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Trevor R. Smith, MDNorthern Utah Kidney Specialists
University of UtahDepartment of Medicine
Division of Nephrology and Hypertension
Northern Utah Kidney Specialists
I have no financial relationships with any entity producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients.
Northern Utah Kidney Specialists
• The Learner will recall the pathophysiology of decompensated cirrhosis and hepatorenal syndrome.
• The Learner will explain the evaluation and management of hepatorenal syndrome.
• The Learner will apply objective data when managing ascites due to decompensated cirrhosis.
Northern Utah Kidney Specialists
Northern Utah Kidney Specialists
• Complications of decompensated cirrhosis such as AKI, ascites, varices, cirrhotic cardiomyopathy and others occur because of:
a) Increased circulatory state by activation of the sympathetic nervous system, RAAS activation and increased ADH
b) Decreased systemic vascular resistance by release of systemic vasodilators
c) Decreased hepatic clearance of vasoactive metabolites such as renin, angiotensin II, aldosterone and vasopressin
d) A and Be) A and Cf) B and Cg) A, B and C
• Definition: diffuse liver fibrosis and abnormal nodules that lack normal organization. The structural changes result in portal hypertension and impaired liver function.
Northern Utah Kidney Specialists
Lancet 2008; 371: 838–51
↓ clearance of: ANP, Glucagon, Renin, ATII, VP,
Aldo
Northern Utah Kidney SpecialistsLiver Int. 2018;38(4):570
Northern Utah Kidney Specialists
SNS, RAAS, ADH
SVR & Effective circulating volume,MAP, HR, CO
VEGF, NO Vasodilators
Hepatol Int. 2018;12(Suppl 1):112
• Compensated: ↑ CO and plasma volume restores ECV.
• Decompensated:↑ vasoconstriction to keep ECV → ascites and renal failure.
Northern Utah Kidney Specialists
• √ The Learner will recall the pathophysiology of decompensated cirrhosis and hepatorenal syndrome.
Northern Utah Kidney Specialists
Northern Utah Kidney Specialists
• AKI occurs in up to 50% of patients with decompensated cirrhosis
• 46% infection, • 32% hypovolemia, • 13% HRS and • 9% intrinsic kidney disease
• 1/3 of patients improve with conservative management• Albumin, IVF
• 2/3 develop persistent renal injury• 40% require dialysis• 60% mortality by 90 days
CJASN 2018, 13(1):16-25.
Northern Utah Kidney Specialists
• A 63 yo M with a 30 year history of EtOH abuse presents to the ER with hematemesis. On examination BP is 74/46 mmHg. His abdomen is distended and tense. Labs reveal a serum sodium of 121, BUN 124, serum creatinine of 3.6 (baseline unknown), T bili24.1, elevated transaminases and a Hgb of 6.8 g/dL.
Treatment of this patient with probable acute kidney injury includes:
a) Transfusion of pRBCs and urgent EGD to evaluate for esophageal varices
b) Diagnostic paracentesis with cell count and culture to evaluate for SBPc) Discontinuing all diuretics and antihypertensive medicationsd) Administration of IV albumin and octreotidee) Administration of vasoconstrictors such as midodrine or
norepinephrine to target a MAP of >82 mmHgf) All the above
Northern Utah Kidney Specialists
Clin Gastroenterol Hepatol.2018;16:162
Northern Utah Kidney Specialists
Clin Gastroenterol Hepatol.2018;16:162
Northern Utah Kidney Specialists
Clin Gastroenterol Hepatol.2018;16:162
Northern Utah Kidney Specialists
Clin Gastroenterol Hepatol.2018;16:162
Northern Utah Kidney Specialists
• ATN: Granular casts, urine osm = serum osm• Nephritis: Proteinuria and hematuria• CKD: baseline Cr, proteinuria, comorbid conditions• Other: Check renal ultrasound for evidence of
abnormal anatomy or obstruction
https://radiopaedia.org/articles/pelviureteric-junction-obstruction-1?lang=ushttps://webpath.med.utah.edu/TUTORIAL/URINE/URINE.html#2
Northern Utah Kidney Specialists
• Diagnosis of exclusion1.Cirrhosis + ascites2. Serum creatinine >1.5 mg/dL3. Not better after 48+ hours of:
-Diuretic withdrawal -Albumin expansion
4. No shock.5. No current or recent treatment with nephrotoxic drugs (?)6. Absence of parenchymal kidney disease
-Proteinuria >500 mg/day, -Microhematuria (>50 RBCs/high power field)-Abnormal renal ultrasound scanning
http://www.icascites.org/about/guidelines/
Northern Utah Kidney Specialists
• Type-1 HRS • Rapid renal failure = 2x serum creatinine to a level greater
than 2.5 mg/dL in <2 weeks.• Precipitating event, ie SBP
• Can occur spontaneously• Acute arterial hypotension → activation of vasoconstrictors
which leads to rapid impairment in liver function and encephalopathy
http://www.icascites.org/about/guidelines/
Northern Utah Kidney Specialists
• Type-2 HRS • “Moderate” renal failure (serum creatinine >1.5 mg/dl)
progressing slowly. • Spontaneous, less association with SBP• Frequent refractory ascites. • Survival
• Ascities without renal failure > HRS type 2 > HRS type 1
http://www.icascites.org/about/guidelines/
• ICU v Non-ICU• ICU- treatment with Norepinephrine + Albumin
• +/- Vasopressin• Non-ICU- treatment with Midodrine + Octreotide + Albumin
• Upcoming therapy: Terlipressin
Northern Utah Kidney Specialists
Northern Utah Kidney SpecialistsGastroenterol Hepatol (N Y). 2015 Apr; 11(4): 220–229.
Ornipressin & Terlipressin: analogs of ADH that cause
preferential splanchnic vasoconstriction
OrOctreotide – somatostatin mimic that decreases splanchnic blood
flowAlbuminMAP Midodrine
Norepinephrine
• Norepinephrine + Albumin
Northern Utah Kidney Specialists
Hepatology. 2002 Aug;36(2):374-80.
• Octreotide + Midodrine + Albumin
Northern Utah Kidney Specialists
Dopamine + Albumin Octreotide + Midodrine + Albumin
Hepatology. 1999;29(6):1690.
• Octreotide + Midodrine + Albumin
Northern Utah Kidney Specialists
Dig Dis Sci. 2007 Mar;52(3):742-8.
Northern Utah Kidney Specialists
Clin Gastroenterol Hepatol.2018;16:162
Northern Utah Kidney Specialists
56%
5%
Hepatology. 2015 Aug;62(2):567-74.
CR + PR
CR + PR
CR
CR
Northern Utah Kidney Specialists
Hepatology. 2015 Aug;62(2):567-74.
Northern Utah Kidney Specialists
Gastroenterology. 1988 Feb;94(2):482-7
Northern Utah Kidney Specialists
Gastroenterology. 1988 Feb;94(2):482-7
>2.8 g/dL
≤ 2.8 g/dL
Northern Utah Kidney Specialists
Terlipressin + albumin v Albumin alone
Terlipressin + albumin v Norepinephrine + albumin
Journal of Clinical Gastroenterology. 52(4):360–367, APR 2018
• Terlipressin + Albumin• Not available in US, awaiting results of Phase 3 trial
(CONFIRM Study)
Northern Utah Kidney Specialists
Northern Utah Kidney Specialists
J Fernández, V Arroyo. Hepatorenal Syndrome. Comprehensive Clinical Nephrology, 5th Edition. 873-882.
Northern Utah Kidney SpecialistsGastroenterol Hepatol (N Y). 2015 Apr; 11(4): 220–229.
Ornipressin & Terlipressin: analogs of ADH that cause
preferential splanchnic vasoconstriction
OrOctreotide – somatostatin mimic that decreases splanchnic blood
flowAlbuminMAP Midodrine
Northern Utah Kidney Specialists
Entire cohort of 91 cirrhotic patients with HRS type 1
Child-Pugh score <10
Child-Pugh score ≥10
Northern Utah Kidney Specialists
Renal Replacement Therapy Transjugular Intrahepatic Portosystemic Shunt
(TIPS)
P=0.961 P=0.034
Northern Utah Kidney Specialists
P=0.000
Response to therapy
Northern Utah Kidney Specialists
CJASN January 2018, 13 (1) 16-25
Northern Utah Kidney SpecialistsCJASN January 2018, 13 (1) 16-25
• High suspicion for HRS• Other causes more likely
• Volume resuscitate with albumin, discontinue diuretics and BP meds
• Treat underlying problem, • Infection or bleeding
• Look for kidney disease• BP target = MAP > 82 mmHg
• Midodrine/octreotide OR norepinephrine• Terlipressin is the future?
• Dialysis for patients eligible for liver transplant
Northern Utah Kidney Specialists
• √ The Learner will recall the pathophysiology of decompensated cirrhosis and hepatorenal syndrome.
• √ The Learner will explain the evaluation and management of hepatorenal syndrome.
Northern Utah Kidney Specialists
Northern Utah Kidney Specialists
• Your 63 yo M with EtOH hepatitis and AKI responds to midodrine/octreotide/albumin and banding of esophageal varices. He is discharged to acute rehab. He is not a transplant candidate because he stopped EtOH on hospital admission. While in rehab he continually experiences abdominal discomfort and distension. Abdominal ultrasound and physical examination reveals the presence of tense ascites.
Besides encouraging sobriety, how do you best manage this patient’s ascites?
a) Weekly paracenteses with post-procedure albumin replacementb) 2g Sodium and 2L fluid restriction dailyc) 2g Sodium restriction, Spironolactone 100 mg daily and Lasix 40
mg dailyd) Palliative care consult because he’s lucky to be alive
Northern Utah Kidney SpecialistsGastroenterol Hepatol (N Y). 2015 Apr; 11(4): 220–229.
Ornipressin & Terlipressin: analogs of ADH that cause
preferential splanchnic vasoconstriction
OrOctreotide – somatostatin mimic that decreases splanchnic blood
flowAlbumin
Spironolactone
MAP Midodrine
Loop diuretics
Northern Utah Kidney Specialists
Hepatology 2013; 1-27
Northern Utah Kidney Specialists
Hepatology 2013; 1-27
Northern Utah Kidney Specialists
• Urine sodium • Use spot urine sodium/potassium ratio
• If ratio is >1, pt should be able to lose fluid• The greater the ratio, the greater the sodium excretion
• 24 hour urine collection• Cumbersome and difficult to interpret• Goal is for urine Na >78 mmol/day
• Non-urinary Na loss is <10 mmol/day• Diuretics should be held if urine sodium <30 mmol/day
• Marker of decreased ECF
Hepatology 2013; 1-27
Northern Utah Kidney Specialists
• Unresponsive to Na restriction and high-dose diuretics (Spironolactone 400 mg/Lasix 160 mg daily)
• Recurs rapidly after paracentesis
• Diuretic failure:• Minimal fluid loss with low urine sodium excretion on
diuretics• Development of complications of diuretics
• Encephalopathy, Cr >2.0, Na <120 mmol/L, K >6.0• Trials show <10% are refractory to optimal therapy (if
adherent)
Hepatology 2013; 1-27
Northern Utah Kidney Specialists
• Serial Paracenteses• Ascites should be able to be controlled with q2 week Rx• Paracentesis >10 L every 2 weeks suggestive of diet non-
adherence• Albumin administration
• Meta-analysis 1225 patients • Reduction in mortality OR 0.64 (95% CI, 0.41-0.98) in the albumin
group.• Albumin dose: 6-8 g/L of volume removed
• 5% Albumin has 5x the sodium of 25% Albumin
Hepatology 2013; 1-27
• √ The Learner will recall the pathophysiology of decompensated cirrhosis and hepatorenal syndrome.
• √ The Learner will explain the evaluation and management of hepatorenal syndrome.
• √ The Learner will apply objective data when managing ascites due to decompensated cirrhosis.
Northern Utah Kidney Specialists
Northern Utah Kidney SpecialistsUniversity of Utah
Department of MedicineDivision of Nephrology and Hypertension
Northern Utah Kidney Specialists
Monique Cho, MDUofU Divison of Nephrology and
Hypertension
Juan Gallegos-Orozco, MD
UofU Transplant Hepatology
Harry Senekjian, MD
Northern Utah Kidney Specialists
Bruce Horowitz, MD
Northern Utah Kidney Specialists
Marcellus Assiago, MD
Northern Utah Kidney Specialists
Northern Utah Kidney SpecialistsUniversity of Utah
Department of MedicineDivision of Nephrology and Hypertension
Northern Utah Kidney Specialists