnose congenital CMV infections. CMV replication is monitored in whole blood or plasma in renal transplant recipients (RTR) and associates with clinical disease. Commercial assays do not detect replication in the salivary gland and there is little data linking detection in saliva with systemic infection and clinical sequelae. Aim: To elucidate the value of detecting CMV in saliva. Methods: RTR (n = 82) were recruited > 2 years after transplantation. An in-house quantitative PCR was used to detect CMV UL54 in saliva samples. CMV DNA was sought in plasma using a commercial assay. Vascular health was predicted using flow mediated dilatation (FMD) and plasma biomarkers. CMV-reactive antibodies were quantified by ELISA and circulating CMV-specific T-cells by an interferon-γ ELISpot assay. Vδ2- γδ T-cells were detected using multicolor flow cytometry reflecting population expansion after CMV infection. Results: The presence of CMV DNA in saliva and plasma associated with plasma levels of antibodies reactive with CMV gB and with populations of circulating Vδ2- γδ T -cells (p < 0.01). T-cells reactive to CMV immediate early (IE)-1 protein were generally higher in patients with CMV DNA in saliva or plasma, but the level of significance varied (p = 0.02–0.16). Additionally, CMV DNA in saliva or plasma associated weakly with impaired FMD. Conclusion: The data suggest that CMV detected in saliva reflects systemic infections in adult RTR. Abstract No. 39 VARIATIONS IN THE CYTOMEGALOVIRUS GENE US28 MAY ALTER IMMUNE RESPONSES IN IMMUNOCOMPRIMISED PATIENTS WATERS Shelley1, LEE Silvia1,2, MUNYARD Kylie1, ARIYANTO Ibnu3, KRESOJE Nina4,5, GAUDIERI Silvana6, LEARY Shay6, IRISH Ashley7, PRICE Patricia1, ALLCOCK Richard4,5 1School of Pharmacy & Biomedical Science, Curtin Health Innovation Research Institute, Curtin University, 2Department of Microbiology, Pathwest Laboratory Medicine, 3Virology and Cancer Pathobiology Research Center, Faculty of Medicine, Universitas Indonesia, 4LotteryWest State Biomedical Facility – Genomics, School of Biomedical Sciences, University of Western Australia, 5School of Human Sciences, University of Western Australia, 6Institute for Immunology and Infectious Diseases, Murdoch University, 7Renal Unit, Fiona Stanley Hospital Background: Human cytomegalovirus (CMV) infections are a common problem after transplantation. Four CMV genotypes are defined by the glycoprotein B (gB) gene, but have have no associations with clinical outcome. Through evolution, CMV has acquired copies of human genes that aid immune evasion or influence pathogenicity. For example, the US28 gene encodes a chemokine receptor and can alter the spread of CMV in the body. Aim: We studied how US28 genotypes may affect pathogenicity. Methods: “Deep sequencing” of CMV is challenging as CMV replicates at low levels so clinical samples contain predominantly human DNA. Enrichment in cell culture is not helpful as it selects for variants lacking immunoregulatory genes. We developed a deep sequencing protocol involving nested PCR to sequence of CMV DNA directly from clinical samples. We sequenced 60 samples (saliva, blood and urine) from Australian renal transplant recipients (RTR n=21), neonates (n=4) and healthy adults (n=7), and Indonesian HIV patients (n=28). Results: Preliminary comparisons of US28 using proprietary software (VGAS) has revealed novel variants differently carried by Indonesian and Australian samples. Amongst the RTR, we identified a strain of CMV that associates with increased levels of CMV gB antibody (which is potentially protective) and associates with higher flow mediated dilatation (ie: better endothelial health). Conclusions: Variations in the chemokine receptor homologue US28 may alter the pathogenic consequences of CMV replication in RTR. We are currently analysing four other CMV genes, UL18, UL40 (NK receptor homologues), UL111a (IL-10 homologue) and US2 (degrades MHC-I) to expand these findings.

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Abstract No. 40 CYTOMEGALOVIRUS (CMV) BURDEN ASSOCIATES WITH MEASURES OF CARDIOVASCULAR HEALTH IN RENAL TRANSPLANT RECIPIENTS AND HEALTHY ADULTS AFFANDI Jacquita1, LEE Silvia2,3, CHIH HuiJun1, WATERS Shelley2, PRICE Patricia2, IRISH Ashley4 1School of Public Health, Curtin University, 2School of Pharmacy & Biomedical Science, Curtin Health Innovation Research Institute, Curtin University, 3Department of Microbiology, Pathwest Laboratory Medicine, 4Renal Unit, Fiona Stanley Hospital Background: Cytomegalovirus (CMV) burden may predict risk of cardiovascular disease. We assessed this in 58 healthy controls and 45 renal transplant recipients (RTR) >2 years after transplantation, stable on therapy who retain a high burden of CMV. Methods: Participants were assessed in 2014 for plasma inflammatory and vasculopathy biomarkers (sIFNAR2, sCD14, CRP, p-selectin, ICAM-1, VCAM-1), and metrics of CMV burden (CMV-reactive antibodies, saliva CMV-DNA and T-cell IFNγ responses to CMV antigens). These were evaluated as predictors of vascular health in 2017 [defined using brachial artery flow mediated dilatation (FMD), carotid intima media thickness (cIMT), pulse wave analysis [augmentation index (Aix@75) and pulse wave velocity (PWV)]. Linear regression models adjusted for age, sex, BMI and eGFR were optimized to identify risk factors. Results: In 2017, RTR had impaired FMD (p<0.001) and PWV (p<0.001). Detectable CMV-DNA (p=0.02) associated with impaired FMD, whilst CMV gB antibody attenuated this effect (p=0.03) (adjusted R2=0.42). In healthy adults, the optimal model predicting FMD (R2=0.22) incorporated high P-selectin (p=0.03) and low ICAM-1 (p=0.03) levels with no significant impact of CMV. Elevated sIFNAR2 (p=0.04) and gB antibody (p=0.06) levels predicted increasing Aix@75 (poor vascular health) in healthy adults (R2=0.4), whilst optimal models for RTR (R2=0.37) linked low sIFNAR2 and CMV IE-1 antibody levels with lower Aix@75 (better vascular health). CMV IE-1 antibody was also protective in relation to PWV in healthy adults (R2=0.55). Conclusion: Measures of active CMV replication were more predictive of impaired FMD in RTR than standard biomarkers, but increased CMV gB antibodies may be protective. Abstract No. 41 INNATE IMMUNE SENSING AND TISSUE REMODELLING OF A BIODEGRADABLE TEMPERING MATRIX SUPPORTED ISLET GRAFT. WALTERS Stacey N1, BAILEY Jacqueline1, CULTRONE Daniele1, ROJAS-CANALES Darling2, DROGEMULLER Chris2, PENKO Danielle2, LOUDOVARIS Thomas3, KAY Thomas3, KORBUTT Gregory4, GREENWOOD John E5, COATES Toby2, GREY Shane T1 1Immunology, Garvan Institute of Medical Research, Sydney, 2Department of Medicine, University of Adelaide, 3Immunology, St Vincent's Institute, Melbourne, 4Department of Medicine, University Of Alberta, 5Burns Unit, Royal Adelaide Hospital The subcutaneous site represents an accessible alternative islet transplant site, but suffers from poor vascularisation. Here we test a clinically proven Biodegradable-Temporising-Matrix; NovoSorb™ (IDT) repurposed from use in burn and wound treatment that may provide a platform for subcutaneous islet-transplants. IDT showed no impact on human islet viability in-vitro (Glucose-Stimulated-Insulin-Secretion). Mouse islets transplanted under the renal capsule of diabetic recipients pre-implanted with IDT resulted in complete recovery and long-term maintenance of euglycemia (>100-days). Neonatal porcine islets (NPI) transplanted with IDT showed increasing porcine insulin production through time (>300-days). Therefore IDT does not interfere with physiological function of human islets, mouse islets and NPI’s. The in-vivo foreign-body- reaction and tissue remodelling of IDT was assessed (Zeiss 7MP two-photon microscope) using transgenic (LysM-GFP+/tdTomTg) mice. Post-operative-day (POD) 7 showed LysM-GFP+-myeloid cells infiltrating the graft. By POD14 LysM-GFP+-myeloid cell-fusion events had occurred evidenced by the presence of giant cells and scattered immature vascular networks with dispersed loose collagen-fibrils had appeared. At POD30 dendritic-like cells were observed and the vascular network was denser and the collagen fibres had increased in thickness. To assess whether innate sensing of the islet graft alone would occur tdTomato red+-islets were transplanted without IDT. 24hrs later LysM-GFP+ myeloid cells were migrating over the surface of the islets and were exhibiting neutrophil like ‘swarming’ behaviour with evident disruption of islet tissue. This analysis reveals a dynamic interaction between the innate-immune system and the islet graft +/- IDT and that IDT can provide a neo-vascularization platform advantageous for subcutaneous islet transplantation.

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Outcomes and Complications#2 Abstract No. 42 METFORMIN REDUCES CALCINEURIN INHIBITOR NEPHROTOXICITY FERNANDO Mangalee1,2, TAYLOR Kylie1,2, AU Amy1,2, HERATH Sanjeeva1,2, ERLICH Jonathan1,2, ENDRE Zoltan1,2 1Department of Nephrology, Prince of Wales Hospital, Sydney, 2Prince of Wales Clinical School, University of New South Wales, Sydney Hypothesis: Calcineurin Inhibitors (CNIs) prevent transplant rejection but cause significant nephrotoxicity. Biomarkers of early CNI nephrotoxicity combined with therapeutic strategies are needed to improve graft survival. As CNIs impair mitochondrial homeostasis, we hypothesised that CNI nephrotoxicity could be ameliorated using metformin. Methods: A rodent model of subclinical CNI nephrotoxicity was developed using daily gavage with 25mg/kg cyclosporine for 14 days. Urine was collected at regular intervals from cyclosporine treated and controls rats, and kidneys were collected on day 14. Established kidney damage biomarker levels were assessed in urine and kidney tissue samples, and label-free quantitative proteomic analysis was used to identify novel urine biomarkers of CNI nephrotoxicity. The effect of metformin on biomarkers levels was evaluated in this subclinical CNI nephrotoxic model using treatment with 200mg/kg metformin daily for 14 days. Informative biomarkers were also evaluated in a human transplant recipient cohort. Results: Subclinical CNI nephrotoxicity occurred in the model with increased urinary KIM-1 levels in cyclosporine treated rats without change in serum creatinine. In addition, urinary clusterin increased while calbindin reduced compared to control rats. Proteomic analysis identified changes in urinary epidermal growth factor and e-cadherin levels as potential novel biomarkers of CNI nephrotoxicity. Metformin treatment reduced subclinical CNI nephrotoxicity and decreased urinary clusterin and KIM-1 levels. Human studies also identified urinary clusterin as a potential biomarker of CNI nephrotoxicity. Conclusion: Urinary clusterin is a potential marker of subclinical CNI nephrotoxicity. Metformin treatment may be a useful preventive treatment strategy.

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MONDAY, 23 March Free Communications 8 Outcomes and Complications#2

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Abstract No. 43 RAPID DETECTION OF KIDNEY TRANSPLANT INJURY BY QUANTIFYING DONOR-DERIVED CELL-FREE DEOXYRIBONUCLEIC ACID VIA MASSIVELY MULTIPLEX POLYMERASE CHAIN REACTION MCKANNA Trudy1, SIGDEL Tara K.2, ACOSTA Felipe1, NAVARRO Samantha1, ZIMMERMANN Bernhard1, DEMKO Zachary P.1, MOSHKEVICH Solomon1, BILLINGS Paul R.1, SARWAL Minnie M.2 1Natera, Inc, 2Dept of Surgery, University of California San Francisco, San Francisco, CA, USA Purpose: Plasma donor-derived cell-free DNA (dd-cfDNA) is a proven marker for allograft rejection kidney transplant (KT) patients. We assessed performance of a novel single-nucleotide polymorphism (SNP)-based massively multiplexed-PCR method targeting 13,392 SNPs to quantify dd-cfDNA and detect rejection. Methods: 217 biopsy-matched samples from 178 KT patients were categorized as active rejection (AR; n=38, 34.2% subclinical) if dd-cfDNA >1% and eGFR <60.0; or non-rejection (NR): borderline (BL; n=72), stable (STA; n=82), and other injury (OI; n=25). Plasma dd-cfDNA was quantified, correlated with rejection status and compared with estimated glomerular filtration rate (eGFR). AR was defined as antibody- and/or T cell-mediated rejection (ABMR/TCMR) as per Banff 2017 criteria. Results: Significant median differences (P<0.0001) were observed in AR vs NR groups for dd-cfDNA: 2.3% vs 0.6% (BL), 0.4% (STA), 0.7% (OI) and eGFR: 45.7 vs 55.9 (BL), 104.5 (STA), 57.4 (OI, Figure 1). The dd-cfDNA assay vs eGFR was associated with higher sensitivity (88.7% vs. 67.8%), specificity (72.6% vs. 65.3%) and AUC (0.87 vs. 0.74). Median dd-cfDNA did not differ significantly between ABMR (2.2%), ABMR/TCMR (2.6%), or TCMR (2.69%) groups (P=0.9). Similar values were observed for in-protocol (n=114) vs. for-cause (n=103) biopsies. Median dd-cfDNA and eGFR were 3.6% and 57.0 for subclinical AR samples at time of biopsy and 2.0% and 40.8 in clinically apparent AR cases, respectively. Conclusions: This novel assay enabled rapid detection of AR by dd-cfDNA and showed superior performance over the existing standard-of-care. Our data suggest that combined dd-cfDNA and eGFR markers can accurately assess AR in KT patients.

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MONDAY, 23 March Free Communications 8 Outcomes and Complications#2

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Abstract No. 44 RELATIVE SURVIVAL IN KIDNEY TRANSPLANT RECIPIENTS WITH DE-NOVO CANCERS VS NON-TRANSPLANT CANCER PATIENTS: A POPULATION STUDY 1980-2016 DE LA MATA Nicole, ROSALES Brenda, KELLY Patrick, WEBSTER Angela School of Public Health, University of Sydney Introduction: Evolution of cancer therapies has improved survival in the general population. For kidney recipients with cancer, balancing transplant function with nephrotoxic and other adverse events of cancer therapies may mean survival gains are not translated. Relative survival accounts for background mortality and shows excess burden for population subgroups. Methods: We aimed to compare relative survival from cancer diagnosis between the general population and kidney recipients in Australia and New Zealand. We included all kidney recipients in 1980-2016 with de-novo cancer post-transplant from ANZDATA. Relative survival was estimated using Ederer II in kidney recipients and compared to relative survival estimates from the general population with cancer, both using the general population as reference, adjusting for age, sex, country and calendar year. Results: Of 3,603 kidney recipients, 2,759 had de-novo cancer post-transplant where 1,612 died over 14,181 person-years. Overall, relative survival was lower among kidney recipients (0.54, 95%CI: 0.52-0.56 at 5 years) compared to the general population with cancer (AU:0.69, NZ:0.61; at 5 years) (Figure 1A). Relative survival remained lower among kidney transplant recipients for colorectal, melanoma, breast and prostate cancer but was comparable for lung cancer (Figure 1B-F). Conclusion: Relative survival was lower among kidney recipients with de-novo cancers, for most cancer types and pronounced in men. Decreased survival may be due to poorer treatment outcomes or access to treatment.

Figure 1. Relative survival from cancer diagnosis in the kidney recipient population and the general population in Australia and New Zealand for: (A) All cancers; (B) Colorectal cancer; (C) Lung cancer; (D) Melanoma; (E) Breast cancer; and (F) Prostate cancer.

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MONDAY, 23 March Free Communications 8 Outcomes and Complications#2

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Abstract No. 45 GRAFT SURVIVAL AND VISUAL ACUITY FOLLOWING SURGICAL VARIATIONS OF CORNEAL TRANSPLANTATION IN EYES WITH FUCHS ENDOTHELIAL DYSTROPHY KEANE MC1, MILLS RAD1,2, COFFEY NE1, COSTER DJ1, JONES VJ1, WILLIAMS KA1 1Australian Corneal Graft Registry, Flinders University, Adelaide, 2Department of Ophthalmology, Flinders Medical Centre, Adelaide Aims: To compare the primary non-functioning graft (PNFG) rate, long-term graft survival, and best corrected visual acuity (BCVA) following penetrating keratoplasty (PK) or variants of partial-thickness endothelial keratoplasty (DSEK or DMEK) for Fuchs endothelial dystrophy (FED). Methods: Analyses on all 4033 corneal grafts for FED registered with the Australian Corneal Graft Registry from 2009-2018. Results: The number of grafts performed annually for FED doubled over 10 years. The rate of PNFG differed significantly amongst grafts (greater for DSEK and DMEK compared with PK, p<0.001). Longer term, poorer Kaplan-Meier graft survival was observed with DMEK compared with DSEK or PK (see figure, both p<0.001) and this difference remained when PNFG were excluded from analysis. While survival of DSEK compared with PK was significantly worse early after graft (p=0.03), there were no significant differences in long-term survival (p=0.134). Pre-graft median BCVA was worse for PK than DSEK or DMEK, and worse for DSEK than DMEK (all comparisons p<0.001). Significant improvement in median BCVA was seen by three months post-graft for DSEK (p=0.019) and DMEK (p=0.001), and at one year post-graft for PK (p=0.022). Significant improvements were observed at yearly intervals to three years post-DMEK, four years post-PK and five years post-DSEK. Median post-graft BCVA was best following DMEK, reaching 6/12 vision by three months. Conclusions: Excellent visual outcomes are attained quickly following endothelial keratoplasty but are counter-balanced by higher rates of PNFG and poorer long-term graft survival. Together these factors contribute to continued, increasing demand on eye banks.

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Abstract No. 46 EVALUATION OF GRAFT FUNCTION AFTER KIDNEY RE-TRANSPLANTATION IN A SINGLE CENTRE IN VIETNAM DANG Ngoc Tuan Anh, HOANG Nu Ngoc Nhung, PHAM, Nhu Hiep Nephrology and Renal Transplant, Hue Central Hospital,Vietnam Aim: To assess the results of kidney re-transplantation performed at Hue Central Hospital, Vietnam. Methods: 815 kidney transplants have been performed at a single hospital since March 2012, all with living donor grafts. 35 (4.3%) were second kidney transplants performed between 2012 and September 2019. Cross matching was by CDC technique in Hue and histopathology specimens were forwarded to HCMC, 90 minutes flight time away. All recipients received the same immunosuppressive regimen with induction therapy of ATG or Basiliximab and maintenance therapy of tacrolimus, MMF and steroids. CMV prophylaxis with Acyclovir was applied for 35/35 (D (+) and R (+)). Long term follow-up in Vietnam is mandated in order to receive subsidized oral immunosuppressive agents. Results: Average recipient age was 44+/-9 years, 26 were male and 9 were female. 32 recipients had initial primary graft survival of >5 years. 9 (25.7%) were HCV positive. 31 (85.6%) recipients had at least 3 HLA matches. 3 cases of acute rejection responded to treatment. All were sensitized, with 23 having PRA <25%, and 2 >80%. 11 (31%) were ABO incompatible. All grafts had primary function and graft survival at one year was 100% (24/24) and five years (4/4). Graft is summarized in attached Table. Conclusion: With carefully selected patients and using living donor grafts, excellent medium-term kidney graft function can be achieved despite limited access to reliable histopathology services.

1 month 3 months 1 year 3 years 5 years

N 35 35 34 14 4

Creatinine mmol/L

85,30±35,40 88,70±12,80 93,62±21,45 92,78±15,06 87,50±9,25

eGFR 81.2 ±10.9

81.6 ±10.4

80.6 ±10.7

81.8 ±11.0

80 ±12.0

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MONDAY, 23 March Free Communications 9 Transplantation Surgery

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Transplantation Surgery Abstract No. 47 TRANSPLANTATION OF KIDNEYS FROM PAEDIATRIC DONORS AGED 1 YEAR AND UNDER: AN ANALYSIS OF THE AUSTRALIAN AND NEW ZEALAND DIALYSIS AND TRANSPLANT (ANZDATA) REGISTRY FROM 1963 TO 2018 YAO Jinna1,2,3, CLAYTON Philip4,5,6, WYBURN Kate7,8, TOVMASSIAN David1,3, CHOKSI Harsham2, LEE Taina9,2,3, LAU Howard1,3, ALLEN Richard1,2,3, YUEN Lawrence1,3, LAURENCE Jerome9,2,1,3, PLEASS Henry1,2,3 1National Pancreas Transplant Unit, Westmead Hospital, Sydney, 2Discipline of Surgery, Sydney Medical School, University of Sydney, 3Westmead Surgical Research and Education Centre, Westmead Hospital, Sydney, 4Department of Medicine, University of Adelaide, 5ANZDATA, 6Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 7Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, 8Discipline of Medicine, University of Sydney, 9Department of Surgery, Royal Prince Alfred Hospital, Sydney Background: Although some evidence suggests transplantation with paediatric kidneys yields good outcomes, there is reluctance to utilise organs from very small paediatric donors. We describe the collective experience of transplantation using kidneys from paediatric donors ≤1 year of age in Australia and New Zealand. Methods: We analysed the ANZDATA registry on all deceased donor kidney transplants from paediatric donors ≤1 year of age from 1963-2018. Statistical significance of cause of graft failure was calculated with Fisher’s exact test. Results: From 1963-1999, 16 transplants were performed (9(56%) adults, 7(44%) children). Donor and recipient characteristics are in table 1. Death-censored graft survival was 50% and 43% at 1 and 5 years, respectively, and was superior in adults (p=0.001). Causes of graft failure included acute rejection (19%), thrombosis (13%), haemolytic uraemia syndrome (6%), cortical necrosis (6%), and death with functioning graft (19%). From 2000-2018, 26 transplants were performed. (25(96%) adults, 1(4%) children) All kidneys were transplanted en bloc. Mean creatinine was 73µmol/L+/-49.1 at 5 years. Death-censored graft survival was 85% at 1 and 5 years. Patient survival was 100% at 1 and 5 years. Causes of graft failure included thrombosis (8%), death with functioning graft (15%) and cortical necrosis (4%). Overall, there was a higher but not statistically significant incidence of graft loss due to vascular thrombosis (25% vs.6%, p=0.158) and acute rejection (25% vs. 3%, p=0.088) in paediatric compared to adult recipients. Conclusion: These results favour the use of small paediatric kidneys donors for adult recipients with selected paediatric recipients under appropriate circumstances. Table 1.

Child (1963-1999) Child (2000-2018) Adult (1963-1999) Adult (2000-2018)

n 7 1 9 25

Donor weight, median (IQR) 14 (12, 15) 10 (10, 10) 12 (10, 15) 11 (10, 12)

Donor gender Female Male

3 (50%) 3 (50%)

0 (0%) 1 (100%)

4 (50%) 4 (50%)

6 (24%) 19 (76%)

Total ischaemia, median (IQR) 14 (8, 19) 14 (14, 14) 14.5 (10, 17.5) 13 (11, 15)

Age at transplant, median (IQR) 4 (1, 10) 16 (16, 16) 46 (40, 50) 45 (37, 48)

Recipient weight (kg), median (IQR) 21 (12, 27) 48 (48, 48) 59 (55, 65.5) 70 (64, 89)

Recipient gender Female Male

3 (43%) 4 (57%)

0 (0%) 1 (100%)

3 (33%) 6 (67%)

9 (36%) 16 (64%)

Waiting time (years), median (IQR) 0.6 (0.2, 1.1) 0.2 (0.2, 0.2) 2.2 (1.1, 4.7) 4.6 (2.7, 5.7)

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Child (1963-1999) Child (2000-2018) Adult (1963-1999) Adult (2000-2018)

Graft number 1 2

7 (100%) 0 (0%)

1 (100%) 0 (0%)

9 (100%) 0 (0%)

21 (84%) 4 (16%)

Abstract No. 48 DUAL KIDNEY TRANSPLANTATION: TWO GOOD OR DOUBLE TROUBLE? HANNA Thomas, TAYLOR Sam, O'MAHONY Kate, DITTMER Ian, LANGLANDS Janice, MANLEY Paul, MUTHUKUMARASWAMY Carl Auckland Renal Transplant Group, Auckland City Hospital Introduction: Dual kidney transplantation (DKT) is an underused strategy to expand the donor pool. The literature offers no consensus on DKT allocation protocols and published outcomes following DKT are limited by selection bias. We aimed to asses our DKT protocol by comparing DKT outcomes with a matched cohort of single kidney transplants (SKT). Methods: Between January 2015 and July 2019 all ECD kidneys were biopsied and allocated to SKT, DKT or discarded according to the histological New Zealand Kidney Score. Donor characteristics between the groups were compared and a matched cohort (1:1) of the SKT group were selected based on significant differences. Complication rates, graft function and survival were compared between the matched SKT control group and all DKTs between 2009-2019. Results: 86 ECD kidney pairs were biopsied and allocated to either SKT- 70, DKT-10 (20 kidneys) or discarded-6 (12 kidneys). Donor age and terminal creatinine were significantly higher in the DKT group compared to the SKT group: 66.9 years vs 62.3 years; p=0.01 and 96.9µmol/L vs 74.8µmol/L; p=0.032, respectively. After matching 1:1 for both variables, 18 SKT recipients were compared to 18 DKT recipients; no significant differences in donor or recipient characteristics remained. The DKT group had significantly better graft function at one month (eGFR 53.4 vs 38.7; p=0.047) and one year (eGFR 60.5 vs 41.8; p=0.051) with no difference in complication rates, graft and patient survival. Conclusions: DKT offers superior graft function compared to matched SKT recipients without compromising safety.

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Abstract No. 49 THE EFFECT OF SURGICAL CLOSURE OF HEMODIALYSIS ARTERIOVENOUS FISTULA AFTER SUCCESSFUL KIDNEY TRANSPLANTATION MARUI Yuhji, YOZA Naoto, MATSUMURA Kaori, USUBA Wataru, AOKI Naoto, NISHI Tomohiro, KATSUOKA Yuichi, NAKAZAWA Ryuto, SASAKI Hideo, KIKUCHI Eiji Department of Urology, St Marianna University School of Medicine,Japan Aim: The hemodynamic burden induced by arteriovenous fistulas (AVF) may contribute the deleterious effect of left ventricular hypertrophy, which may subside by AVF closure after successful kidney transplant shown by case reports. But the influence on the kidney graft remained a matter of debate. So, we investigated the impact of the closure on the graft function after kidney transplantation. Methods: We compared changes in transplanted kidney function before and after AVF closure for 28 recipients who underwent the surgical closure between 2011 and 2018. The t-test was used for statistical examination. Results: Patients, median age 50 years, underwent the surgical AVF closure with a median period of 28 months from kidney transplantation. Compared to the mean eGFR(ml/min) before AVF closure, which was 48.0±10.5, and the means after 1 month, 3 months, 6 months, and 1 year, which were 49.8±11.6, 50.5±11.9, 49.6±12.4 and 49.0±11.7 respectively, the graft function was significantly improved after 1 month and 3 months (p<0.05). In a case where the brain natriuretic peptide (BNP) was measured before and after the closure, the eGFR improved as BNP decreased. (figure) Conclusions: The improved cardiac function possibly due to AVF closure may have had a positive impact on the kidney graft function. Given the result of an improvement trend of the graft function in the short term, with definite indications such as heart failure due to high flow AVF, painful aneurysm and aesthetic reasons, the surgical AVF closure appears to be safe and reasonable in well-functioning kidney recipients. Figure Change of BNP and eGFR after AVF closure

64.0

66.0

68.0

70.0

72.0

74.0

0.0

5.0

10.0

15.0

20.0

25.0

30.0eGFR

eGFR ml/min

PRE 1POM 3POM 6POM 12POM

BNP pg/dl

BNP

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Abstract No. 50 TOTAL PANCREATECTOMY WITH ISLET AUTOTRANSPLANTATION FOR CHRONIC PANCREATITIS: AN AUSTRALIAN PERSPECTIVE TOVMASSIAN David1,2, YOON Peter1, YAO Jinna1,3, HAWTHORNE Wayne1,4,5, YUEN Lawrence1,3, ALLEN Richard1,3, LAURENCE Jerome1,3, O'CONNELL Philip1,6, ROGERS Natasha1,6, PLEASS Henry1,3 1National Pancreas Transplant Unit, Westmead Hospital, Sydney, 2Western Clinical School, University of Sydney, 3Discipline of Surgery, Sydney Medical School, University of Sydney, 4Transplantation Laboratory, Westmead Millennium Institute, Westmead Hospital, Sydney, 5School of Medicine, Faculty of Health Sciences, University of Sydney, 6Discipline of Medicine, University of Sydney Background: Chronic pancreatitis is a debilitating disease with insidious onset characterised by fibrosis, loss of parenchymal function and pancreatic calcification. Total pancreatectomy is known to alleviate pain symptoms associated with chronic pancreatitis however patients suffer from difficult to manage diabetes mellitus post-operatively. Brittle diabetes is the major contributor to morbidity and mortality associated with total pancreatectomy. Islet autotransplantation allows patients to have a period of insulin free survival and can be protective against developing brittle diabetes. Methods: We retrospectively reviewed all patients (n=4) who underwent total pancreatectomy with islet autotransplantation within the past 5 years. Primary outcomes measured included 30-day mortality, post-operative pain and period of insulin independence. Results: A total of 4 patients underwent total pancreatectomy with islet autotransplantation with mean BMI of 19.2 ± 4.6. All patients were alive at 1 year after surgery. Mean units of insulin required at 30 days post-op was 11 ± 2.9 per day. All patients remained insulin free 1 year post islet autotransplant. The mean C-peptide level at day 1 post-op was 0.23 vs 0.31 at day 30 (p=0.36). All patients were successfully weaned off opiate analgesia within 30 days post-op. Conclusion: Total pancreatectomy with islet autotransplantation offers the ability to treat symptoms for patients with chronic pancreatitis and improve their post-operative morbidity associated with diabetes. Our sample size is low in this pilot study and further research is necessary to ensure this procedure is safe and efficacious.

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Abstract No. 51 THE USE OF DECEASED DONOR VESSELS IN KIDNEY TRANSPLANTATION LEE Taina1, VERRAN Deborah1, LAURENCE Jerome1,2, PULITANO Carlo3,2,4 1Transplant surgery, Royal Prince Alfred Hospital, Sydney, 2Discipline of Surgery, Sydney Medical School, University of Sydney, 3Transplant surgery, University of Sydney, 4Institute of Academic Surgery, Institute of Academic Surgery Background: The use of iliac vessels from a third party deceased donor may help address technical challenges in renal transplant surgery, particularly living donor transplantation where there may be short donor allograft vessels. Methods: Analysis of donor and recipient data from a retrospective case series of living donor renal transplant recipients following vascular reconstruction with deceased donor vessel extensions at Royal Prince Alfred Hospital. Results: Between 2004-2018, 26 recipients met inclusion criteria out of 495 living donor transplants performed, of which, 11(42%) received the right kidney and 15(58%) received the left kidney. 10 allografts underwent only venous reconstruction, 2 underwent only arterial reconstruction and 14 underwent both. Nine(35%) of these allografts also had >1 donor artery. The mean(SD) secondary warm ischaemic time was 35(+/-10) minutes. The mean(SD) recipient BMI was 27(+/-4). Mean(SD) creatinine at 90 days was 183(+/-180) and of these recipients, 3(12%) had delayed graft function. At a median follow-up of 1791 days, there were 5 graft losses, of which 2 were lost due to death with a functioning graft(Figure 1). Causes of graft loss included recurrent disease, chronic allograft nephropathy and rejection. One graft was lost at 5 days with vascular thrombosis associated with severe acute rejection in an ABO incompatible transplant. Eight rejection episodes occurred in seven recipients over mean period of 306 days. Conclusions: The use of third party deceased donor vessels is a safe technique, which can facilitate renal allograft implantation in technically challenging cases.

0 2000 4000 60000

50

100

Figure 1: Death Censored Graft Survival

Survival (days)

Perc

ent s

urvi

val

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Abstract No. 52 OPTIMISING A MOUSE MODEL OF RENAL ISCHEMIA REPERFUSION INJURY PEFANIS Aspasia1,2, MCRAE Jennifer M1, BONGONI Anjan K1, IERINO Frank L3,2, COWAN Peter J1,2 1Immunology Research Centre, St Vincent's Hospital, Melbourne, 2Department of Medicine, University of Melbourne, 3Department of Nephrology, St Vincent's Hospital, Melbourne Background: Ischemia-reperfusion injury (IRI) following transplantation results in delayed graft function, amplified rejection and long-term fibrosis. Studying the pathogenic mechanisms of IRI is complicated by variation in experimental mouse models. Subtle changes in temperature, anesthesia, mouse age/sex and strain/colony differences can influence results. Aim: To characterize a mouse model of renal IRI which can be used to study mechanisms of injury and evaluate therapeutic renoprotective strategies. Methods: 10-12 week old male C57BL/6 mice were administered ketamine/xylazine anesthesia prior to a right nephrectomy followed by left renal pedicle clamping for 18, 20, 22 or 24 min. Samples were collected 24 hrs post-reperfusion assessing renal injury and inflammation. A separate cohort of mice underwent 18 min ischemia, with samples collected at various timepoints post reperfusion assessing the kinetics of injury/inflammation. Results: Renal injury was proportional to ischemia time (Figure 1). The gene expression of kidney injury (KIM-1/NGAL p<0.0005) and inflammation (IL-1β/MIP-2 p<0.05) markers were progressively upregulated with increased ischemia time. At time points analyzed to date, peak injury occurred 24 hrs post reperfusion (Creatinine p<0.01; Tubular injury score p<0.05). Gene expression of KIM-1 and NGAL were maximally upregulated at 24hrs post reperfusion (p<0.001), with markers of inflammation highest at 24hrs (IL-1β p=0.033) and 72hrs (IL-33/ TNFa/ TLR2/ TLR4 p<0.001). Conclusion: We have characterized a model of renal IRI showing a relationship between ischemia time, renal injury and the upregulation of various relevant genes. This model provides a platform to test novel therapeutic agents aimed at minimizing renal IRI and improving transplant outcomes.

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Abstract No. 53 COMPARISON OF IN VITRO SUPPRESSION OF CD4+CD25-T EFFECTOR CELL PROLIFERATION BY TH2-LIKE TREG AND NAIVE TREG USING A REFINED FLOW CYTOMETRY BASED ASSAY RAKESH Prateek1,2, VERMA Nirupama1, BEDI Sukhandeep1, TRAN Giang1,3, ROBINSON Catherine3, HODGKINSON Suzanne1,3, HALL Bruce1,3 1School of Medicine, University of New South Wales, Sydney, 2School of Medicine, Liverpool Health Service and University of New South Wales, South Western Sydney Clinical School, Liverpool, NSW, 3Liverpool Health Service and University of New South Wales, South Western Sydney Clinical School, Liverpool, NSW Aims. Naïve CD4+CD25+T regulatory cells (Treg) activated by antigen and rIL-4 generate Ts2 cells expressing IL-5Rα. Ts2 cells activated with rIL-5 and specific antigen generate more potent Th2-like Treg. Accurate assessment of specific in vitro suppression of effector cells is difficult due to presence of stimulator cells and Treg. We assessed the suppression by Th2-like Treg using a refined flow cytometry based assay. Methods. Th2-like Treg were generated by 4d culture of CD4+CD25+ tTreg from naïve DA rats with PVG-stimulators and rIL-4 to generate Ts2 cells, which were further cultured with PVG-stimulators and rIL-5 for 3d. Serially diluted freshly isolated CD4+CD25+ tTreg or Th2-like Treg were co-cultured for 5-7 days with constant number of CD4+CD25-T DA effector cells and PVG thymic stimulator cells. Suppression of CD4+CD25-T cell proliferation was analysed using FACS, and flow cytometry to assess the number of undivided CTV+ CD4+CD25-T effector cells after exclusion of CFSE+ stimulator cells and CD25-PE+ Treg. Results. CD4+CD25-T cells typically proliferated 5-6 cycles by 5d, consistent with 1-2% of original responder population proliferating against alloantigen. tTreg suppressed T effector cell proliferation at ratios of 1:1 to 1:4 (Treg:Responder). With Th2-like Treg, CD4+CD25-T cell proliferation was suppressed up to 1:128 or 1:512 in both 5 and 7 day cultures. Conclusion. This assay specifically assessed the suppression of effector cells, avoiding interference from stimulator cells or Treg and confirmed that the two-step activation of tTreg, first with IL4/antigen then IL-5/antigen, could induce highly potent Treg that suppress at high in vitro ratios of 1:128. Abstract No. 54 IN VIVO IDENTIFICATION OF GENES ASSOCIATED WITH KIDNEY GRAFT FIBROSIS MA Xiaoqian, LU Bo, CAO Qi, ZHAO Yuanfei, HU Min, YI Shounan, O'CONNELL Philip Centre for Transplant and Renal Research, Westmead Millennium Institute, Westmead Hospital, Sydney Aims: Our previous GoCAR multicenter study has identified a set of 13 genes with independent prediction for the development of fibrosis at 1 year after kidney transplantation. The aim of this study was to identify which one of these genes is important in associated with kidney graft fibrosis in in a mouse model of transplantation. Methods: BALB/c mouse-derived kidneys were transplanted into C57Bl6/J recipients. A single dose of MR1(CD154) Ab injection was given 24h before transplantation in MR1 treatment group. Another native kidney of recipients was removed at day 3 post transplantation. Kidney grafts were harvested at day 30 post transplantation. Sirius red was performed to evaluate the fibrosis development. Real-time PCR and Western blot were used for analysis of relevant gene and protein expression, respectively within grafts. Results: Grafts from MR1 treated mice displayed a significant reduction of Sirius red staining in the tubular interstitium and significantly lower mRNA levels of COL I and FN when compared to controls, indicating reduced accumulation of ECM and significantly delayed fibrosis development in MR1 treated recipients. Interestingly, mRNA expression of CHCHD10 (which is the mitochondrial gene involved in energy and membrane repair) and its protein level were significantly upregulated in control group compared to the MR1 treatment group detected by real-time PCR and Western blot. Discussion: The results suggested that CHCHD 10 may be involved in the signaling pathway of fibrosis and its real function is being under further study using CRISP/CAS9 technique.

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Abstract No. 55 ASSESSING CYTOMEGALOVIRUS IMMUNITY IN POST LUNG TRANSPLANT RECIPIENTS LI Jenny1, GARDINER Brad1, OATES Clare1, LIN Jie1, JALALI Sedigheh1, CRISTIANO Yvonne2, LEVVEY Bronwyn2, BROOKS AG1, SNELL GI3, WESTALL GP3, SULLIVAN LC1,3 1Department of Microbiology and Immunology, University of Melbourne, 2Alfred Hospital, Melbourne, 3Lung Transplant Service, Alfred Hospital, Melbourne Introduction/Aim: Cytomegalovirus (CMV) disease causes significant morbidity and mortality in lung transplant recipients. Current guidelines use pre-transplant serology to guide antiviral prophylaxis. Immunological monitoring may allow for tailoring of antiviral prophylaxis to a patient’s risk of infection. In this study we aimed to determine if commercially available assays, QuantiFERON-CMV and T-Track-CMV (ELISpot assay), and HLA-CMV tetramer staining, could predict risk of CMV disease in lung transplant recipients. Methods: We retrospectively analysed QuantiFERON-CMV data and frozen peripheral blood mononuclear cells (PBMCs) from 34 lung transplant recipients transplanted from 2014 to 2015. T-Track-CMV was performed per manufacturer’s instructions using cryopreserved PBMCs. Human leukocyte antigen (HLA) typing was obtained and HLA-CMV tetramer staining was performed. CMV viral load in both serum and bronchoalveolar lavage (BAL) post-transplant were obtained from patients’ medical records and correlated to assay results. The predictive ability of the assays was determined using Kaplan Meier curves. Results: QuantiFERON-CMV and T-Track-CMV assays were predictive of high level CMV viraemia. In both assays, 6% of assay positive recipients developed high level viraemia compared to 94% of assay negative recipients. In contrast, 53% of QuantiFERON-CMV positive recipients and 44% of T-Track-CMV positive recipients developed high level allograft infection. Additionally, 90% of recipients who were CMV seropositive pre-transplant were HLA-CMV tetramer positive which did not correlate with CMV disease development post-transplant. Conclusion: Our study demonstrates that commercially available immune monitoring assays may predict high level viraemia post-transplant. Further improvement is required for prediction of replicating CMV in the allograft and validation of clinical utility. Abstract No. 56 RENAL TRANSPLANT SCREENING FOR ADVANCED COLORECTAL NEOPLASIA IN THE WELLNESS CLINIC TAN Rachel Yi Ping1,2, VAN DER JEUGD Jane2, JUNEJA Rajiv1,2, BARBARA Jeffrey1,2 1Department of Nephrology, Flinders Medical Centre, Adelaide, 2College of Medicine and Public Health, Flinders University, Adelaide Aim: To determine whether it is appropriate to screen for advanced colorectal neoplasia with immunochemical faecal occult blood testing (iFOBT) for human haemoglobin in the renal transplant population. Method: The screening period for this retrospective study was from 1st July 2014 to 30th June 2019 on renal transplant recipients who were invited to attend the wellness clinic conducted by a Nurse Practitioner. iFOBT x2 during that time period were requested on an annual basis for those patients who attended the wellness clinic. Renal transplant recipients with positive iFOBT were referred for colonoscopy. Advanced colorectal neoplasia was defined as an adenoma of at least 10 mm in diameter, villous features, high-grade dysplasia or colorectal cancer. Results: 44% (n=103) of prevalent renal transplant recipients attended the wellness clinic. Baseline characteristic were 84% (n=63) male, with a mean age of being transplanted at 50 years old and 7.17 years post renal transplant. 66% (n=68) of this subgroup underwent iFOBT x2 on at least one occasion. 33.8% (n=23) of initial iFOBTs were found to be positive and were referred for colonoscopy. 69.5% (n=16) had colonoscopies. Of those, 12.5% (n=2) revealed advanced colorectal neoplasia, 25% (n=4) had non-advanced colorectal neoplasia and the remainder 62.5% (n=10) with normal or insignificant pathology. One patient within the normal subgroup developed colorectal cancer within two years after iFOBT screening and colonoscopy. Conclusion: Screening for advanced colorectal neoplasia post renal transplantation with iFOBT may be considered worthwhile in this at-risk population.

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Abstract No. 57 EFFECT OF DIET ON HUMAN ISLET FUNCTION CHEUNG Charmaine1, BURNS Heather1, STOKES Rebecca1, GUNTON Jenny1,2 1Department of Endocrine and Metabolism, The Westmead Institute for Medical Research, 2Department of Endocrine and Metabolism, Westmead Hospital, Sydney AIM: The aim of the research is to use “humanised mice” which are diabetic mice transplanted with human islets to test whether different diets affect the function and survival of human islets. METHODS: Immunodeficient RAG1-null mice (C57Bl/6 genetic background) were used for human islet transplant. Prior to transplant, diabetes was induced by alloxan. 17 female and 5 male mice each received 2000IEQ human islets under the kidney capsule from donors with normal glucose tolerance. Eight weeks after transplantation 2 mice did not have resolution of diabetes and were excluded. Mice with functioning grafts (n=20) were placed on high-fat diet (HFD, 45% of calories from fat) or continued on normal chow (n=10 each). Glucose tolerance test (GTT) were performed before and after diet. Energy expenditure was measured by using Promethion metabolic cages. RESULTS: Mice fed HFD had significant weight gain by 8 weeks of diet (≥3g) and their random-fed BGL were higher (2-3mmol/L) than mice from the same human donors eating chow. On formal GTT, mice fed HFD showed deterioration of their glucose tolerance compared to chow-fed animals. The effect was more pronounced with donor 278 than donor 281 but glucose tolerance deteriorated for both sets of islets. At cull, mice eating HFD had obvious fatty liver changes. CONCLUSION: Consumption of HFD showed detrimental effects on human islets even though the donors had normal glucose tolerance.

Figure 1: GTT results pre diet vs Chow vs HDS on 16 weeks post diet commencement for female mice from different donor H281 and H278. Significantly higher BGL readings observed in HFD group at 15 minutes and 30 minutes after glucose administered for donor Islets H278.

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Abstract No. 58 THE USE OF FREESTYLE LIBRE FLASH GLUCOSE MONITORING SYSTEM TO MONITOR BLOOD GLUCOSE LEVELS IN A DIABETIC PORCINE MODEL PENKO Daniella1,2, NITSCHKE Jodie1,2, JOHNSTON Julie1,2, MATHEWS Loren3, JOHNS Daniel3, MUIRHEAD Robb3, PULLAN Caitlin3, DROGEMULLER Christopher4,2, TORPY David5,2, KUCHEL Timothy3, COATES P. Toby H2,1 1Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 2Department of Medicine, University of Adelaide, 3South Australian Health and Medical Research Institute, Preclinical Imaging and Research Laboratories, SAHMRI, 4Royal Adelaide Hospital, 53Endocrine and Metabolic Unit, Royal Adelaide Hospital Introduction:Abbott Laboratories Flash Glucose Monitoring System, FreeStyle Libre, is a recent clinical innovation to monitor blood glucose levels (BGL) of Diabetics. The system involves self-application of a sensor with attached probe onto upper arm measuring interstitial glucose levels. The system continuously monitors glucose-levels, identifying fluctuations improving regulation. The sensor can be worn for up to 2 weeks, reducing need for repetitive self-monitoring using blood glucose strips. However, accuracy discrepancies were noted between measuring interstitial versus blood glucose-levels. This study assessed the device in a large diabetic porcine model, to investigate the ease of using the FreeStyle Libre monitoring glucose levels and its accuracy. Method:Landrace pigs were rendered diabetic by chemical destruction of the beta cells or removal of the pancreas. The sensor was inserted into the skin adjacent to dorsal neck vertebrae. Intra-venous glucose tolerance test (IVGTT, 0.5g glucose/kg) was performed over 120 minutes, recording BGL readings via sensor and self-monitoring using a glucose meter. Glucose-levels were monitored twice daily using the scanner up to 75 days following diabetes induction. Results:The device successfully continuously monitored glucose-levels, enabling management of diabetes via exogenous insulin. A few failures lead to momentary read errors, requiring replacement of the sensor. However, this may be due to the nature of working with large animals and site of application. Scanner IVGTT data followed a similar trend to traditional self-monitoring using test strips. A lag was observed in scanner glucose-levels versus test strip, as reported elsewhere. Conclusion:The device was well-tolerated, demonstrating a novel application and off-label use of this system in a large animal setting. Abstract No. 59 IN VITRO ACTIVATION OF HUMAN CD4+CD25+CD127LO TREG SUBPOPULATIONS VERMA NIRUPAMA D1,2, AL-ATIYAH Ranje1, TRAN GIANG1,2, HODGKINSON SUZANNE J1,3,4, HALL BRUCE M1,3,5 1Immune Tolerance Group, Ingham Institute of Applied Medical Research, 2South Western Sydney Clinical School, University of New South Wales, Sydney, 3Department of Medicine, University of New South Wales, Sydney, 4Department of Neurology, Liverpool Hospital, 5Renal Unit, Liverpool Hospital Background: Human T regulatory cells (CD4+CD25+CD127loFoxp3+) population is heterogenous. It can be divided into three subpopulations; Population I (Pop I) as CD25+CD45RA+ naïve Treg, Pop II as CD25hiCD45RA-

highly activated Treg and Pop III as CD25+CD45RA-. Activated Treg express chemokine receptors of activated T cells, including CXCR3 (Th1) and CCR6 (Th17), that promote their migration to inflammation site. Culture of whole Treg population with alloantigen and rIL-2 increased proportion of Population II (activated Treg). Here, we investigated the effect rIL-2 and allostimulation on activation on individual populations. Methods: Healthy human blood was subjected to PBMC isolation using standard Ficoll method. PBMC were stained with CD4, CD25, CD127 and CD45RA. Subpopulations within Treg (CD4+CD127loCD25+) were sorted and cultured for 4 days with rIL-2 and alloantigen (allo). Multicolour flow cytometry assessed changes in Treg subpopulations. Results: Pop I lost Foxp3 in absence of allo or rIL-2. Culture with both (allo/rIL-2) produced cells with higher Foxp3 and CD25 expression, which expressed CD45RA, and had increased expression of CCR4 but not CXCR3 and CCR6. Pop II or III were not increased. Pop II died when cultured alone or with allo. Activation with rIL-2 alone or with allo increased expression of Foxp3 and CD25, maintained CCR4 and CXCR3 expression and increased CCR6+ cells. Pop III when cultured with IL-2, had mixed changes, some cells expressed less Foxp3 while others shifted to Pop II. Conclusions: Each Treg subpopulation has a different pathway of activation. These studies may identify a way to grow antigen-specific Treg for therapy.

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Abstract No. 60 CHARACTERISATION OF DONOR-DERIVED LYMPHOCYTES IN THE CIRCULATION OF LUNG-TRANSPLANT RECIPIENTS STANKOVIC Sanda1,2, CHRISTIANO Yvonne3, WESTALL Glen3, LEVVEY Bronwyn3, BROOKS Andrew1,2, SNELL Gregory3, SULLIVAN Lucy1,2,3 1Department of Microbiology and Immunology, University of Melbourne, 2Peter Doherty Institute for Infection and Immunity, 3Lung Transplant Service, Alfred Hospital, Melbourne The presence of donor-derived lymphocytes in the circulation of transplant recipients has been associated with graft dysfunction. Conversely, other studies indicate that the presence of donor-derived lymphocytes may actually induce tolerance to the transplanted organ. To investigate if donor-derived lymphocytes are present in a lung transplant setting and to better characterise their temporal difference in circulation, we investigated by flow cytometry peripheral blood mononuclear cells (PBMCs) at regular intervals post-transplant. Samples from 2 weeks to 18 months were analyzed for presence and phenotype of donor-derived lymphocytes. We find that at 2 weeks post-transplant most recipients have some detectable donor-derived lymphocytes in circulation but after this point they are largely absent. Phenotypically, these cells consist largely of CD3+ T cells and NK cells, with up to 4% of circulating lymphocytes being of donor origin at 2 weeks post-transplant. Interestingly, Using Ki67 as a marker of proliferating cells, we find they undergo proliferation at early time-points, indicating their potential contribution to immune responses within the recipient. In conclusion, donor-derived lymphocytes are common in the circulation of lung transplant recipients. Their exact role in the immunology of recipient will be a target of our future research. Abstract No. 61 USE OF HLA EPITOPES IN A VIRTUAL CROSSMATCH (VXM) TO BETTER ASSESS LUNG TRANSPLANT (LTX) COMPATIBILITY HIHO Steven1,2, SULLIVAN Lucy2,3, WESTALL Glen2, SNELL Greg2 1Tissue Typing Laboratory, Australian Red Cross Blood Service, 2Lung Transplant Service, Alfred Hospital, Melbourne, 3Doherty Institute Introduction: In the era of using solid phase assays to identify potential anti-human leukocyte antigen (HLA) donor specific antibodies (DSAs), the use of a virtual crossmatch (vXM) as an assessment of compatibility has increased. vXM has many benefits over a cell based assay, including decreased turn-around time and reduced cold ischemia times thus allowing a wider geographical range for potential donors. However, a vXM does not assess the level of HLA compatibility, which has recently been shown to be associated with LTx outcomes. Here we investigate in a retrospective cohort how a vXM incorporating existing HLA DSA and epMM could have predicted outcomes. Methods: We analysed 310 primary LTx undertaken 2008-2015. Recipients and donors were high resolution HLA typed for all HLA loci. HLA antibody testing was performed using Luminex Single Antigen Beads and cumulative MFI cut-offs >5000 were deemed positive for vXM. HLAMatchmaker (v2.1) was used to determine epMM. CLAD was diagnosed using ISHLT guidelines. Kaplan Meier analysis with long-ranked tests was used in comparing groups. Results: Neither HLA class I or class II pre-LTx DSA was associated with CLAD-free survival, although numbers were low due to intentional avoidance of existing DSA. epMM alone showed no significance to CLAD-free survival. However, combining epMM and avoidance of pre-tx DSA was significantly associated with improved patient survival (p<0.001). Conclusion: Here we demonstrate, how the inclusion of epMM to vXM would improve the compatibility assessment and provide clinicians greater confidence in recipient selection for deceased donors.

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Abstract No. 62 EARLY CESSATION OF PATIENT CONTROLLED ANALGESIA (PCA) LAPAROSCOPIC DONOR NEPHRECTOMY KEOGH Kandice1, LAWSON Malclm2, PRESTON John2, WOOD Simon2, GRIFFIN Anthony3, RHEE Handoo2 1Department of Surgery, Princess Alexandra Hospital, Brisbane, 2Urology and Transplant Surgery, Princess Alexandra Hospital, Brisbane, 3Transplant Surgery, Princess Alexandra Hospital, Brisbane Background: Patient controlled analgesia (PCA) systems are frequently employed in the post operative management of surgical patients however evidence regarding their impact has been mixed. Patients undergoing laparoscopic donor nephrectomy represent a special cohort given the exceptional health and altruistic circumstances of their surgical procedure. Aims: The aim of this study was to assess the proportion of patients using PCA systems post operatively and whether the use of PCA impacted duration of inpatient stay and recovery. Methods: A single center retrospective cohort analysis was performed on all patients who underwent laparoscopic during a four year period. Patients for inclusion were identified via a prospectively managed database. Information regarding patient demographics, duration of stay, delivery of analgesia and occurrence of complications was collected from electronic medical records. Results: There were 94 patients who underwent surgery. The cohort consisted of 53% female patients with an average age of 51 years. 88% (n=83) of patients were commenced on PCA analgesia as a part of routine post operative order. A large proportion of PCAs were ceased on post operative day one (68%). Average admission duration did not differ significantly between those using a PCA (3.27 days) and those with as required analgesia (3.27 days). For those with oxycodone PCAs increased usage in the immediate post op period was correlated with longer admission (p=0.02). The most frequent side effect associated with PCA use was nausea (26%). Despite this the overall use of antiemetics did not differ between PCA and PRN patients (p=0.66). Conclusion: In this study, PCAs did not appear to significantly change the post operative outcomes for patients. This may be due to early cessation of PCAs with clear evidence for delayed recovery in patients who require or have PCAs for longer.

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Abstract No. 63 DOES DONOR TERMINAL, ADMISSION OR BEST ESTIMATE GLOMERULAR FILTRATION RATE PREDICT KIDNEY TRANSPLANTATION OUTCOMES? IRISH Georgina Laura1,2,3, COATES Toby3,4, CLAYTON P A2,3,4 1Oxford Kidney Unit, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom, 2South Australian Health and Medical Research Institute (SAHMRI), Adelaide, Australia, 3Department of Medicine, University of Adelaide, 4Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital Aim: When assessing deceased kidney donors, a key factor is donor kidney function. It is unclear whether terminal, admission, or the best of terminal and admission estimated glomerular filtration rate (eGFR) best predicts outcomes. We aimed to examine which eGFR measure most accurately predicts recipient outcomes. Methods: Using data from the Australia and New Zealand Organ Donor (ANZOD) and Dialysis and Transplant (ANZDATA) Registries, we included adult recipients of deceased donor kidney-only transplants over 2003-2017. We created multilinear regression models for the outcomes of recipient eGFR at 6 and 12 months. We compared the models using F test and adjusted R squared. We constructed Cox proportional hazards models for the outcomes of graft survival and death censored graft survival. Results: 7303 transplant recipients were included in the analysis. There was strong evidence of an association between terminal, admission and best donor eGFR and 6 and 12 month recipient eGFR (figure1). The models performed similarly, although adjusted R squared values were slightly better for terminal eGFR at 6 months and admission eGFR at 12 months. The Cox proportional hazard models showed eGFR was a strong predictor of graft survival, and terminal and best eGFR were better predictors than admission eGFR. The C statistics for discrimination were similar across all models. Conclusions: In deceased kidney donors, admission, terminal and best eGFR are all strongly associated with recipient kidney function. Terminal and best eGFR were slightly better than admission eGFR at predicting graft survival. Multilinear regression Cox Proportional Hazard Model Outcome 6 month eGFR 12 month eGFR

Death Censored Graft Survival

Overall Graft Survival

Beta coefficient (SE)

F test statistic p value

Adjusted R squared

Beta coefficient (SE)

F test statistic p value

Adjusted R squared

Hazard Ratio (95% CI)

Wald test p value

Harrel’s C statistic

Hazard Ratio (95% CI)

Wald test p value

Harrell’s C statistic

Terminal eGFR

0.072 (0.009)

9.31 P<0.0001 0.28

0.068 (0.009)

7.88 p<0.0001 0.28

0.94 (0.92-0.96)

20.30 p=0.0004 0.65

0.96 (0.95- 0.98)

19.71 p=0.0001 0.66

Admission eGFR

0.050 (0.010)

3.85 p=0.0002 0.27

0.054 (0.011)

4.59 p<0.0001 0.27

0.95 (0.92-0.98)

9.67 p=0.0464 0.65

0.97 (0.95-0.99)

9.21 p=0.01 0.65

Best eGFR

0.090 (0.011)

8.99 p<0.0001 0.28

0.090 (0.012)

8.25 p<0.0001 0.28

0.94 (0.91-0.97)

16.24 p=0.0027 0.65

0.96 (0.94-0.98)

15.49 P=0.0004 0.66

Figure 1: Test statistics and point estimates for multilinear regression and Cox proportional hazard models

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Abstract No. 64 INVESTIGATION OF FALSE POSITIVE LUMINEX RESULTS USING SURROGATE FLOW CROSSMATCHING DOWNING Jonathan, VUKOVIC Irena, SUTANTO Michael, WONG Zo-Ee, LE Cindy, DEY Jacqueline, HOGAN Jessie, DE SANTIS Dianne, MARTINEZ Patricia Clinical Immunology, PathWest Investigation of False Positive Luminex Results using Surrogate Flow Crossmatching Accurate Human Leucocyte Antibody (HLA) profile information is essential for safe and equitable allocation of solid organ transplants. The Luminex Single Antigen Bead (SAB) assay is sensitive and highly specific; however, the SAB assay is known to generate false positive results which could potentially deny access to transplant. We report the investigation of a number of cases of suspected false positive reactivity in the SAB assay using flow cytometry ‘surrogate crossmatches’ (FCXM). In all cases patient serum was screened using the One Lambda SAB assay and the surrogate crossmatches were performed using the ‘Halifster’ protocol. In three patient sera where HLA-A*11:02 was identified (in the absence of A*11:01) as the only class I specificity, FCXM was performed with a surrogate cell positive for HLA-A*11:02. The MFI of the A*11:02 reactivity was 12,997, 2300 and 3522 respectively. T and B cell flow crossmatch results were negative for all three. Commonly a reactivity pattern against DP1, DP5 and DR53 was also observed. One patient, RA, was tested by FCXM against a cell possessing DP5 (DP5 MFI=2424) and gave a negative B cell result (MCS of -46). Another serum, KA, was tested by FCXM against two cells possessing DR53 (MFI=2378) and gave a B cell MCS of -28 and -107 respectively. Patient JD showed reactivity with every DRB1 bead in the SAB panel, including against self DRB1 antigens. When tested by FCXM against cells possessing DRB1*03:01 (MFI, 7920) and DRB1*14:08 (DRB1*14:01 MFI, 5061) the B cell FCXM was negative (MCS of 17). These cases show the importance of performing further investigative testing where suspicion exists in the SAB result. Whilst some of the antigens included in this report involve low expression loci (i.e. DRB4 and DPB1), the presence of a negative FCXM suggests the SAB reactivity should be viewed with caution. Abstract No. 65 UNDERSTANDING AND ATTITUDES TOWARD ACCEPTING AN INCREASED VIRAL RISK DONOR IN PATIENTS ACTIVE ON THE KIDNEY TRANSPLANT WAITING LIST KANSAL Arushi1, DENDLE Claire2,3, KANELLIS John3,4, MULLEY William3,4 1Renal Transplant Unit, Monash Medical Centre, Melbourne, 2Infectious Diseases Unit, Monash Medical Centre, Melbourne, 3Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne, 4Nephrology and Renal Transplant, Monash Medical Centre, Melbourne Acceptance of increased viral risk donors (IVRDs) has increased internationally. Victoria recently implemented a state-wide IVRD information sheet and consent form (PICF) for potential recipients. Aims: To assess characteristics of patients willing to accept IVRDs and reasons influencing decision‐making. Methods: All 149 patients active on the kidney transplant waiting list at our centre were posted the IVRD PICF and a survey designed to assess their understanding of risk and willingness to accept an IVRD kidney. Responses were obtained via mail or telephone. Results: During the study period, 48 patients underwent transplantation, 15 were removed from the waiting list, and one died. 74 of the remaining 85 patients completed the survey. 28 patients (37.8%) would accept an IVRD, with the most commonly cited reason being to reduce wait‐time. 26 patients (35.1%) would not accept, most commonly due to concern about infection, whilst 20 patients (27%) were undecided. Accepting patients had a longer mean wait‐time (4.7±4.2 vs 2.7±2.7 years,p=0.048) and a higher median (IQR) calculated PRA(%) (97(9‐99) vs 1.5(0‐97.5),p=0.023) relative to those not accepting. Age and sex were not different between groups. The median acceptable infection risk from transplantation was 1 in 1000 for accepting patients. A higher proportion of patients unwilling to accept reported an incomplete understanding (19% vs 3%) of the PICF. The most feared potential infection was HIV. Conclusions: Increased waiting time and greater HLA sensitisation were associated with an increased likelihood of accepting an IVRD. The impact of patient education on IVRD acceptance requires further examination.

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Abstract No. 66 T-CELL ADOPTIVE IMMUNOTHERAPY FOR BK NEPHROPATHY JAHAN Sadia1, SCUDERI Carla1, FRANCIS Leo2, KHANNA Rajiv3, JOHN George1 1Renal Unit, Royal Brisbane Hospital, 2Department of Pathology, Royal Brisbane Hospital, 3 QIMR Berghofer Medical Research Institute Introduction: BK virus (BKV) nephropathy occurs in 1-10% of kidney transplantation recipients with suboptimal therapeutic options. Case: A 54-year-old received a transplant in March 2017. BKV was detected at 3.6 x 102 copies/mL within a month of transplantation leading to halving of mycophenolate and addition of Leflunomide when counts increased. Allograft histology in December showed polyomavirus nephropathy leading to infusions of immunoglobulin and cessation of mycophenolate. In February 2018 cidofovir and ciprofloxacin were commenced. In April, tacrolimus was reduced while introducing Everolimus. Blood BKV count increased and a second graft biopsy in August 2018 showed increasing polyoma virus and subsequent biopsy in September 2018 for worsening renal function showed 30% of tubule reactivity for SV40. BKV reactive T cells were isolated from the patient’s daughter, expanded and infused over 10 sessions, each of 3.6 x 107 copies/mL cells starting late September. The fourth allograft biopsy in November 2018 demonstrated involvement of BKV in 50% of tubules. Allograft function continued to decline, requiring maintenance haemodialysis from December 2018. An allograft nephrectomy after 6 months showed ~ 80% interstitial fibrosis with <1% SV40. We conclude that the T-cell adoptive immunotherapy had reduced BKV load, but with extensive infection, despite viral clearance, attendant fibrosis and tubular atrophy caused graft failure. Conclusions: T-cell adoptive immunotherapy for BKVAN requires to be trialled early in the course of illness for its efficacy. The process of viral clearance appears to occur over many months again underlining need for early adoptive immunotherapy. Abstract No. 67 TREATMENT OF SAPOVIRUS INFECTION IN A RENAL TRANSPLANT PATIENT MYAT, Lin Lin, MAY, Stephen Department of Nephrology, Tamworth hospital, NSW Case: 32-year-old female with a past history of ESRF secondary to IgA nephritis presented with severe diarrhoea 11 months after a non-complicated LR kidney transplant. She was on standard immunosuppression with prednisone, myfortic and tacrolimus. Her creatinine had increased from a base line of 126 µmol/l, eGFR 49 to 204, eGFR 27 with high tacrolimus level of 29µ gm/l. Stool cultures were positive for Sapovirus which from the literature is difficult to treat without reduction or cessation of mycophenolyate. It is associated with prolonged viral shedding often > 300 days. She was given a course of nitazoxide over 3 days with rapid resolution of her diarrhoea and a return to baseline creatinine without reduction of her immunosuppression. Her stool culture had rapid resolution of Sapovirus PCR This case adds to a very limited literature using of nitazoxide in transplantation and is possibly the first case of Sapovirus successfully treated with nitazoxide without reduction of immunosuppression.

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Abstract No. 68 THE SURGICAL MANAGEMENT OF URETERIC COMPLICATIONS IN RENAL TRANSPLANTATION: A 10-YEAR REVIEW OF OUTCOMES AT A TERTIARY CENTRE. LEE Alice1, SALTER Sherry1,2, JAYA Joseph1,2, SUH Nancy3, SAUNDER Alan2 1Department of General Surgery, Monash Medical Centre, Melbourne, 2Department of Vascular and Transplantation Surgery, Monash Medical Centre, Melbourne, 3Department of Nephrology Surgery, Melbourne Health Background: Ureteric complications cause significant morbidity in renal and simultaneous pancreas-kidney (SPK) transplantation. This review of medical records identified transplant patients with ureteric complications necessitating surgical intervention from a tertiary centre over 10 years. This case series of surgically managed ureteric complications may be used for training and education. Methods: The hospital medical records were reviewed to identify patients at Monash Health, Victoria, Australia, who underwent renal or SPK transplantations from 1st June 2009 to 31st May 2019 with subsequent surgical intervention for ureteric complications. A detailed analysis of operation reports, biochemistry, pathology, radiology and outpatient data enabled the authors to identify the type of complication, surgical management, and outcome. Results: A total of 893 renal and SPK transplants were performed over the 10-year period. Ten of these (1.12%; 7 renal, 3 SPK) had ureteric complications required operative repair. Five of the 10 had ureteric leaks (0.56%); 3 had ureteric strictures (0.34%); 1 had ureteric obstruction from extraluminal compression (0.11%); and 1 had both leak and stricture (0.11%). All 10 patients underwent ureteric reimplantation. Two patients required more than one operation for their ureteric complication. No graft loss or surgical mortality occurred. All 10 patients currently have functioning kidney transplants and none require maintenance dialysis. Conclusion: We report a low rate (1.12%) of ureteric complications in our renal and SPK transplants. Our standard corrective procedure of ureteric reimplantation is proving successful, confirming that appropriate surgery can rectify ureteric complications in renal transplant patients. Abstract No. 69 SERIOUS INFECTIONS ARE COMMON AMONG HIV-INFECTED KIDNEY TRANSPLANT RECIPIENTS: A SINGLE-CENTRE EXPERIENCE HERON JE1, GILLIN A1, LEE F2, JARDINE MJ3,4, CHADBAN SJ1,5, WYBURN K1,5, GRACEY DM1,6 1Renal & Transplantation Unit, Royal Prince Alfred Hospital, Sydney, 2Department of Immunology, Royal Prince Alfred Hospital, Sydney, 3The George Institute for Global Health, University of New South Wales, Sydney, 4Renal Unit, Concord Repatriation and General Hospital, Sydney, 5Kidney Node, Charles Perkins Centre, University of Sydney, 6Sydney Medical School, University of Sydney Introduction: Chronic kidney disease is increasingly prevalent among people living with HIV. Transplantation is now the preferred treatment for End Stage Kidney Disease in people with HIV, as international data has shown favourable recipient and graft outcomes, and comparable rates of infectious complications. Methods: We conducted a retrospective review of kidney transplants performed in HIV-infected recipients at our centre. Data were extracted from ANZDATA and medical records between 2007 and 2018. Results: Five deceased donor kidney transplants were performed in five HIV-infected recipients. All recipients were male. Follow-up ranged from 28 days to 5.7 years, with a total 10.1 patient-years of follow-up. Average waiting time was 4.6 years (range: 0.7 to 9.5 years). Recipients were induced with corticosteroids and anti-CD25; one recipient received IVIg. Three patients required changes to their ART at transplant because of drug interactions or viral resistance. None had immediate graft function, and three required dialysis. Acute rejection occurred in three recipients, all within ten days of transplantation. During follow-up, two suffered non-fatal cardiovascular events and one recipient died of sepsis and post-transplant lymphoproliferative disease, with a functioning graft. No other cancers occurred. No cases of death-censored allograft loss occurred; mean one-year creatinine was 195micromol/L (range: 173 to 276micromol/L). A high rate of serious infectious complications was observed, including bacterial infections, BK nephropathy, invasive CMV, pulmonary aspergillosis and disseminated Strongyloides. One episode of HIV viraemia occurred. Conclusion: Serious infections were common among HIV-infected transplant recipients at our centre. Allograft function was acceptable, despite frequent early rejection episodes.

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Abstract No. 70 MALAKOPLAKIA CAUSING DIARRHOEA AND WEIGHT LOSS IN A RENAL TRANSPLANT RECIPIENT ELLIOTT Rachel1, MAJONI William1, CAMPBELL Kirsty2, KHAN Afaq3 1Department of Nephrology, Royal Darwin Hospital, 2Department of Gastroenterology, Royal Darwin Hospital, 3Department of Pathology, Royal Darwin Hospital We present a case of malakoplakia in a renal transplant recipient with diarrhoea and weight loss. A 62 year old Indigenous male from remote Northern Territory was admitted with severe hyponatraemia to 107mmol/L and acute kidney injury with significant diarrhoea. This occurred on a background of 20kg unintentional weight loss over a 6 month. His past history was significant for end stage kidney disease due to presumed diabetic nephropathy treated with haemodialysis and subsequent deceased donor renal transplant in 2013. Maintenance immunosuppression included tacrolimus, prednisolone and mycophenolate mofetil. Initial tests were significant for a positive faecal occult blood test and low level cytomegalovirus viraemia at 1003 copies/mL. He underwent gastroscopy and colonoscopy which revealed varying polypoid lesions throughout the large bowel. Histological examination revealed Michaelis-Gutman bodies with calcium deposition evident on von kossa stain. A presumptive diagnosis of malakoplakia was made, likely due to infectious aetiology. Malakoplakia is a rare chronic granulomatous disease thought to be due to an acquired deficiency of bactericidal activity of macrophages. More commonly found in genitourinary tract, there are few reported cases of malakoplakia in gastrointestinal system and other organ systems. This case draws attention to the need to consider infectious causes of diarrhoea in transplant recipients.

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Abstract No. 71 PREVALENCE OF AT1R ANTIBODY AMONG MALAYSIAN MULTI-ETHNIC KIDNEY TRANSPLANT RECIPIENTS JALALONMUHALI Maisarah1, CAROLL Robert2,3, DEAYTON Sue4, EMERY Tim3, HUMFREYS Ian3, LIM Sue Jin1, NG Kok Peng5, LIM Soo Kun5, COATES Toby2,4 1Department of Medicine, University Malaya Medical Centre, Kuala Lumpur, 2Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 3Transplantation Immunology Laboratory, Australian Red Cross Blood Service, Adelaide, 4Transplant Immunobiology Laboratory, Australian Red Cross Blood Service, Adelaide, 5University Malaya Medical Centre, Kuala Lumpur, Background: Antibody mediated rejection (ABMR) is one of the major cause of allograft dysfunction in kidney transplant recipient. Routinely the patients need to be screened for HLA-donor specific antibodies (DSAs) before proceeding for transplantation. This measure is to reduce the rate of ABMR and graft loss. Unfortunately, ABMR could still happen in those with negative DSA. This clinical phenomenon possibly due to the non-HLA antibodies (ie: AT1R-Ab). Thus, knowing its prevalence is substantially important in our cohort. Methodology: All sera for AT1R-Ab were collected at UMMC, Kuala Lumpur, Malaysia. The sera were centrifuged and kept refrigerated at -80°C before being transported to the South Australian Transplantation and Immunogenetics Laboratory (SATIS). Enzyme-linked immunosorbent assay kit (One Lambda) was used for detection of AT1R-Ab and it was performed according to the manufacturer’s instructions. The level of > 17.1 U/mL was considered to be AT1R-Ab positive; 10.1 - 17.0 U/mL at risk, and < 10.0 U/mL negative. Results: A total of 115 sera were received from 99 potential and post KTR. Out of these 68 sera were collected pre-transplantation and 47 sera were post-transplantation. Among the pre-transplant sera 32/68 (47%) were negative, 24/68(35%) were at risk and 12/68(18%) were positive. While in the post-transplant sera 27/47 (57%) were negative, 14/47 (30%) and 6/47 (13%) at risk and positive respectively. Table 1 showed the demographic and immunological characteristics of the study patients. Variable Negative (N=49) At Risk (N=36) Positive (N=14) P=value Age (mean + SD) 43.35 ± 11.72 40.19 ±10.50

34.14 ±8.36

0.021

Gender, male 26 (53.1%) 20 (55.6%)

9 (64.3%)

0.760

Ethnicity Malay Chinese Indian

17 (34.7%) 31 (63.3%) 1 (2%)

11 (30.6%) 21 (58.3%) 4 (11.1%)

2 (14.3%) 11 (78.6%) 1 (7.1%)

0.274

Dialysis Access No Access AVF Dialysis Catheter Tenckhoff Catheter

15/49 (30.6%) 23/49 (49.6%) 6/49 (12.2%) 5/49 (10.2%)

13/31 (41.9%) 13/31 (41.9%) 3/31 (9.7%) 2/31 (6.5%)

4/14 (28.6%) 8/14 (57.1%) 0/14 (0%) 9/14 (9.6%)

0.542

Preformed HLA-DSA 7/21 (33.3%) 13/19 (68.4%)

5/7 (71.4%)

0.052

Table 1: Demographic and immunological characteristics of the study population Conclusion: The prevalence of positive pre-transplant AT1R-Ab was 18% and 35% were at risk in our pre-transplant cohort. AT1R-Ab were significantly higher in younger age group. It would be interesting to look at their transplant outcome and analyzing the treatment that were given.

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Abstract No. 73 BONE MINERAL DENSITY IN PAEDIATRIC KIDNEY TRANSPLANT RECIPIENTS HAWTHORNE Madeline1, CRAIG Elizabeth2, KENNEDY Sean1,2 1School of Women's & Children's Health, University of New South Wales, Sydney, 2Department of Nephrology, Sydney Children's Hospital Corticosteroids are thought to be major contributors to low bone mineral density (BMD) after transplantation, however the role of calcineurin inhibitors (CNI) or mTOR inhibitors is less understood. In this study we describe the results of dual-energy x-ray absorptiometry (DEXA) scans performed in a single-centre cohort of paediatric kidney transplant recipients and explore patient and treatment based factors that may contribute to low BMD. DEXA scans were performed every 2 years after transplant, up to the age of 18 years. Low BMD was defined as having a DEXA z-score ≤ -2 standard deviations, according to age-related ranges. Variables included in analyses were age, gender, height and weight, time since transplant, primary renal disease, immunosuppressant class, current estimated glomerular filtration rate and number of rejection episodes. The study included 38 recipients with median age of 15.4 years (IQR 4.3) at the most recent DEXA scan and a median time since transplant of 3.6 years (range 1 to 11). All were receiving corticosteroids, 26 (68.4%) were receiving CNIs and 11 (28.9%) were receiving a mTORI. 15 had received high dose steroids for at least one episode of rejection. 15 (39.5%) recipients had a low BMD. Those with a low BMD had lower height z-scores (p=0.02) and were more likely to be receiving mTORI than a CNI (OR 7.9, CI 1.4-43.5. p=0.02 in multivariable analysis). There were no other significant differences between groups. This is the first study to link mTORI use in transplantation with low BMD. Abstract No. 74 RENAL ALLOGRAFT TORSION AND PSEUDOANEURYSMS OF THE PANCREATIC ARTERY FOLLOWING SIMULTANEOUS PANCREAS-KIDNEY TRANSPLANTATION: A CASE REPORT TAN Sarah1, TAN Rachel1,2, CEHIC Gabrielle3,4, WU Michael5,6, KANELLIS John7,8, BARBARA Jeffrey1,2 1Department of Nephrology, Flinders Medical Centre, Adelaide, 2College of Medicine and Public Health, Flinders University, Adelaide, 3Department of Nuclear Medicine, Flinders Medical Centre, Adelaide, 4South Australian Medical Imaging (SAMI), 5Department of Surgery and School of Clinical Sciences, Monash Health, 6Monash University, Melbourne, 7Department of Nephrology, Monash Health, 8Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne Background: We report two unusual complications of simultaneous pancreas-kidney transplantation (SPKT) occurring in the one patient. Case report: A 39-year-old man with end-stage renal failure secondary to type 1 diabetes mellitus underwent successful SPKT in October 2018. Three months later, he presented with acute renal allograft failure and returned to dialysis. Renal scintigraphy showed a central photopenic region and angiogram showed absent flow in the renal transplant artery without treatable thrombus and the incidental finding of two pseudoaneurysms of the transplant pancreas Y-graft. He remained dialysis-dependent for three weeks before spontaneous partial recovery of graft function and repeat renal scintigraphy showed significant improvement in perfusion with no evidence of vascular insult. However, in April 2019 he was readmitted with a sudden deterioration in renal graft function again necessitating haemodialysis. Clinical examination and renal scintigraphy confirmed that the renal allograft had shifted from the left iliac fossa to the midline. Within 18 hours he had been dialysed, travelled interstate and had undergone surgical exploration where torsion of the renal allograft was confirmed and nephropexy performed. In this case, the kidney was initially implanted in the left retroperitoneum via a midline transperitoneal approach, which predisposes it to this risk. The patient regained reasonable renal allograft function (eGFR 41) and remains dialysis-independent with good pancreatic graft function. Conclusion: Renal allograft torsion should be considered post-SPKT in patients presenting with AKI and absent or minimal arterial flow. Although most published case reports describe surgical management of pseudoaneurysms post-SPKT, our case demonstrates successful conservative management.

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Abstract No. 75 COMPARISON OF THE EFFECT OF SINGLE VS DUAL ANTIPLATELET AGENTS ON POST-OPERATIVE HAEMORRHAGE AFTER RENAL TRANSPLANTATION: A SYSTEMATIC REVIEW AND META-ANALYSIS AGOSTINHO Nelson1,2, LEE Taina1,2, D'SOUZA Kenneth3, YAO Jinna1,2, LAM Susanna1,2, HAMEED Ahmer4, PULITANO Carlo1,2, YUEN LAWRENCE4, JOSEPH David Morris1,2, QASABIAN Raffi1,2, SANDROUSSI Charbel1,2, CHADBAN Steven5,6, YING Tracey5,6, CELERMAJER David7,6, PLEASS Henry2,4, LAURENCE Jerome Martin1,2,4 1Transplant Department, Royal Prince Alfred Hospital, Sydney, 2Institute of Academic Surgery, University of Sydney, 3School of Medicine, University of Sydney, 4Department of Surgery, Westmead Hospital, Sydney, 5Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, 6Department of Medicine, University of Sydney, 7Department of Cardiology, Royal Prince Alfred Hospital, Sydney Aim: A significant proportion of renal transplant patients have cardiovascular comorbidities for which they receive treatment with antiplatelet agents. The aim of this study was to systematically review the current literature reporting perioperative outcomes for patients receiving dual antiplatelet therapy (DAPT) compared to single antiplatelet therapy (SAPT) at the time of kidney transplantation with particular reference to the risks of postoperative haemorrhage. Methods: Embase, Medline and Cochrane databases were utilized to identify articles reporting outcomes of renal transplant recipients on SAPT and DAPT. These outcomes were compared using a random effects model meta-analysis where appropriate. Results: Five articles were incorporated in the analysis, including 120 receiving DAPT, and 772 SAPT group. There was a significantly higher risk of post-operative haemorrhagic events in the DAPT group compared to the SAPT group (RR 1.58, 95% CI 1.19 – 2.09, p = 0.001). There were insufficient data to analyse the risks of thrombotic complications or cardiovascular events. Conclusions: The use of DAPT was associated with a higher risk of post-operative haemorrhage compared to the use of SAPT. This finding is consistent with the existing literature on the non-transplant, non-cardiac surgery population.

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Abstract No. 76 UTILISATION OF PERIOPERATIVE INTRAVENOUS FLUIDS IN DECEASED DONOR KIDNEY TRANSPLANTATION IN AUSTRALIA AND NEW ZEALAND: A CROSS-SECTIONAL SURVEY COLLINS Michael1,2, REIDLINGER Donna2, FAHIM Magid2,3, HAWLEY Carmel2, CHADBAN Steven2,4,5 1Department of Renal Medicine, Auckland District Health Board, 2Australasian Kidney Trials Network, University of Queensland, Brisbane, 3Department of Nephrology, Princess Alexandra Hospital, Brisbane, 4Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, 5Kidney Node, Charles Perkins Centre, University of Sydney Background: Peri-operative intravenous (IV) fluids are a critical aspect of care in deceased donor kidney transplantation. Balanced low-chloride crystalloids such as Plasma-Lyte® 148 (Plasmalyte) may be associated with better graft function compared with 0.9% sodium chloride (normal saline), although definitive efficacy and safety data are lacking. Aims: To determine (1) the standard-of-care (SOC) for peri-operative IV fluids at renal transplant hospitals in Australia and New Zealand, and (2) the level of support for a trial of Plasmalyte versus normal saline with an endpoint of graft function. Methods: A cross-sectional survey of nephrologists and transplant directors at transplant hospitals in Australia and New Zealand was conducted in 2016. One survey per hospital was included in this analysis. Descriptive statistics are reported for fluids used, and for attitudes to participation in a potential trial. Results: The survey response rate was 85% (15/18 adult and 7/8 paediatric hospitals). Normal saline was the primary fluid used intraoperatively at 14/22 (64%), and post-operatively at 18/22 (87%) hospitals (see Figure). There was some intra-operative use of Hartmann’s (3/22, 14%) and Plasmalyte (4/22, 18%) but little use post-operatively. Ten hospitals (45%) reported using variable amounts of hypotonic solutions (typically 5% dextrose) post-operatively along with the primary SOC fluid. Eighteen hospitals (82%) expressed interest in participating in a blinded trial of Plasmalyte vs normal saline. Conclusions: While there is some variation in fluid types used in deceased donor kidney transplantation, normal saline is the standard-of-care at the majority of hospitals. There is sufficient equipoise to justify a trial. Figure. Fluids used as standard of care for deceased donor kidney transplantation at hospitals in Australia and New Zealand

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Abstract No. 77 PARVOVIRUS B19 INDUCED DIABETES MELLITUS IN A RENAL TRANSPLANT RECIPIENT PARK Yeung Ae1, CHOW Kevin V1,2, MASTERSON Rosemary1,2 1Department of Nephrology, Royal Melbourne Hospital, 2Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne Case: A 41-year-old man with end stage kidney disease secondary to IgA nephropathy presented with an episode of hyperglycaemia (BGL 51.8mmol/L) 11 weeks post renal transplant, on a background of recently diagnosed refractory anaemia secondary to parvovirus B19 (PVB19) infection. Given his elevated anti-GADAb, low c-peptide and positive parvovirus PCR, the diagnosis of PVB19-associated immune pancreatic islet cell damage with resultant diabetes was confirmed. HLA typing revealed the patient to be homozygous for HLA-DR 4/4, which confers one of the highest risks for type 1 diabetes mellitus. He was commenced on basal-bolus insulin regime, regular intravenous immunoglobulin infusions and reduced immunosuppression. Despite these measures, 12 months later, the patient remains PVB19 PCR positive with persistent insulin-dependent diabetes although his anaemia has resolved. PVB19 infections can present as refractory anaemia in context of immunosuppression and have been described to precipitate autoimmune conditions. Although the pathophysiology of PVB19 associated diabetes remains unclear, it has been suggested that the virus plays a role in the induction of autoantibodies such as anti-GAD antibody and anti-IA-2 antibody. In the context of renal transplantation, immune-mediated diabetes secondary to PVB19 infection has been rarely reported. Conclusions: PVB19 infections should be considered as a cause of post-transplant diabetes mellitus particularly if accompanied by significant hyperglycaemia and refractory anaemia. In renal transplant recipients with known susceptible HLA typing to autoimmune diabetes, monitoring for PVB19 infection may need to be considered to facilitate early detection of PVB19 infection and potentially reduce immunosuppressive dose before permanent pancreatic B cell damage occurs. Abstract No. 78 MANAGING TUBERCULOSIS TRANSMISSION RISK TO EXPOSED KIDNEY TRANSPLANT RECIPIENTS LI Jennifer1, GILROY Nicky2, CHO Jin Gun3, BAG S4, ROGERS Natasha5, CHAPMAN Jeremy Robert5 1Centre for Transplant and Renal Research, Westmead Institute for Medical Research, Westmead, Sydney, 2Department of Infectious Diseases, Westmead Hospital, Sydney, 3Department of Respiratory Medicine, Westmead Hospital, Sydney, 4Discipline of Public Health, Westmead Hospital, Sydney, 5Department of Renal Medicine, Westmead Hospital, Sydney Drug-resistant tuberculosis (TB) in solid organ transplant recipients is a challenging issue and recommendations for screening of recipients exposed in the post-transplant period remains limited. Aims: Evaluate the risk of transmission and treatment challenges of transplant recipients exposed to drug-resistant TB. Methods: A single-centre, retrospective cohort study of patients from Westmead Hospital were identified through contract tracing to an index case: a kidney transplant patient diagnosed with isoniazid-resistant, active pulmonary TB visiting the outpatients clinic between January to May 2018. Screening involved symptomatology survey, interferon-γ release assay (IGRA), tuberculin skin test (TST) and a chest x-ray (CXR). High risk patients were reviewed at a multi-disciplinary (MDT) clinic. Patients were followed up for 12-months. Results: 122 transplant patients were identified and 90 (74%) agreed to screening. Majority had either IGRA and/or CXR but only 49% patients partook in TST screening. During the 12-month follow up period, no cases of active transmission were detected. Six of 17 patients referred to the MDT were commenced on rifabutin for inadequately treated latent TB. Conclusion: Screening and managing the transmission risk for TB in our transplant patients was a challenging exercise, driven by the immunosuppressed risk group, high infectivity and drug resistant profile. Despite our conservative approach to screening, we did not detect any case of transmission of active TB in our cohort. Furthermore, rifabutin is a viable alternative to isoniazid for chemoprophylaxis in resistant cases but requires close monitoring and drug titration to avoid the pitfall of suboptimal immunosuppression in transplant recipients.

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Abstract No. 79 ASSOCIATION BETWEEN SOCIOECONOMIC STATUS, PRE-EMPTIVE REPEAT TRANSPLANTATION AND MORTALITY POST KIDNEY ALLOGRAFT FAILURE WONG Yun Hui Sheryl1, WONG Germaine2, MCDONALD Stephen3, CLAYTON Philip3, JOHNSON David4, HAWLEY Carmel4, VIECELLI Andrea5,6, PILMORE Helen7, WALKER Rachael8, ROBERTS Matthew9,10, LOK Charmaine11,12, POLKINGHORNE Kevan13,14, BOUDVILLE Neil1,15, LIM Wai Hon1 1Department of Nephrology, Sir Charles Gairdner Hospital, Perth, 2Department of Nephrology, Westmead Hospital, Sydney, 3Department of Nephrology, Royal Adelaide Hospital, 4Department of Nephrology, Princess Alexandra Hospital, Brisbane, 5Department of Nephrology, Mater Institute, Brisbane, 6School of Medicine, University of Queensland, Brisbane, 7School of Medicine, University of Auckland, 8School of Nursing, Eastern Institute of Technology, 9Department of Nephrology, Box Hill Hospital Victoria, 10Department of Medicine, 11Department of Nephrology, Toronto General Hospital, 12School of Health Sciences, McMaster University, 13Department of Renal Medicine, Monash Medical Centre, Melbourne, 14School of Medicine, Monash University, Melbourne, 15School of Medicine, University of Western Australia, Perth Background: Low socio-economic status (SES) is associated with reduced rates of pre-emptive kidney transplantation (PEKT) and poor health outcomes in patients with end-stage kidney disease.However, it remains unclear whether a similar association exists post-kidney allograft failure. Methods: Using ANZDATA registry, the associations between residential postcode-derived SES (Index of Relative Socioeconomic Advantage and Disadvantage [IRSAD] of the general Australian population) and likelihood of second PEKTand all-cause mortality post-first kidney allograft failurewere examined using logistic and competing risk analyses, respectively. Results: Of 2221 patients who experienced first allograft failure between 2005-2017, 772 (34.8%) patients were of the lowest SES (IRSAD quintiles 1+2) and 519 (23.3%) in the highest SES (quintile 5). Fifty-nine patients received a second PEKT, of which 57 (97%) were live-donor transplants. Compared to patients in the highest SES, patients in the lowest SES were more likely to be Indigenous, have vascular comorbidities and live remotely. They were also less likely to receive a second PEKT (adjusted OR 0.43 [95%CI 0.22-0.85]; p=0.015) and were more likely to die post-allograft failure (adjusted sub-distribution HR 1.32[1.04-1.66]; p=0.022), with second kidney transplant considered as a competing event. Restricting the analysis to those aged 60 or less at time of first allograft failure, the association between lowest SES and odds ofsecond PEKT was similar (adjusted OR 0.49 [95%CI 0.24-0.98]; p=0.043). Conclusion: Compared with high SES, low SES is associated with a reduced likelihood of pre-emptive repeat transplantation and a higher risk of all-cause mortality post-first kidney allograft failure.

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Abstract No. 80 INCIDENCE AND RISK FACTORS OF POLYOMAVIRUS (BK) INFECTION IN KIDNEY AND KIDNEY PANCREAS (SPK) TRANSPLANT RECIPIENTS ALLAN Lachlan1, YAO Jinna1, AMARATUNGA Rajith1, PLEASS Henry1, WONG Germaine2 1Department of Surgery, Westmead Hospital, Sydney, 2Department of Nephrology, Westmead Hospital, Sydney Background: BK virus is a major cause of allograft loss in transplant recipients. The incidence and risk factors of BK infection varies considerably depending on patient and centre characteristics. Aim: To determine the incidence and risk factors of BK infections (viraemia and nephropathy (BKVAN)) in kidney and SPK transplant recipients. Methods: We conducted a cohort study of kidney and SPK transplant recipients between January 2017 and July 2018. BK viraemia was defined as any detectable viraemic load. LASSO and multivariable logistic regression were conducted to select the key factors that predict the incidence of BK viraemia and BKVAN. Results: A total of 66 kidney transplant and 31 SPK transplants were included in the analysis and followed up for 211 person-years. The one-year incidence of BK viraemia and BK VAN were 34% and 15%, respectively. A total of 78 patients (80%) had tacrolimus levels higher than 15ng/ml in the first week post-transplant. The three most important factors (OR 95%CI) for BK viraemia were (Figure 1): coefficient of variation (CV) of tacrolimus trough level within the first month after transplantation (1.05 (1.02-1.10)), age at transplantation (0.97 (0.96-1.00) and day 7 total tacrolimus dose (1.13 (0.98-1.31)). CV of tacrolimus trough level within the first month remain the strongest predictor for BKVAN (1.06 (1.01 – 1.11)). Conclusion: The one-year incidence of BK viraemia among kidney and SPK transplant recipients was high. The most important factor for predicting BK reactivation in transplant recipients was the increased variation of tacrolimus trough levels within the first month post-transplantation. Figure 1.

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Abstract No. 81 “HYPERACUTE” T CELL MEDIATED REJECTION (TCMR) OF A STABLE RENAL ALLOGRAFT FOLLOWING PD1 BLOCKADE FOR RECURRENT HEAD AND NECK SQUAMOUS CELL CARCINOMA (HNSCC) ROWLANDSON Matthew1, TREVILLIAN Paul1,2, MALLESARA Girish3, FORMBY Mark4, HARDSTAFF Ruth1 1Newcastle Transplant Unit, John Hunter Hospital, Newcastle, 2School of Epidemiology and Public Health, University of Newcastle, Newcastle, New South Wales, Australia, 3Department of Medical Oncology, Calvary Mater Newcastle, 4Department of Pathology, John Hunter Hospital, Newcastle Introduction: HNSCC is a common post-transplant malignancy amongst Australians and carries a poor prognosis. Trials of checkpoint immunotherapy have shown improved survival in patients with recurrent HNSCC compared to platinum-based therapies. Its use in organ transplant recipients, dependent on maintenance immunosuppression, is likely to be problematic but there are few reports. We describe a case of “hyperacute rejection” in a stable living donor renal transplant recipient after PD-1 inhibition with Nivolumab. Case Report: A 64 year old male received a living unrelated kidney transplant 9 years ago for ADPKD (6/6 HLA mismatch, no DSAb’s,ABOi (anti-B,1:32). TCMR (Banff 1b) at 3 months treated with pulse Methylprednisolone/Thymoglobulin with biopsy proven resolution. Subsequently the eGFR maintained at ~80 ml/min for the next nine years. In 2016 he developed right tonsil SCC treated with apparently curative chemo-radiation. Mycophenolate was ceased. In 2019 his SCC reoccurred with unresectable invasive disease which required tracheostomy. He failed chemotherapy and, with consent, was given Nivolumab. Two weeks after second dose he presented with a swollen tender graft and anuria. Imaging suggested thrombosed graft. He required urgent graft nephrectomy. Histology showed diffuse interstitial haemorrhage with focal infarction and diffuse, heavy, subintimal T-cell infiltration in arteries of all sizes and peri-venously. Thromboses were not seen, C4d was negative and there were no DSAb’s. The patient returned to dialysis. Conclusion: This case demonstrates aggressive T-cell mediated vascular rejection that may follow the use of checkpoint blockade. It gives insight into the likely important role of expression of PDL1 in allograft immuno-tolerance.

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Abstract No. 82 VALIDATION OF PARENTHOOD EVENTS REPORTED TO AUSTRALIA AND NEW ZEALAND DIALYSIS AND TRANSPLANT (ANZDATA) REGISTRY WITH THE MULTI-JURISDICTIONAL PERINATAL DATA COLLECTIONS. HEWAWASAM Erandi1,2, DAVIES Christopher3,2, GULYANI Aarti4, MCDONALD Stephen5,3,2, CLAYTON Philip5,3,2, JESUDASON Shilpanjali5,2 1ANZDATA, 2Faculty of Health and Medical Sciences, University of Adelaide, 3ANZDATA, 4School of Pharmacy and Medical Sciences, University of South Australia, 5Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital Aims: The ANZDATA registry collects parenthood event data for men and women receiving renal replacement therapy (RRT). We aimed to validate the parenthood events reported to ANZDATA with the Perinatal Data Collections (PDC). Method: Using probabilistic data linkage, ANZDATA (1970-2016) was linked to PDC capturing mandatory data on births ≥20 weeks gestation or birthweight >400 grams (1991-2013) in New South Wales (NSW), South Australia (SA) and Western Australia (WA). The birth register was used to link fathers to mothers and their babies within the perinatal datasets. We compared births reported to ANZDATA from 1991-2013 with gestational age ≥20 weeks or birthweight >400 grams, to births identified within the PDC with the same timeframe. Results: Of 2,891,295 births, 1425 babies were born to 898 women and 2457 babies were born to 1481 men who ever received RRT. Of these, 228 births occurred after 150 mothers started RRT, while 655 births occurred after 403 fathers started RRT. Linking ANZDATA with PDC identified more parenthood events than those reported to ANZDATA, particularly from fathers (Table 1). A few parenthood events reported to ANZDATA were not reported to PDC, upon investigation most of these appeared to be overseas or interstate births but require further exploration. Conclusions: ANZDATA parenthood event reporting and data can now be validated. We will explore potential causes of discrepancy between the PDC and ANZDATA. Having identified these births, detailed perinatal data that was not captured by ANZDATA can be analysed to better understand the impact of RRT on pregnancy outcomes. Table 1. Parenthood events directly reported to ANZDATA compared with those identified through the data linkage to Perinatal Data Collections (PDC)

Mother receiving RRT Father receiving RRT

Dialysis* Transplant* Dialysis* Transplant*

Parenthood events reported to PDC, births (mothers/fathers) 21 (16) 207 (134) 148 (106) 507 (297)

Parenthood events reported to both PDC and ANZDATA, births (mothers/fathers) 17 (14) 159 (110) 53 (46) 176 (133)

Parenthood events reported to PDC but not to ANZDATA, births (mothers/fathers) 4 (2) 48 (24) 95 (60) 331 (164)

% of births not reported to ANZDATA 19% 23% 64% 65%

*Same parent may be represented both in dialysis and transplant cohorts depending on the renal replacement therapy at the time of conception Abbreviations: RRT, renal replacement therapy; PDC, Perinatal Data Collections; ANZDATA; Australia and New Zealand Dialysis and Transplant Registry

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Abstract No. 83 MANAGEMENT OF TRANSPLANT KIDNEY AUTOLOGOUS SAPHENOUS VEIN GRAFT ANEURYSM HANLON Lucy1, AGOSTINHO Nelson1, HEWA-GEEGANAGE Shanika1, LEE Taina1, GILLIN Adrian2, VERRAN Deborah1, LAURENCE Jerome Martin1,3 1Transplant Department, Royal Prince Alfred Hospital, Sydney, 2Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, 3Institute of Academic Surgery, University of Sydney Aim: Saphenous vein graft aneurysms (SVGA) after renal transplants are a documented rare vascular complication. There are no standard management guidelines, but endovascular treatment is often used in preference to surgery because of the complexity of the surgery and potential for graft loss. Method: This presentation outlines the case of a 45 year old female with a history of renal transplant with an autologous saphenous vein interposition graft between the donor renal artery and recipient iliac artery that became complicated by an aneurysm. The aneurysmal segment included upper and lower polar arteries and so was not amenable to endovascular management. Results: The patient underwent explanation of the donor kidney, perfusion ex situ with preservation solution and back table resection of the aneurysm, followed by reconstruction using deceased donor iliac vessels. The kidney was then re-transplanted 21 years after its initial implantation. The patient was discharged from hospital on post-operative day 5 with a functioning transplant graft. Conclusion: Explanation, resection and reconstruction ex situ is a technically feasible solution to late transplant renal artery aneurysm where endovascular treatment is not feasible.

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Figure 1: A) Computer tomography reconstruction of recipient right internal iliac artery (yellow arrow) showing SVGA (white arrow) with upper and lower pole renal arteries (blue arrow) B) SVGA sac opened showing ostia of upper and lower pole renal arteries (yellow arrows) C) SVGA sac opened (yellow arrow) with ostia of upper and lower pole arteries originating from renal artery D) Reconstruction of renal artery using a donor iliac artery Y graft to upper and lower pole arteries (yellow arrow) E) Retransplanted kidney with reconstructed renal artery anastomosed to recipient iliac artery (yellow arrow) and vein (white arrow) F) Resected SVGA

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Abstract No. 84 LIVE KIDNEY DONOR ALLOGRAFT LITHIASIS: A SYSTEMATIC REVIEW OF STONE RELATED MORBIDITY IN DONORS YAO Jinna1,2, TOVMASSIAN David1, LAU Howard1,3, LEE Taina4,2, ALLEN Richard1,2, YUEN Lawrence1, LAURENCE Jerome4,2,1, PLEASS Henry1,2 1National Pancreas Transplant Unit, Westmead Hospital, Sydney, 2Discipline of Surgery, Sydney Medical School, University of Sydney, 3Department of Urology, Westmead Hospital, Sydney, 4Department of Surgery, Royal Prince Alfred Hospital, Sydney Background: Nephrolithiasis is a common incidental finding during live donor work up. However, its long term clinical significance to the donor is unclear. Donor safety is inherently the primary concern for the donor surgeon. The ramifications of stone recurrence in a solitary kidney are important concerns which influences donor eligibility. Methods: We conducted a systematic review to summarise the totality of published evidence on stone related morbidity of live donors with incidental finding of nephrolithiasis. Results: Ten studies and 162 live donors with asymptomatic urolithiasis were identified. The prevalence of incidental urolithiasis amongst live donors was 5.8%. Eight (4.9%) patients had bilateral stones. Eleven (6.8%) patients had their contralateral kidney without stones donated. In eight studies, positive metabolic work up and previous stone disease was a contraindication to donation. At median follow up of 20.6 months (2-79.3), there was one (0.6%) donor who had a stone related event. This patient had donated their contralateral kidney without a stone. Conclusions: Surgeons who participate in kidney donor selection should remain the advocate for the donor. It would appear that the risk of stone related morbidity in kidney donors is low but not insignificant. In the absence of robust long term outcome data, incidental urolithiasis found during live donor work up should not be an impediment to donation with the caveat that risk of stone related morbidity should be minimised by donating the kidney with the stone. Recurrent stone formers, bilateral stone disease and those with metabolic abnormalities should be excluded from donation. Abstract No. 85 IMPACT OF KIDNEY TRANSPLANT TRAINING ON SECOND WARM ISCHAEMIA TIME AMARATUNGA RA1, ALLAN L1, YAO J1, ROBERTSON P2, KABLE K2, ROGERS N2, WONG G2, ALLEN R2, RYAN B2, YUEN L2, PLEASS H2 1Department of Surgery, Westmead Hospital, Sydney, 2Renal Transplant Unit, Westmead Hospital, Sydney Background: Second warm ischaemia time (SWIT) is independently associated with outcomes in kidney transplantation. SWIT is defined as the time from kidney removal from cold storage to reperfusion and incorporates vascular anastomosis time. A SWIT longer than 30 minutes appears to be associated with an increased risk of DGF, reduced allograft survival and overall patient survival. The aim of this study was to assess the impact of trainee involvement on SWIT and subsequent graft outcomes. Method: We conducted a cohort study of 50 deceased donor kidney transplants at our institution between 2017 and 2018. Data collected included SWIT, serum creatinine levels, DGF and graft failure. Exclusion criteria included live donor, dual kidney and simultaneous pancreas and kidney transplants. Results: All fifty transplants had trainees perform at least 50% of the arterial and venous anastomoses. The median SWIT was 27.5+/-9 minutes. DCD kidneys made up 40% of cases. KDPI ranged from 4–98 with a mean of 57. Median one year creatinine was 120+/-53 umol/L. The rate of DGF was 54% (n = 27). The rate of graft failure was 26% (n = 13) and 0% (n = 0) at one month and one year respectively. Conclusion: In our institution where trainees perform a significant role in the vascular anastomosis of kidney transplants we found a similar SWIT to that which is reported in the literature. Despite the higher rate of DGF, which is likely related to the KDPI and DCD kidney rate in our cohort, graft function was preserved at 1 year follow up.

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Abstract No. 86 ANALYSING THE EFFECT OF A CLOSED INCISION NEGATIVE PRESSURE WOUND THERAPY (CINPWT) SYSTEM ON SURGICAL SITE INFECTIONS AND WOUND COMPLICATIONS IN KIDNEY TRANSPLANT RECIPIENTS. A PROPENSITY SCORE MATCHED ANALYSIS LAM Susanna1,2, HUYNH Annie1, LAURENCE Jerome1,2,3 1Transplantation Services, Royal Prince Alfred Hospital, Sydney, 2Discipline of Surgery, Sydney Medical School, University of Sydney, 3Department of Surgery, Institute of Academic Surgery Wound complications including surgical site infections (SSI) affect 3-27% of kidney transplant recipients. Successful strategies to prevent wound complications include the use of a closed incision negative pressure wound therapy (ciNPWT) system. However, there is no data on the use of ciNPWT in kidney transplant recipients. The aim of this study was to determine the effectiveness of ciNPWT in preventing wound complications in kidney transplant recipients. Methods: Kidney transplant recipients over the age of 18, with a BMI > 25kg/m2, were included. A prospective cohort of recipients utilised the ciNPWT system as a dressing and results were compared with a retrospective cohort of recipients who used standard dressings. We applied propensity score matching to the analysis. Results: There were 87 patients who underwent a kidney transplant, 61 had a standard surgical dressing and 26 had a ciNPWT dressing. After PSM, there were 26 matched pairs in each group. Surgical site infections (SSI) rates were similar for both standard dressing and ciNPWT groups in the unmatched cohort (8.2% vs 11.5%, p = 0.621). In the PSM cohort, SSI were also similar between the two groups (7.7% vs 11.5% p=0.638). Wound complications were similar for both standard dressing and ciNPWT groups in the unmatched cohort (27.9% vs 19.2%, p= 0.396). In the PSM cohort results were also similar between the two groups (38.5% vs 19.2% p = 0.126). Conclusion: There is no difference in wound complications and SSI in kidney transplant recipients who have used the ciNPWT system compared to standard dressings. Abstract No. 87 SELECTIVE URETERIC STENT INSERTION IN RENAL TRANSPLANT PATIENTS RANA Abdul Ahad, OLAKKENGIL Santosh, BHATTACHARJYA Shanthanu, RUSSELL Christine, DIAS Brendan Central and Northern Adelaide Renal Transplant Services (CNARTS), Royal Adelaide Hospital, Adelaide Introduction: Routine ureteric stent insertion for renal transplant still remains a matter of debate and at best controversial. It is believed that routine ureteric stent insertion reduces the risk of major ureteric complications but may increase the risk of urinary tract infections in an immunosuppressed patient. Many studies show reduction in major ureteric complications by routinely using JJ stent insertion during renal transplantation although the urinary tract infection rate is higher in patients with JJ stents and thus the controversy continues. The Royal Adelaide Hospital Renal Transplant centre decided to test Selective ureteric stent insertion and assess the rates of UTI and MUC in patients with routine stent insertion against those with selective stent insertion. Objectives: To assess the incidence of UTI and major ureteric complications in patients undergoing selective and routine prophylactic ureteric stent insertion in renal transplant. Methods: We conducted a retrospective study on patients undergoing renal transplant at The Royal Adelaide Hospital to assess for differences in rates of UTI and MUC in a group of patients who had selective JJ ureteric Stent insertion and those who had routine ureteric stent insertion. All patients had stent insertion before early 2017 but since then selective ureteric stent insertion was taken up. 63 patients underwent selective ureteric stent insertion since june 2017, 63 patients were taken from before June 2017 who had routine stent insertion. Both these groups were assessed for UTI within 4-6 weeks, as stents are usually removed within 6 weeks in the unit. The two groups were also assessed for Major ureteric complications (Urine leak). After the initial assessment more patients were found to have UTI with routine ureteric stent insertion but the number was not statistically significant likely due to the sample size furthermore more patients data was collected and selective ureteric stent insertion number went up to 136. Results: Initially 63 patients underwent routine stent insertion. 26 patients had UTI (41%) within 4-6 weeks of renal transplantation. One patient had urine leak from this group of patients. A total of 63 patients underwent selective ureteric stent insertion, 28 (44.44%) patients had ureteric stent insertion, 12 patients (42.85%) had UTI and one patient had a urine leak. 35 patients had stent insertion in the selective stent insertion group and 7 patients (20%) had UTI and one patient also had a urine leak in this group. Subsequently after collection of more data it was found that 26 (19.1%) out of 136 patients had UTI in the selective stent group which was found to be significant and 8 patients had a urine leak which was still comparable to the routine stent insertion group. Conclusion: Selective ureteric stent insertion has shown to reduce urinary tract infections with comparable major ureteric complications in renal transplant patients.

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Abstract No. 88 SPONTANEOUS RENAL ALLOGRAFT RUPTURE IN A PAIR OF DECEASED DONOR KIDNEYS: A CASE REPORT TOVMASSIAN David1,2, YOON Peter1, YAO Jinna1,2, YUEN Lawrence1, ALLEN Richard1,3, LAURENCE Jerome4,3, PLEASS Henry1,3 1National Pancreas Transplant Unit, Westmead Hospital, Sydney, 2Western Clinical School, University of Sydney, 3School of Medicine, University of Sydney, 4Renal Transplant Unit, Westmead Hospital, Sydney Renal allograft rupture (RAR) is a rare and potentially fatal complication of renal transplantation. RAR is most commonly associated with acute rejection however it has also been noted in cases of severe acute tubular necrosis or renal vein thrombosis. We herein report a case of two patients who underwent renal transplantation from the same deceased donor. Both recipients had identical spontaneous RAR post-operatively at the middle to inferior pole of the kidney. Neither patient had any evidence of rejection or acute tubular necrosis on biopsies nor did they have renal vein thrombosis. The donor cause of death was however traumatic with a fall from height. One recipient had a capsulotomy performed whereas the other had wound packing and re-exploration in 48 hours. The kidneys were both salvaged and the recipients remain well with good renal function. Abstract No. 89 OPTIMAL SURGICAL MANAGEMENT OF RENAL HYPERPARATHYROIDISM KRIGE AJ1,2,3, BOCHNER MA2, KOLLIAS J2, WHITFIELD RJ2, BINGHAM JMM2 1Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 2Department of Surgery, Royal Adelaide Hospital, 3School of Medicine, Faculty of Health Sciences, University of Adelaide Secondary and tertiary hyperparathyroidism are major complications of chronic renal failure, and can persist following renal transplantation. The optimal surgical treatment of renal hyperparathyroidism is uncertain. We examined our experience with an audit of consecutive cases at our centre. In a single-centre retrospective audit of a 10 year period, we compared outcomes between total parathyroidectomy with autograft and subtotal parathyroidectomy. The theatre database ORMIS was utilised to capture all parathyroidectomies over the study period, with this list filtered for operations performed for renal hyperparathyroidism. Patient records were accessed to determine reason for referral (secondary/tertiary hyperparathyroidism), dialysis/transplant status, type of operation, weight of resected tissue, duration of post-operative calcium infusion, length of stay (LOS), calcium and parathyroid hormone (PTH) trends and complications. These data were compared between groups, with exclusion of MIP and re-exploration operations. Of all patients undergoing parathyroidectomy for renal hyperparathyroidism (n=78), the majority were performed for tertiary hyperparathyroidism. 42% had functioning transplants or required definitive management of hyperparathyroidism before being waitlisted for transplantation. 55 patients underwent subtotal parathyroidectomy and 23 had total parathyroidectomy with autograft, with the remainder undergoing MIP or re-exploration. Median LOS was significantly less in the subtotal parathyroidectomy group (4 days vs 6 days in total parathyroidectomy, p=0.029), with a trend toward shorter duration of post-operative calcium infusion. There was no significant difference in the post-operative calcium and PTH levels over time. Subtotal parathyroidectomy is not inferior to total parathyroidectomy with autograft, and may result in shorter duration of post-operative calcium infusion and LOS.

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Abstract No. 90 PRE-TRANSPLANTATION NATIVE NEPHRECTOMY IN POLYCYSTIC KIDNEY DISEASE: AN OVERVIEW OF INDICATIONS AND CASE REPORT. PERERA Dinushi, YAO Jinna, ALLAN Lachlan, PLEASS Henry Department of Surgery, Westmead Hospital, Sydney Background Patients with autosomal dominant polycystic kidney disease (ADPKD) develop multiple expanding renal cysts over time. Approximately 50% of patients develop end-stage kidney disease which may require renal replacement therapy, including transplantation. There remains discussion regarding the need for, and optimal timing of native-nephrectomy in ADPKD. Current indications for pre-transplantation native nephrectomy include pain, haemorrhage, infection and a need to create space for donor kidney implantation. Case Report We present the case report and clinical images of a 49 year-old male with ADPKD presenting with recurrent cyst infections, fluid overload and malnutrition secondary to massive polycystic kidneys. He required optimization of nutrition, fluid overload, coagulopathy and was commenced on haemodialysis. He was planned for bilateral nephrectomies for management of chronic cyst infections and to allow for future donor kidney implantation given the significant size of the native kidneys. He underwent open left nephrectomy (specimen weight 7.5kg) and washout of a subphrenic abscess. Right nephrectomy was abandoned due to intraoperative haemodynamic instability. He progressed well post-operatively and recovered with no complications. Conclusion Our case reflects current views on pre-transplantation native nephrectomy in polycystic kidney disease, namely its suitability in the settings of pain, infection, haemorrhage and to create space for donor kidney implantation. Careful preoperative planning and optimisation needs to occur to minimise significant morbidity and mortality.

Figure: Left native nephrectomy specimen, weight 7.5kg

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Abstract No. 91 IMPACT OF PROLONGED COLD ISCHAEMIC TIME IN AN OVINE MODEL OF RENAL TRANSPLANTATION KRIGE AJ1,2, JOHNSON JK1, RUSSELL CH1, PALMER LJ3, COATES PTH1,2 1Central Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, 2School of Medicine, University of Adelaide, 3School of Public Health, University of Adelaide Prolonged cold ischaemia is an inevitable occurrence in a portion of kidneys for transplantation in Australia due to our large transplantation catchment areas and the current accepted method of static cold storage (SCS) organ preservation. At times cold ischaemic time (CIT) approaches the upper acceptable limit of 24 hours. It is widely accepted in the literature that increased CIT has an impact on both short- and subsequently long-term graft outcomes. We have examined the effect of short and prolonged CIT on the outcomes of renal transplants using an ovine renal auto-transplantation model. 2 groups of sheep underwent left nephrectomy and kidney auto-transplantation into the left neck with anastomosis to jugular vein and carotid artery and ureter brought out to skin as a urostomy. Kidneys in both groups were preserved using standard SCS preservation. In group 1 CIT was limited to <90 minutes and in group 2 CIT approached 24 hours. All sheep were followed up for 1 week post transplantation, undergoing daily biopsies of the transplant kidney and daily collection of urine samples from both the transplant kidney via urostomy and the contralateral non-transplanted kidney via indwelling urinary catheter. Biopsies were assessed for histopathology, and urine samples for urinary biomarker Kidney Injury Molecule-1 (KIM-1) using ELISA. This allowed comparison of KIM-1 between native and transplant kidneys and correlation of urinary KIM-1 with histopathological findings in the transplant in order to determine the short term impact of prolonged cold ischaemia on the graft. Abstract No. 92 A BIOETHICAL ARGUMENT FOR INCREASING ABORIGINAL LIVING KIDNEY DONATION WEIGHTMAN Alison1,2,3 1Monash Bioethics Centre, Monash University, Melbourne, 2Royal Adelaide Hospital, 3Department of Nephrology, Royal Darwin Hospital Distributive justice is a key principle of modern-day Western bioethics. This means allocation of healthcare resources, including kidney transplants, ought to occur in a manner that enables equal access for all Australians. Inequalities in allocation are only ethically permissible if there is benefit to the least advantaged (for example, extra funding to programs supporting disadvantaged groups). Given the disproportionately high incidence of kidney disease among Aboriginal Australians, it would be expected that renal transplantation, including living donor kidneys, would be more accessible to Aboriginal people to help address this pre-existing disparity. Unfortunately, Aboriginal people are the least able to access living donor kidney transplants. Australian transplantation units rarely accept Aboriginal donors, due to concerns about higher rates of donor adverse outcomes including kidney failure and diabetes. I suggest this response is unjustifiably paternalistic, as it prevents Aboriginal donors and recipients from making their own choices about the acceptability of the risks and sacrifices of donation. Renal transplants offer incontestable gains in health, quality of life and life expectancy in comparison to dialysis, with the potential added benefits of returning to family and country. While the duty of non-maleficence makes it impossible to overlook the significant negative outcomes experienced by some donors, the potential gains to recipients together with the harms of restricted access to living donor transplantation may be sufficient to outweigh these. I argue that we should consider a more permissive approach to Aboriginal living kidney donor assessment, in order to better promote donor autonomy and address social injustice.

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AUTHOR INDEX

NOTE: Numbers refer to abstract number, not page number. Bold numbers indicate presenting author. ACOSTA Felipe 43 ADHIKARY Sam 17 AFFANDI Jacquita 40 AGOSTINHO Nelson 75, 83 AL-ATIYAH Ranje 59 ALEXANDER Ian 36 ALEXANDER Stephen 2, 4,16, 18, 33 ALLAN Lachlan 80, 85, 90 ALLCOCK Richard 39 ALLEN Richard 13, 47, 50, 84, 85, 88 AMARATUNGA Rajith 80, 85 ANDERSON Patricia 25 AOKI Naoto 49 ARIYANTO Ibnu 39 AU Amy 42 BAG S 78 BAILEY Jacqueline 41 BAMPTON Tristan 29 BARBARA Jeffrey 56, 74 BARRY Lucinda 21 BARRY Simon 15, 34 BEDI Sukhandeep 53 BERTOLINO Patrick 36 BHATTACHARJYA Shanthanu 87 BILLINGS Paul R. 43 BINGHAM JMM 89 BOCHNER Ma 89 BONGONI Anjan K 52 BOUDVILLE Neil 79 BOWEN David 36 BROOKS Ag 55 BROOKS Andrew 60 BURNS Heathe 16, 57 BUSSELL Lauren 11 CAMPBELL Kirsty 70 CAO Qi 4, 18, 54 CARROLL Robert 15, 34, 71 CATTERALL Tara 28 CAVAZZONI Elena 35, 37 CEHIC Gabrielle 74 CELERMAJER David 75 CHADBAN Steve 31, 69, 75, 76 CHAMBERS Daniel 10 CHAN Doris 72 CHANDRASEGARAM Manju 10 CHAPMAN Jeremy 78 CHEN John 27, 29 CHEUNG Charmaine 57 CHEW Hong Chee 12, 30 CHEW Yi Vee 16, 25, 33 CHIH Huijun 40 CHO Jin Gun 78 CHOKSI Harsham 47 CHOW Kevin V 77

CHRISTIANO Yvonne 60 CLAYTON Phil 6, 22, 23, 24, 26, 31, 47, 63, 79, 82 COATES P. Toby 15, 19, 22, 27, 29, 34, 41, 58, 63, 71, 91 COFFEY Ne 45 COLLINS Michael 76 CONNELLAN Mark 12 CORBETT Matthew 13 COSTER DJ 45 COUPER Richard 27, 29 COWAN Peter 52 CRAIG Elizabeth 73 CRAIG Jonathan 14 CRISTIANO Yvonne 55 CROSS Nick 22 CROWHURST Thomas 11 CULTRONE Daniele 41 CUTHBERTSON Peter 17 D'COSTA Rohit 5, 20 D'ORSOGNA Lloyd 9 D'SOUZA Kenneth 75 DANG Ngoc Tuan Anh 46 DAVIES Christopher 6, 82 DE LA MATA Nicole 8, 35, 37, 44 DE ROO Ronald 33 DE SANTIS Dianne 9, 64 DEAYTON Sue 71 DEMKO Zachary 43 DENDLE Claire 65 DEY Jacqueline 64 DIAS Brendan 87 DITTMER Ian 22, 48 DOWNING Jonathan 9, 64 DOYLE A 1, 3, 30 DROGEMULLER Christopher 29, 34, 41, 58 DUDEK Nadine 36 EDWARDS Suzanne 11 ELLIOTT Rachel 70 ELLIS Patrick 33 EMERY Tim 71 ENDRE Zoltan 42 ENDRE Zoltan 42 ERLICH Jonathan 42 ETHERTON Colleen 29 FAHIM Magid 76 FARIDI Pouya 36 FERNANDO Mangalee 42 FORMBY Mark 81 FRANCIS Leo 66 FURNISS Hayley 7 GANTUMUR Narangerel 34

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GAO Ling 1, 3, 12, 30 GARDINER Brad 55 GASPI Renan 33 GAUDIERI Silvana 39 GILLIN A 69, 83 GILROY Nicky 78 GOODWIN Melissa 21 GRACEY DM 69 GRANGER Emily 12 GREENWOOD John 41 GREY Shane. 32, 41 GRIFFIN Anthony 62 GUJARI Diba 22 GULYANI Aarti 26, 82 GUNTON Jenny 57 HALL Bruce 53, 59 HAMEED Ahmer 33, 75 HANLON Lucy 83 HANNA Thomas 48 HARDSTAFF Ruth 81 HARRIS David 18 HAWLEY Carmel 76, 79 HAWTHORNE Madeline 73 HAWTHORNE Wayne 16, 25, 33, 50 HEDLEY James 8, 35, 37 HERATH Sanjeeva 42 HERON Je 69 HEWA-GEEGANAGE Shanika 83 HEWAWASAM Erandi 26, 82 HICKS M 1, 3, 12, 30 HIHO Steven 61 HOANG Nu Ngoc Nhung 46 HODGKINSON Suzanne 53, 59 HOGAN Jesse 9, 64 HOLMES-LIEW Chien-Li 11 HOLMES Mark 11 HOPE Christopher 15, 34 HUGHES Peter 6, 7, 23 HUMFREYS Ian 71 HU Min 4, 16, 18, 33, 64 HURTADO Plinio 19 HUYNH Annie 86 IERINO Frank 52 IRISH Ashley 38, 39, 40 IRISH Georgina 63 JABBOUR A 1, 30 JACKSON Angela 93 JAHAN Sadia 66 JALALI Sedigheh 55 JALALONMUHALI Maisarah 71 JANSZ Paul 12 JARDINE Meg 14, 69 JAYA Joseph 68 JESUDASEN Shilpanjali 26, 82 JIMENEZ Elvira 25 JOHN George 66 JOHNS Daniel 58 JOHNSON David 79 JOHNSTON Julie 58, 91 JOHNSTON Sonya 11

JONES Daryl 7 JONES VJ 45 JOSEPH David Morris 75 JUNEJA Rajiv 56 KABLE K 85 KANELLIS John 7, 26, 65, 74 KANSAL Arushi 65 KARUNIA Jevin 18 KASSAHN Karin 27 KATSUOKA Yuichi 49 KAUSMAN Joshua 6, 23 KAWANISHI Yujiro 12 KAY Thomas 28, 41 KEANE M 45 KELLY Patrick 8, 31, 35, 37, 44 KENNEDY Sean 73 KEOGH Kandice 62 KEUNG Karen 33 KHAN Afaq 70 KHANNA Rajiv 66 KHURANA Sanjeev 29 KIKUCHI Eiji 49 KIM Juewan 15, 34 KIRATA Svjetlana 29 KOLLIAS J 89 KORBUTT Gregory 41 KOS Cameron 28 KRESOJE Nina 39 KRIGE AJ 89, 91 KUCHEL Timothy 58 LAM Susanna 75, 86 LANGLANDS Janice 48 LARKINS Nicholas 6, 72 LAU Howard 47, 84 LAURENCE Jerome 13, 33, 47,50, 51, 75, 83, 84, 86, 88 LAWSON Malclm 62 LE PAGE Amelia 6 LEARY Shay 39 LE Cindy 64 LEE Alice 68 LEE F 69 LEE Silvia 38, 39, 40 LEE Taina 47, 51, 75, 83, 84 LEONG Mario 36 LEVVEY Bronwyn 5, 20, 55, 60 LI Jennifer 2, 78 LI Jenny 55 LIM Soo Kun 71 LIM Sue Jin 71 LIM Wai 22, 79 LIN Jie 55 LIU Xiao 34 LLOYD Megan 38 LOK Charmaine 79 LOUDOVARIS Thomas 28, 29, 41 LU Bo 4, 18, 54 LU David B 33 MACDONALD PS 1, 3, 12, 30 MACKIE Fiona 6

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MAJONI William 70 MALLESARA Girish 81 MANLEY Paul 48 MARIANA Lina 28 MARTIN Dominique 22 MARTINEZ Patricia 9, 64 MARUI Yuhji 49 MASTERSON Rosemary 77 MATHEWS Loren 58 MATSUMURA Kaori 49 MAY Stephen 67 MA Xiaoqian 54 MCCARTHY Hugh 18 MCDONALD Mark 5, 20, 21 MCDONALD Stephen 22, 26, 79, 82 MCDOWELL Joseph 32 MCKANNA Trudy 43 MCMICHAEL Lachlan 24 MCRAE Jennifer M 52 MENON Madhav 4 MEYBODI Farid 13 MIFSUD Nicole 36 MILLS Rad 45 MIRAZIZ Ray 33 MOSHKEVICH Solomon 43 MUIRHEAD Robb 58 MULLEY William 65 MUNYARD Kylie 39 MURPHY Barbara 4 MUTHUKUMARASWAMY Carl 48 MYATT Lin Lin 67 NAKAZAWA Ryuto 49 NATALE Patrizia 14 NAVARRO Samantha 43 NEO Eu Ling 29 NG Kok Peng 71 NICHOLSON Leigh 4, 16 NISHI Tomohiro 49 NITSCHKE Jodie 58 O'CONNELL Philip 4, 16, 25, 50, 54 O'LEARY Michael 8, 35, 37 O'MAHONY Kate 48 O’GRADY Greg 33 OATES Clare 55 OKAHARA Shuji 5, 20 OLAKKENGIL Santosh 87 OPDAM Helen 5, 7, 20, 21 P’NG Chow H 33 PALMER Lyle 22, 27, 91 PALMER Suetonia 14 PAPAS Evan 28 PARK Yeung Ae 77 PAUL-HENG Moumita 36 PEFANIS Aspasia 52 PENKO Danielle 41, 58 PERERA Dinushi 90 PERKINS Griffith 19, 34 PHAM Nhu Hiep 46 PILCHER David 5, 20 PILMORE Helen 79

PLEASS Henry C. 33, 47, 50, 75, 80, 84, 85, 88, 90 PLEASS Henry 47, 50, 84, 88 POLKINGHORNE Kevan 79 PRESTON John 62 PRICE Patricia 38, 39, 40 PULITANO Carlo 51, 75 PULLAN Caitlin 58 PURCELL Anthony 36 QASABIAN Raffi 75 QIAN Yi Wen 16 RADFORD Toni 29 RAKESH Prateek 53 RRAMACHANDRAN Vidiya 37 RANA Abdul Ahad 87 RAWLINSON William 37 RAZAVIAN Mona 14 REIDLINGER Donna 76 RHEE Handoo 62 ROBERTS Matthew 79 ROBERTSON Paul 33, 85 ROBINSON Catherine 53 ROGERS Natasha 2, 4, 16, 33, 50, 78, 85 ROJAS-CANALES Darling 41 ROSALES Brenda 8, 35, 37, 44 ROWLANDSON Matthew 81 RUOSPO Marinella 14 RUSSELL Christine 87, 91 RUSSEL Oscar 22 RYAN B 85 SAGLIMBENE Valeria M 14 SALTER Sherry 68 SANDERS Jo 7 SANDROUSSI Charbel 75 SARWAL Minnie 43 SASAKI Hideo 49 SAUNDER Alan 68 SCAFFIDI Jacqueline 15 SCHEUER SE 1, 3, 12, 30 SCOTT Hamish 27 SCUDERI Carla 66 SELCK Claudia 28 SHARLAND Alexandra 36 SHAW Karli 18 SHI Bree 31 SIGDEL Tara K. 43 SLADDEN Timothy 10 SLUYTER Ronald 17 SMITH Georgia 22 SNELL Greg 5, 11, 20, 55, 60, 61 SON Eric Taeyoung 36 SOTO Claudio 12 STANKOVIC Sanda 60 STOKES Rebecca 57 STRIPPOLI Giovanni F 14 SUH Nancy 68 SULLIVAN Lucy 55, 60, 61 SUTANTO Michael 9, 64 SWAMINATHAN Suda 72 SYPEK Matthew 6, 23

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TANG Joanne 26 TANG Sooling 16 TANG Tianfeng 4 TAN Rachel 56, 74 TAN Sarah 74 TAYLOR Kylie 42 TAYLOR Sam 48 THOMAS Gordon 33 THOMAS Helen 28 TOEWS Maeghan 22 TORPY David 58 TOVMASSIAN David 47, 50, 84, 88 TRAN Giang 53, 59 TREVILLIAN Paul 81 USUBA Wataru 49 VAN DER JEUGD Jane 56 VERMA Nirupama 53, 59 VERRAN Deborah 51, 83 VIECELLI Andrea 79 VILLANUEVA Jeanette 1, 3, 12, 30 VUKOVIC Irena 64 WALKER Rachael 79 WALLACE Gordon 34 WALLER Karen 8, 35, 37 WALTERS Stacey 32, 41 WANG Yuan Min 18 WATERS Shelley 38, 39, 40 WATSON Alasdair 12 WATSON Debbie 17

WEBSTER Angela 8, 14, 26, 35, 37, 44 WEIGHTMAN Alison 92 WESTALL Glen 55, 60, 61 WHITFIELD RJ 89 WILLIAMS K 45 WILLIAMS Lindy 25 WONG Germaine 6, 22, 33, 79, 80, 85 WONG Yun Hui Sheryl 79 WONG Zo-Ee 64 WOOD Simon 62 WU Denghao 27 WU Michael 74 WYBURN Kate 8, 23, 35, 37, 47, 69 XU Bo 33 YAO Jinna 47, 50, 75, 80, 84, 85, 90 YEO Aeneas 11 YERKOVICH Stephanie 10 YEUNG David 11 YING Tracey 31, 75 YI Shounan 16, 54 YOON Peter 50, 88 YOZA Naoto 49 YUEN Lawrence 33, 47, 50, 75, 84, 85, 88 YUE Zhilian 34 ZAMMIT Nathan. 32 ZHANG Chris 33 ZHANG Geoff 16, 18 ZHAO Yuanfei 16, 54 ZHENG Guoping 4 ZIMMERMANN Bernhard 43

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The Transplantation

Society of Australia and

New Zealand Inc.

ABN 90 796 930 798

SOCIETY OFFICERS

Toby Coates (President)

Helen Pilmore (Vice President)

Natasha Rogers (Secretary)

Bronwyn Levvey (Treasurer)

COUNCILLORS

Nick Cross Kate Wyburn

Kelly MacDonald Christine Russell

Nick Shackel Philip Clayton

Andrew Jabbour Fiona Mackie

Nigel Palk (ATCA Representative)

PAST PRESIDENTS AG Ross Sheil James Biggs

Anthony JF d’Apice Kerry Atkinson

Ian FC McKenzie Tom Mandel Bruce Hall

Jeremy Chapman Mauro Sandrin Stephen Lynch Randall Faull

Philip O’Connell Josette Eris

Frank Ierino Peter Macdonald

Geoffrey McCaughan Steve Chadban

Stephen Alexander

EXECUTIVE OFFICER Sommer Twycross

145 Macquarie Street Sydney NSW 2000

Australia Tel: (02) 9256 5461 Fax: (02) 9241 4083

E-mail:[email protected] Web: www.tsanz.com.au

NOTICE OF ANNUAL GENERAL MEETING

The Annual General Meeting of the Transplantation Society of Australia and New Zealand held on Monday 30th July 2019 in the Refectory, The Holme Building, Sydney University at 5.00pm.

Present: 53 members of the Society were present at the meeting which was chaired by the President, Professor Steve Alexander, who welcomed everyone to the meeting.

Also in attendance: Mrs Nieves Piaggio, Executive Officer and Ms Katie Graham, Administrative Officer

1. APOLOGIESDr Robert Carroll

2. CONFIRMATION OF THE MINUTESThe minutes of the Annual General Meeting held on 30th April2018 were passed as a true record.

Moved: Toby CoatesSeconded: Shane Grey

3. BUSINESS ARISING FROM THE MINUTESConstitutional changes to be discussed in the secretary’s report

4. PRESIDENT’S REPORTProfessor Steve Alexander started by thanking the transplantcommunity. He also thanked everyone for attending and advisedthat attendance was up from last year with over 300 registrations.He then went on to thank the convenors Natasha Rogers and BillMulley (ASM), Michael Collins and Karen Keung (PGC), KarenDwyer and Leyla Aouad (Masterclass) and Bronwyn Levvey andAndrew Jabbour (Cardiothoracic Symposium). He thensummarised the various projects that TSANZ had underaken andthanked the retiring Council members Dr Rob Carroll (Treasurer),Dr Nick Cross (NZ), A/Prof. Nick Shackel and told members thatthe Society would be in good hands under the new PresidentProfessor Toby Coates and President Elect Associate ProfessorHelen Pilmore.All in attendance:

1. Confirmed the election of members of CouncilA/Professor Kate Wyburn, and Dr Philip Clayton

2. Ratified that the cardiac position be an additional position andfor A/Professor Andrew Jabbour to continue as ex officiocardiac representative on Council until the next election in2021.

3. Endorsed that the current TSANZ Council appoint the NationalDirector of NZ Kidney Transplantation, Dr Nick Cross, as ex-

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officio representative from New Zealand.

4. Agreed that the unfilled New Zealand council position be held by the next person standing at this year’s election, Dr Fiona Mackie, until the next election in 2021.

5. TREASURER’S REPORT – presented by the Incoming Treasurer A/Prof Bronwyn

Levvey Bronwyn confirmed increase in registration at this year’s AGM and the Society’s financial stability. She advised of an increase of sponsorship at this year’s ASM with expenses for meetings and awards remaining stable. She then referred the membership to the Financial Report of 31st December 2018 and proposed that it be accepted Moved: Helen Pilmore Seconded: Shane Grey

6. SECRETARY’S REPORT

Natasha Rogers, the Honorary Secretary, confirmed that the number of members was stable with an approximate 50/50-member split. However, only a small number were students and encouraged all to let their students know that membership with TSANZ was only $22. She then presented a Motion for an increase in full membership (both to Australia and New Zealand members) of $50 to be split over two years. $25 starting in 2020 and again in 2021. The idea of a “Research Levy” fund was also presented. Moved: Christine Russell Seconded: Shane Grey

She then then presented members with the proposed constitution changes as outlined in “Annexure 1” (attached). Changes were passed unanimously.

7. REPORT ON ADVISORY COMMITTEES/WORKING GROUPS

Toby Coates advised membership that the Advisory Committees and Working Groups were working well as was the TLRG meetings with OTA.

8. SCIENTIFIC PROGRAM & EDUCATION COMMITTEE REPORT (SPEC)

Toby, thanked this year’s organisers of all 4 meetings. He confirmed that the attendance figures had exceed 2018 and stated that the move out of Canberra had been very positive.

He then thanked Dan Chambers and Kelli MacDonald for their time as co-chairs of SPEC and confirmed the appointment of Dr Wai Lim and Dr Lucy Sullivan as the new co-chairs He confirmed that the 2020 ASM would be held from 22-24 March at the Adelaide Convention Centre and that the convenors would be Dr Phillip Clayton and Dr Eu Ling Neo. Other meetings taking place - Machine Perfusion Workshop, the PGC, Masterclass, Liver meeting and TNA/ATCA.

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9. LIAISON WITH SCIENTIFIC SOCIETIES

No discussion 10. GENERAL BUSINESS

Geoff McCaughan ask whether registration fees had increased in the past few years. Steve Alexander confirmed that they had remained stable with TSANZ providing a very subsidised rate for students to encourage them to attend as well as become members. He reiterated that student membership fees were only $22. He also stated that, in the past few years, the cost of the ASM had been capped as well as the amount of the awards however, TSANZ were still offering Early Career Researchers Awards, Ian McKenzie Award, the Aviva Award, Lafferty Award (biennial), Travel Awards and the TTS Mentee/Mentor Awards. Geoff McCaughan then asked whether TSANZ would address the China issue? Steve Alexander stated that it gets addressed by different members of the transplanting community at various times. Steve then welcomed the incoming Council members – A/Professor Kate Wyburn, Dr Phillip Clayton, A/Professor Andrew Jabbour and Dr Fiona Mackie and congratulated Steven McDonald as the chair of NIKTT and Jacqui Hughes as the Deputy Chair.

There being no further business the meeting closed at 5.20pm.

Toby Coates Natasha Rogers

President Honorary Secretary

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President’s Report Nearly six months into 2020 and obviously so much has happened and, the Transplantation Society of Australia and New Zealand (TSANZ) as the peak body that represents the transplantation sector, has been playing a leading role at all levels. Despite COVID-19 being the major defining event of 2020, other important Australasian issues have also been happening in the Transplant space. Paired Kidney Exchange with New Zealand In partnership with the Australian and New Zealand governments TSANZ, and particularly the Renal Transplant Advisory Committee (RTAC), have taken a major step forward by the establishment of the Trans-Tasman Australian and New Zealand Paired Kidney Exchange (ANZKX) program. The program which was announced in September 2019 has increased the number of pairs in the exchange and increased use of altruistic donors. This has been a major undertaking. Thanks and due credit need to go Nick Cross, Ian Dittmer, John Irvine, Carl Muthu, Peter Hughes and from the laboratory side, Heather Dunkley and Linda Cantwell as well as ANZKX coordinators Jo Burton (NZ) and Emma Vanhardeveld (Australia). From the Organ and Tissue Authority (OTA) Jude Harrison and Amanda Nicol also played critical roles in getting the final product to work, culminating in the first Trans-Tasman 5-way exchange taking place in October 2019. Organ Match The updating for the National Organ Match system (NOMS) has been a huge task for members of the TSANZ. The seamless transition from the old system to the new was the product of a lot of very hard work and planning. In particular, I would like to acknowledge – Narelle Watson and Rhonda Holdsworth as well as all state laboratory directors: Ian Humphries (SA) Mary Diviney (VIC), Lyanne Weston and Narelle Watson NSW, Dianne De Santis (WA) and Alisha Thornton (QLD). Also, within the state laboratories, the tissue typing laboratory subject matter experts who willingly contributed their time and expertise to create the final product. Acknowledgement also needs to go to the Organ Match Strategic Governance committee Jude Harrison and David Childs (transplant). The potential for the new Organ Match system to deliver a more responsive organ allocation system is significant and represents a fantastic new opportunity in Australian transplantation. For New Zealand transplantation, the Organ Match system supports the ANZKX. Virtual and Flow Crossmatching With changes in tissue typing for organ transplantation, the CDC crossmatch has been phased out worldwide necessitating a change to “virtual” crossmatching – a technique that relies on high level molecular typing and sophisticated antibody determination to determine tissue compatibility. Behind the scenes, TSANZ and OTA have organised the new Virtual Crossmatch working group, chaired by Dr Ross Francis. At the same time, the Tissue Typing laboratories have been implementing new protocols for flow cytometric cross matching, which will be performed on the night in order to match sensitised transplant recipients. These changes in technology will bring transplantation into line with other nations worldwide, who have already implemented virtual cross matching techniques for organ allocation.

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The President’s Report

National Indigenous Kidney Transplant Taskforce - NIKTTThe TSANZ acknowledge the efforts of Stephen McDonald (Chair), Jacqui Hughes (Deputy Chair), and members of the NIKTT secretariat and operations committee including: Natasha Rogers, Eleanor Garrard, Jude Harrison, Kelli Owen, Kim Rawson and Matilda D’Antoine. Key achievements are:

• Provision of eight equity and access sponsorships amounting to $1.04 million.o These initiatives span across four jurisdictions and include: delivery of outreach

kidney transplant education and assessment in rural and remote areas; establishment of transplant focussed patient mentor pilot projects and Indigenous reference groups and strengthening the Aboriginal and Torres Strait Islander health workforce in kidney transplant settings.

• Commencement of the NIKTT data project, which is being delivered through ANZDATA.o 29 units are participating in this initiative, which involves the collection of additional

pre-transplant data points; it is anticipated the findings will improve our understanding of the inequities that affect Indigenous patients throughout the journey to waitlisting and transplantation.

• Successful hosting of the National Indigenous Dialysis and Transplantation Congress(NIDTC) in Alice Springs in October 2019.

o Over the course of the three-day event, around 130 delegates from all over Australiapartook in workshops to generate innovative approaches to tackling kidney disease inequities that affect Indigenous Australians.

• The establishment of a partnership with the Lowitja Institute to deliver a review into existinghealth service interventions that target cultural bias.

o The review will draw upon Australian and international approaches to describe wherecultural bias fits in relation to other cultural and bias models from an Indigenous perspective.

o Australian studies and examples will then form the basis of a comprehensive analysisof cultural bias interventions designed to address equity, access and health outcomes for Aboriginal and Torres Strait Islander Australians.

o The findings will be made available to the Commonwealth and the broadercommunity in the form of a policy report.

Ernst and Young Review of Organ Donation, Retrieval and Transplantation SystemThe “EY review” as it is also known was a major piece of work undertaken as a review of the Australian organ donation, retrieval and transplantation system, which began in June 2018 and was published February 2020. Many members of the TSANZ participated in the EY review process, and the TSANZ has been asked for its comments in regard to its implementation. Of the 57 recommendations, TSANZ and the TLRG have pushed hard for increased resourcing downstream for transplant units recognising the major stress that increased transplant activity has on transplant units. Following the release of the final report, a committee of government officials representing all jurisdictions and OTA will oversee a comprehensive assessment of the Final Report’s recommendations and development of a future national strategy. It remains unclear in the current environment how many of the recommendations of the EY review will eventually be implemented. The TSANZ Council will monitor the activity and recommendations of the jurisdictional committee to ensure that a clinical input to any final recommendations be applied.

COVID-19 and Organ Transplantation in AustraliaEveryone of course has been impacted by COVID-19, which will undoubtedly change theway we live and practice transplantation in Australia, New Zealand and worldwide. The

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emerging pandemic caused the TSANZ Council and TSANZ Scientific Program and Education Committee (SPEC) to issue an early cancellation of the Adelaide Annual Scientific Meeting, which was due to be held in March of 2020, more about this below. From a society point of view, TSANZ played a key role in the formation of the COVID-19 National Transplantation and Donation Rapid Response Taskforce. Membership of the task force, co-chaired by the TSANZ President and the Chair of the Transplant Liaison Reference Group (TLRG), Professor Steve Chadban covered all the chairs of the TSANZ Advisory Committees and subject matter experts from the Donation sector lead by Dr Helen Opdam. The Taskforce was a joint effort with the OTA, and has met weekly during the evolving pandemic producing a weekly communique. The Taskforce was central in the decision to suspend kidney transplantation in Australia, and then to help re-initiate the program when conditions improved. It’s important to note the role of Professor Kate Wyburn who, as RTAC chair, coordinated the state transplant programs and provided communication to non-transplant nephrologists through the weekly webinars with the Australian and New Zealand Society of Nephrology (ANZSN). Remarkable throughout the pandemic, Donate Life Australia continued to provide extraordinary service to the transplant sector. Heart, lung, liver and paediatric kidney transplant programs were not suspended and continued to provide lifesaving organs for Australians. In New Zealand, Organ Donation New Zealand (ODNZ) continued its work, enabling the NZ programs to continue throughout the pandemic. There was a remarkable spirit of cooperation and mutual recognition and respect of roles that was the flavour of the organ and tissue sector during this time. The weekly meetings have produced 14 communiques to date, which document the evolution of pandemic in Australia and the transplant sectors response to it. None of this was more evident than when the time came to restart programs and kidney transplantation began again in a staged manner across Australia. TSANZ and the Transplant Nurses Association (TNA) teamed up with Transplant Australia (TA) to provide updates to patients, which were distributed on our website and on TA and Kidney Health Australia’s (KHA) websites. The society is grateful to Chris Thomas from TA and A/Professor Shilpa Jesudason from KHA for their help in getting patient specific advice as widely distributed as possible. TSANZ Annual Scientific Meeting 2021 A tremendous amount of planning went into the March 2020 TSANZ program, by the SPEC and our meeting coordinators. The program, with a wide range of topics, held with other affiliated meetings was designed to give a broad transplantation experience for our wide membership – from Donor Coordinator and Transplant Nurses to basic science and clinical transplant specialists. As we all know now, this meeting was cancelled. However, great efforts from the SPEC and in particular our office staff, has turned around what was a potential disaster. After discussion, the Council determined that the ASM should be held again in Adelaide in 2021. The Adelaide Convention Centre has agreed to move the booking to March 2021 without loss of any deposit. withdraw sponsorship from the TSANZ meeting, but kept their faith with our group and kept their sponsorship current. We are closely watching how things unfold with the international travel situation regarding attendance of our invited overseas speakers, and planning for virtual sessions as needed. Thanks again to the meeting convenors Eu Ling Neo and Philip Clayton and the chairs of our SPEC, Lucy Sullivan and Wai Lim, for their hard work in these exceptional circumstances. TSANZ Office Staff and COVID-19 Our society runs efficiently due to the very hard work of our Executive Officer Nieves Piaggio, our Senior Project Officer Kim Rawson and our Admin Support Officer Roslyn Davies. Early in the COVID-19 outbreak, our team transitioned to working from home, and have been delivering excellent service from there. Recognising that the Society was going to

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take a significant financial loss due to the cancellation and postponement of the Annual Scientific Meeting, TSANZ initiated an application to the Federal Government’s Job Keeper scheme, and our office staff were successful in getting this subsidy – further saving significant funds for the Society. The entire Council on behalf of the membership would like to thank again our excellent office staff for their flexibility, loyalty and dedication to our mission in transplantation. TSANZ Website As we enter the increasingly virtual world, our staff pointed out that the current TSANZ website was not for purpose and well overdue for an upgrade. Council approved a revamped website design, after a tender process, to allow Pioneer Websites to develop the new platform. The improved features will include enhanced facilities for educational content for our members and enhanced communication with our membership. Likewise the Annual Dinner, which was to be held at the Adelaide Town Hall has been transferred without loss of deposit to March 2021. It was most heartening to see that over 90% of Society members kept their registration fees with the Society and did not require a refund. This is an obvious indication of the value of the meeting to our members and bodes well for next year. I would also like to provide a vote of thanks on behalf of the Society to our Industry Partners and Commercial Colleagues, who did not TSANZ Elections in October As the year progresses it is now time for elections for the new council and, of course, I strongly encourage you all to consider nominating for the council. There are 7 positions to fill under our incoming president, Helen Pilmore. Those remaining on the council are Kate Wyburn, Philip Clayton and the new ATCA President, Paul Robertson. Finally, of course, just to thank all of our TSANZ Council, the Advisory Committees and most importantly everyone in the transplantation community from students, nurses, coordinators, tissue typers, Donate Life staff, ICU professionals, physicians and surgeons who keep the business of transplantation in Australia and New Zealand going. Toby Coates TSANZ President

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TSANZ Membership List

129 * Denotes ATCA/TSANZ Member # Denotes TNA/TSANZ Member

TSANZ Membership List

AUSTRALIAN CAPITAL TERRITORY

Carney, G Cunningham, J* Falk, M Kwan, T Mehakovic, E Simeonovic, C

NEW SOUTH WALES

Adam, N* Adhikary, S Alexander, S Allen, R Anderson, P Anthony, C Aouad, L Au, E Bird, K Burns, H Burns, T # Burton, M # Calisa, V Cao, J Cao, L Chadban, S Chan, E Chanda, S * Chen, J Chen, T Cheung, C Chew, Y Chew, H Chong, C Collett, J Conway, J Cooper, B Correas, M # Coulshed, S Craig, E # Crawford, M Cuthbertson, P Datson, L * Davidson, D * Dcunha, U De La Mata, N Didsbury, M

Diep, J Dobrijevic, E Durkan, A Erlich, J Fazekas de St Groth, B Fernando, M Fritis-Lamora, R * Gallagher, M Gallagher, A Gao, L George, C Geraghty, N Gillies, A Glanville, A Gracey, D Graham, A Granger, E Grey, S Griffiths, D * Habijanec (nee Belmar), B # Haghighi, K Hahn, D Haigh, S * Hameed, A Hanson, C Harkess, M Havryk, A Hawthorne, W Heer, M Heron, J Hibberd, A Hicks, M Hodgkinson, S Howell, M Hu, M Huang, D Hultin, S Imran, M Iyer, A Jabbour, A James (nee Ryding), L Jameson, C Jardine, M Jayasinghe, K Jha, S Jimenez Vera, E Ju, X Kable, Kaeser, M

Kelly, J Kelly, P Kennedy, S Keung, K Kim, S Koutalistras, N * Kubitskiy, A Kwan, J Lai, S Lam, V Lan, P Le Page, A Lee, V Lee, T Leong, M Lewis, D Li, Y Li, J Lin, R Liuwantara, D Lu, D Luxton, G Ma, S Macdonald, P Mackie, J Mackie, F Mahony, H Mahony, J Majumdar, A Malouf, M Manera, K Mawson , J # May, S Mazid, S McCaughan, G McGinn, S McIvor, L # McKenzie, J Mears, D Melick, G Mitchell, A Munro, C # Murugasu, R Muthiah, K Nabb, L Nankivell, B Naresh, C Natfaji, A Nicholson, L O'Connell, P

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TSANZ Membership List

130 * Denotes ATCA/TSANZ Member # Denotes TNA/TSANZ Member

Paul, P # Paul, M Phoon, R Piaggio, N Pleass, H Pollock, C Prakash, M Pulitano, C Pussell, B Rakesh, P Ralph, A Rasko (nee Strasser), S Rawlinson, W Reimann, F Richards (nee Mackay), K Ritchie, A Robertson, M Robertson, P * Robinson, C Rogers, N Rosales, B Roxburgh, S Sandery, B Scholes-Robertson, N Seifert, N * Sen, S Shackel, N Shahrestani, S Sharland, A Sharma, A Shen, Y Shingde, R Shun, A Siew, S Silveira, P Simpson, A Singer, J Skalicky, D Son, E Spicer, T Sprott, P Stein, A * Stormon, M Sud, K Talaei Zanjani, N Tang, J Tangirala, N Thomson, I Tong, A Trevillian, P Tuh, B Utsiwegota, M # Van Reede Van Oudtshoorn (nee Larkins), E # Vughan, E

Verma, N Verran, D Villanueva, J Virtue, S # Volovets, A Waller, K Walters, S Wan, S Wang, C Watson, D Webster, A Williams, L Wong, G Wong, M Wong, N Woodhouse, E Wright, J Wu, H Wyburn, K Wyld, M Yao, J Yi, S Ying, T Yong, K Zahorowska, B Zammit, N Zhang, G Zhao, Y El-Rashid, M Grooby, K * Haloob, I Laurence, J Moawadh, M Raman, A Ross, C * Scheuer, S Sgorbini, M #

NORTHERN TERRITORY

Brown, M Cairnes, S * Cass, A Elliott, R Hughes, J Karepalli, V Lawton, P Majoni, S Thiele, I

QUEENSLAND

Abbott, W Bettens, P # Brooks, E Burke, M

Byrne, S Campbell, S Carey, J * Chambers, D Chan, S Coco, T * Cossart, A Divithotawela, C Eldridge, A # Fawcett, J Fiene, A Francis, R Francis, A Gartlan, K Griffin, A Hardie, I Hawley, C Henden, A Hill, G Hilton, L # Hollett, P Hopkins, P Isbel, N Jarrett, M # Javorsky, G Jegatheesan, D Kanagarajah, V Le Texier, L Leisfield, P # Lockwood, D Lynch, S MacDonald, K Macdonald, G Mallett, A Markey, K Martins, P McSweeney, W McTaggart, S Minnie, S Mon, S Mudge, D Porra, M # Preston, J Reiling, J Rixon, S # Robson, A Rourke, F * Sinclair, K Sinnya, S Sladden, T Staatz, C Steptoe, R Stuart, K Tallis, C Tan, A

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TSANZ Membership List

131 * Denotes ATCA/TSANZ Member # Denotes TNA/TSANZ Member

Tey, S Van Eps, C Varelias, A Viecelli, A Wilkinson, A Winks (nee Bruce), L # Wong, J Rhee, H

SOUTH AUSTRALIA

Bampton, T Barbara, J Barnett, D Bateman, S Bhattacharjya, S Bimal Gujari, D Bragg, K # Brooke-Smith, M Carroll, R Clayton, P Coates, P Crowhurst, T Dolan, P Drogemuller, C Duncan, K * Faull, R Hodak, A # Holmes, M Holmes-Liew, C Hope, C Irish, G Jastrzebski, N * Jessup, C Jesudason, S John, E * Juneja, R Kang, K Kapojos, J Keane, M Kette, F Khanal, N Kim, J Krige, A Ladhani, M Lett, B McDonald, S McMichael, L Mills, R Mohan Rao, M Muller, K Neo, E Palk, N Passaris, G Pavathuparambil Abdul Manaph, N

Perkins, G Radford, T # Rao, N Rojas-Canales, D Russ, G Russell, C Salehi, T Sivanathan, K Stead, S Sypek, M Tan, B Tan, R Tan, S Venkataraman, K Weightman, A Williams, N * Wu, D

TASMANIA

Gan, J Graver, A Jose, M Kirkland, G

VICTORIA

Andrew, N # Angus, P Atkinson, A Barraclough, K Bateman, K # Bergin, P Blair, S Bourne, B # Brown, F Butler, E Byrne, A Cantwell, L Cheong, J Chow, F Chow, K Choy, S Cocco, N Cohney, S Coughlan, T Cowan, P Crosthwaite, A Dave, V Devine, C # Dhital, K Dwyer, K Dwyer, B * Ellis, C # Fang, D Fink, M Fisicaro, N

Ford, S Fuller, L # Gardner-Dixon, P # Gock, H Goh, S Goldman, A # Goodman, D Gopal, B Gow, P Grynberg, K Hardikar, W Hedley, J Hiho, S Holdsworth, R Hughes, P Hughes, T * Idel, I Ierino, F Ireland, K # Jaw, J Jones, R Kameshwar, K Kanellis, J Kansal, A Kathiravelu, H # Katsoulis, J Kausman, J Kay, T Kennedy, E # Kerr, P Kos, C Kotecha, S Kuo, S Lanteri, M Lee, D Leong, K Leung, P Levin, K Levvey, B Lew, A Li, J Lian, M Ling, J Loudovaris, T Luscombe, B # Maney, O # Mariana, L Martin, D Martin (nee Ngu), K Masterson, R McGiffin, D McRae, J Menahem, S Metz, D Miach, P

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TSANZ Membership List

132 * Denotes ATCA/TSANZ Member # Denotes TNA/TSANZ Member

Michell, I Mulley, W Mullins, K # Murphy, S Nicholls, K Paizis, K Paraskeva, M Pavlovic, J # Pefanis, A Perini, M Pimentel, A Ramessur Chandran, S Rea, A * Roberts, V Robertson, A Rozenkov, V Ryan, J Salter, S Salvaris, E Sandiford, M # Saunder, A Shipp, A * Sinclair, M Snell, G Somerville, C Stankovic, S Starkey, G Stedman, H # Steinberg, A Steven, M Suh, N Sullivan, L Ta, J Ta'eed, A Tait, B Tan, S Testro, A Thomas, H Thomson, N Trapani, J Tupper, K # Vago, A # Van Hardeveld, E # Walcott, J Walker, R Wang, B Westall, G Whitlam, J Wilson, S Bongoni, A Hodgson, A *

WESTERN AUSTRALIA

Adams, L Boan, P

Corsair, N # Dart, S Delriviere, L Dembo, L Do Nguyen, H Downing, J Fazackerley, C # Fidler, S Garas, G Goddard, K He, B Howson, P Irish, A Jamboti, J Larbalestier, R Larkins, N Lavender, M Lim, W Lucas, M Manickavasagar, R Mou, L Musk, M Nanayakkara, C Ng, Z Perry, G Phillips, J Prosser, A Putrino (nee Chua), S Puttagunta, H Schuamann, M * Soraru, J Sunderland, A Swaminathan, R Tassone, G Waters, S Yeo, R

NEW ZEALAND

Langlands, J * Sprenger, L * Ahmed, J Allawati, H Chatterjee, A Clark, C Collins, M Cross, N Dittmer, I Donnellan, S Dunckley, H Evans, H Ferguson, F # Hanna, T Hecker, B Irvine, J Johnston, M #

Leikis, M Manley, P McNally, A McWilliams, T Munn, S Muthu, C Nagaraju, G Pilmore, H Prestidge, C Roake, J Roberts (previously Sheikh), A Ruygrok, P Shettigar, R Walker, R Wasywich, C Yasutomi, M

INTERNATIONAL MEMBERS

Altamimi, A Bhasin, M Bond, G Ericzon, B Ferrari, P Hancock, W Ison, M Jalalonmuhali, M Kleemann, F Koulmanda, M Mainra, R Marui, Y Matsunami, H Neil, D Rao, P Taylor, C

HONORARY LIFE MEMBERS

Monaco, A Morris, P Biggs.AM, J Bishop, A Chapman AC, J Hall, B Sheil, A Williams, K d'Apice, A Marshall, V McKenzie, I Miller, J Nossal, G

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TSANZ Membership List

133 * Denotes ATCA/TSANZ Member # Denotes TNA/TSANZ Member

AFFILIATE ORGANISATIONS

Australian Transplant Coordinators Association (ATCA)

Transplant Nurses Association (TNA) The Transplantation Society (TTS)

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TSANZ Fun Run/Walk; Meeting Point and Map of Course