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Predisposing Conditions, Predisposing Conditions, Management and Prevention of Management and Prevention of
Chronic Kidney Disease Chronic Kidney Disease
Dr FA Arogundade Dr FA Arogundade FMCP FWACP, ISN FellowFMCP FWACP, ISN Fellow
Consultant Nephrologist,Consultant Nephrologist,Obafemi Awolowo University,Obafemi Awolowo University,
Ile-Ife.Ile-Ife.
Definition of CKDDefinition of CKD
• Progressive and persistent deterioration in Progressive and persistent deterioration in kidney structure and function, ultimately kidney structure and function, ultimately resulting in accumulation of nitrogenous resulting in accumulation of nitrogenous waste and disruption of acid base waste and disruption of acid base homeostasis. homeostasis.
• In addition, CKD also leads to derangements In addition, CKD also leads to derangements of the kidney’s osmoregulatory, metabolic of the kidney’s osmoregulatory, metabolic and endocrine functions. and endocrine functions.
• Now CKD can be staged (KDOQI)Now CKD can be staged (KDOQI)
Stage 5
Stage
1
Stage 4
Stage 3
Stage 2
GF
R >
90
GF
R 6
0-89
GFR 15-29G
FR
30-
59
GFR <15
Staging of CKD
Prevalence of CRF is largely unknown Prevalence of CRF is largely unknown
• Conceivably high due to the high Conceivably high due to the high prevalence of diseases that cause prevalence of diseases that cause chronic renal failure:chronic renal failure:
• HYPERTENSION: > 15% in adultsHYPERTENSION: > 15% in adults
• DIABETES MELLITUS:>2.5-4.0% DIABETES MELLITUS:>2.5-4.0%
• Chronic inflammation – endemicity Chronic inflammation – endemicity of malaria, Hepatitis B,C, & HIVof malaria, Hepatitis B,C, & HIV
• Socio-cultural practicesSocio-cultural practices
• OthersOthers
Prevalence of CKD in NigeriaPrevalence of CKD in Nigeria
0
10
20
30
40
50
60
%
<90 90 - 99 100 - 109
Male
Female
mmHg
0
10
20
30
40
50
60
%
<90 90 - 99 100 - 109
Male
Female
mmHg
Blood pressure distribution in respondentsBlood pressure distribution in respondents(13.6% had HT, only 3.6% were previously diagnosed)(13.6% had HT, only 3.6% were previously diagnosed)
Systolic Blood pressureSystolic Blood pressure Diastolic Blood pressureDiastolic Blood pressure
Ulasi et al. Medical screening by NAN, 2005Ulasi et al. Medical screening by NAN, 2005
47
110
0 134
0 7 0 00
20
40
60
%
nil trace 30 100 500
Male
Female
mg/dl
The grading of proteinuria in respondentsThe grading of proteinuria in respondents(19% had proteinuria)(19% had proteinuria)
Ulasi et al. Medical screening by NAN, 2005Ulasi et al. Medical screening by NAN, 2005
NHANES III16,800
US Population CKD PrevalenceStage % number1 GFR:>90 3.3 5.9
millions2 89-60 3 5.33 59-30 4.3 7.64 29-15 0.25 400,0005 <15 0.2 345,000Total 11 19.2
Garg AX et al. Albuminuria and renal insufficiency prevalence guides populationscreening: results from the NHANES III. Kidney Int 2002; 61: 2165 – 2175.
AusDiab11,247
• Population-based cross-sectional study to determine the prevalence of DM,Obesity,CVD Risk factors,and Indicators of Kidney disease in Australian adults
• 11,247 Participants– Renal impairment 9.7%– Haematuria 3.7%– Albuminuria 6%– Proteinuria 0.6 %
Total 16%
Chadban et al, Prevalence of kidney damage in Australian adults: The AusDiab Kidney Study. J Am Soc Nehrol 2003, 14: S131 – S138.
• CRF accounts for 8–12% of hospital medical admissions
• CRF is a leading cause of mortality among adults
Sentinel study: based on available hospital data
• Prevalence of 300-400 per million population
Hospital Data
Akinsola, 1989; Kadiri et al 1997; Akinsola et al, 2004. Arogundade et al 2005
0
100
200
300
400
500
600
700
800
1989 1991 1993 1995 1997 1999 2001 2003
Total medicaladmissionsCRF admissions
0
2
4
6
8
10
12
14
16
18
1989 1994 1999
CRFadmissions aspercentage ofMedicaladmissions
NHANESNHANES
4%4%
NHANESNHANES
96%96%
Aus-DiabAus-Diab
9.7%9.7%
Aus-DiabAus-Diab
90.3%90.3%
Documented causes in Nigeria
• Hypertension– Benign– Malignant
• Chronic glomerulonephritis – – Causes unknown in the majority– Occurs post-infection
• Parasite – malaria; • Bacteria – sore throat or skin infections;• Helminths – Schistosoma, Filaria• Viruses - Hepatitis B, C, HIV• Fungal
– Toxins: Bleaching creams / soap
Other documented causes in Nigeria
• Diabetes MellitusDiabetes Mellitus
• Chronic urinary tract infection Chronic urinary tract infection
• Obstructive UropathiesObstructive Uropathies
• Drugs – Analgesic abuseDrugs – Analgesic abuse
• Inherited kidney disease-ADPKDInherited kidney disease-ADPKD
• Connective Tissue Disease - SLE, RAConnective Tissue Disease - SLE, RA
• OthersOthers
0
10
20
30
40
50
60
70
1989-1993
1994-1998
1999-2003
HypertensionCGNDiabetic NephropathyObstructive UropathyTIN
Arogundade et al, 2005
Objectives of Clinical EvaluationObjectives of Clinical Evaluation
Establishing that there is CKDEstablishing that there is CKDDefining the likely aetiologyDefining the likely aetiologyDetermining occurrence/presence of Determining occurrence/presence of
complicationscomplicationsAssessing prognosis and survivalAssessing prognosis and survival
Clinical Evaluation – Hx & ExaminationClinical Evaluation – Hx & Examination
Polyuria & NocturiaPolyuria & Nocturia Frothiness of urineFrothiness of urine OliguriaOliguria Symptoms of prostatismSymptoms of prostatism Features of uraemiaFeatures of uraemia Use of Analgesics, Hg containing Use of Analgesics, Hg containing
creams/soaps, other drugs, local herbscreams/soaps, other drugs, local herbs Past Medical Hx – HT, DM, Body Swelling etc.Past Medical Hx – HT, DM, Body Swelling etc. Family Hx – Renal Ds, Family Hx – Renal Ds, Social Hx – Alcohol, SmokingSocial Hx – Alcohol, Smoking
Clinical Evaluation – Hx & ExaminationClinical Evaluation – Hx & Examination
Presence of HTPresence of HTPresence of oedemaPresence of oedemaPresence of PallorPresence of PallorPresence of Uraemic featuresPresence of Uraemic featuresPresence of heart failurePresence of heart failurePresence of retinopathyPresence of retinopathy
InvestigationsInvestigations
BloodBlood ChemistryChemistry
E/U/CrE/U/Cr Ca, Po4,Ca, Po4, Alb, Chol, lipid profileAlb, Chol, lipid profile
HaemogramHaemogram Blood cell countsBlood cell counts SerologySerology Clotting profileClotting profile
UrineUrine MicroscopyMicroscopy ChemistryChemistry
Full urinalysisFull urinalysis 24 Hour profile24 Hour profile
ImagingImaging USSUSS CXRCXR ECHOECHO
ECGECG Renal BiopsyRenal Biopsy
ManagementManagement
• ConservativeConservative– Control of risk factorsControl of risk factors
• ModifiableModifiable• Non modifiableNon modifiable
• RRTRRT– PDPD– HDHD– TransplantTransplant
CKDCKDHypertension
Proteinuria
Lipids
Smoking
alcohol
Weight
Risk Factors/Markers for progressive CKD
Cal-phos
Anaemia
Nutrition
Gender
Race
Ageing
Card.VD
CKDCKD
DM
Infectns
BP BP Classificat.Classificat.
SBPSBP
mmHgmmHg
DBPDBP
mmHgmmHg
Lifestyle Lifestyle Modific.Modific.
Initial Drug TreatmentInitial Drug Treatment
Without Without Compelling Compelling Indic.Indic.
With With Compel. Compel. Indic.Indic.
NormalNormal <120<120 <80<80 Encour.Encour. No No antihypertenantihypertensive neededsive needed
Drugs for Drugs for compel. compel. Indic.Indic.Pre-HTPre-HT 120-139120-139 80-8980-89 YesYes
Stage 1Stage 1 140-159140-159 90-9990-99 YesYes Thiazide + Thiazide + othersothers
Drugs for Drugs for compel. compel. Indic. + Indic. + antihypertantihypertensivesensives
Stage 2Stage 2 >>160160 >>100100 YesYes 2 drug 2 drug combinationcombination
JNC VII Classification and management of BP for adultsJNC VII Classification and management of BP for adults
• 75.7% had hypoalbuminaemia ( mean ± SD for serum albumin; 29.5 ± 7.2 g/L).
• 88.9% had anaemia (Packed Cell Volume,‘PCV’ <33%) Mean± SD; 24.2 ± 7.0%).
• Arogundade et al , 2005
Hypertension
<125/75
Proteinuria
<1g/d
Lipids
<5SmokingSTOP
Alcohol
Weight
CKD Prevention – Modifiable risk factors
= CVD Protection
DM
<7%ALB
Ca-Ph<4.5
PCV 33-36
Choice of Antihypertensives• Regimens that include angiotensin-converting
enzyme inhibitors (ACEIs) are more effective than regimens that do not include ACEIs in slowing progression of both diabetic and non-diabetic kidney disease.
• Combination therapy of ACEI and angiotensin receptor blocker (ARB) slows progression of both diabetic and non-diabetic kidney disease more effectively than either single agent.
• ACEIs appear to be more effective than beta-blockers and dihydropyridine calcium channel blockers in slowing progressive kidney disease.
• Beta-blockers may be more effective in slowing progression than dihydropyridine calcium channel blockers, especially in the presence of proteinuria.
Choice of Antihypertensives
RRT RRT AVAILABILITYAVAILABILITY AFFORDABILITYAFFORDABILITY USEFULNESSUSEFULNESS LIMITATIONSLIMITATIONS
PDPD Not readilyNot readily Not AffordableNot Affordable 1. Diff. vasc. 1. Diff. vasc.
AccessAccess
2. Uncotr. HD 2. Uncotr. HD
HT.HT.
3. Low HCT not3. Low HCT not
desiring transf.desiring transf.
1. Softwa. 1. Softwa. sourcsourc
2. Infections2. Infections
3. Mechanical3. Mechanical
4. Obesity4. Obesity
HDHD ReadilyReadily Not affordableNot affordable 1. Easy1. Easy
2. Time constr.2. Time constr.
3. 3.
1. Hypotensn.1. Hypotensn.
2. Reactions2. Reactions
3. Inf transm.3. Inf transm.
4. Blood loss4. Blood loss
TXTX ReadilyReadily Not affordableNot affordable 1. Best QOL1. Best QOL
2. Cheap ultim.2. Cheap ultim.
3. Best profile3. Best profile
1. Planning1. Planning
2. Organ Sourc2. Organ Sourc
3. Infrastruc. 3. Infrastruc.
4. Donor Probl4. Donor Probl
ReferenceReferencess
Akinsola et al, Akinsola et al, 20002000
Arije et al, 1992&95, Arije et al, 1992&95, Bamgboye 2002, Bamgboye 2002, Arogundade et al, Arogundade et al, 20052005
Arije et al, Arije et al, 1992&95, 1992&95, Arogundade et Arogundade et al, 2004 & 2005al, 2004 & 2005
Arije et al, Arije et al, 1992&95, 1992&95, Arogundade et Arogundade et al, 2004 & 2005al, 2004 & 2005
Fig 1: COMPARING HRQOL IN THE PATIENT'S GROUPS
0
5
10
15
20
25
30
Liv
ing
rela
ted
Recip
ien
ts (
Gro
up
II)
Em
oti
on
ally
rela
ted
Recip
ien
ts
(Gro
up
III)
Main
ten
an
ce
haem
od
ialy
sis
Pati
en
ts (
Gro
up
I)
Patients Groups
Nu
mb
er o
f P
ati
en
ts
Karnofsky Score =90 Karnofsky Score = 80 Karnofsky score = 70 Karnofsky score = 50
Fig 2: Correlation between Quality of Life
Scores and Age in all studied subjects
(r=-0.363, P<0.0001)
AGE (years)
70605040302010
HR
QO
L S
core
s
100
90
80
70
60
50
Fig 3: Correlation between Quality of Life
Scores and Serum Creatinine in all subjects
(r=-0.502, P<0.0001)
Serum Creatinine (mg/dl)
181614121086420
HR
QO
L S
core
s
100
90
80
70
60
50
Fig 4: Correlation between Quality of Life
Scores and Haemoglobin (g/dL) in all subjects
(r=0.705, P<0.0001)
Haemoglobin (g/dL)
18161412108642
HR
QO
L S
core
s100
90
80
70
60
50
Preventive NephrologyPreventive Nephrology Primary PreventionPrimary Prevention
Aims at preventing kidney disease from occurring at allAims at preventing kidney disease from occurring at all Calls for knowledge of Calls for knowledge of
risk factors that predispose to renal diseaserisk factors that predispose to renal disease risk factors that initiate renal damage.risk factors that initiate renal damage. modification, removal, or avoidance of factors.modification, removal, or avoidance of factors. development of a positive health seeking attitude and development of a positive health seeking attitude and
behaviourbehaviour Secondary PreventionSecondary Prevention
Aims at identifying factors that aid or hasten progression Aims at identifying factors that aid or hasten progression of kidney disease and/or accelerate loss of kidney of kidney disease and/or accelerate loss of kidney function, and preventing or removing such factors. While function, and preventing or removing such factors. While a few of these factors are not modifiable, majority of them a few of these factors are not modifiable, majority of them could be modified, controlled or completely avoided.could be modified, controlled or completely avoided.
Tertiary PreventionTertiary Prevention
CKDCKDHypertension
Proteinuria
Lipids
Smoking
alcohol
Weight
Risk Factors/Markers for progressive CKD
Cal-phos
Anaemia
NutritionGender
Race
Ageing
Card.VD
CKDCKDDM
Infectns
Non ModifiableNon Modifiable ModifiableModifiable
Hypertension
<125/75
Proteinuria
<1g/d
Lipids
<5SmokingSTOP
Alcohol
Weight
CKD Prevention – Modifiable risk factors
= CVD Protection
DM
<7%ALB
Ca-Ph<4.5
PCV 33-36
Tertiary Prevention
Hypertension
<125/75
Proteinuria
<1g/d
Lipids
<5SmokingSTOP
Alcohol
Weight
DM
<7%ALB
Ca-Ph<4.5
PCV 33-36
Tertiary Prevention ContdTertiary Prevention Contd
• Control of HTControl of HT
• Use of EPO & Parenteral Iron Use of EPO & Parenteral Iron
• Use of Vit D analoguesUse of Vit D analogues
• Use of Phosphate sequestering agentsUse of Phosphate sequestering agents
• Control of hyperlipidaemiaControl of hyperlipidaemia
• Control of InfectionsControl of Infections
• Control of Heart FailureControl of Heart Failure
When do we refer to Nephrologists When do we refer to Nephrologists
CKD 4 & 5CKD 4 & 5Resistant HTResistant HTPersistent proteinuria / haematuriaPersistent proteinuria / haematuriaDifficulty achieving Bld sugar controlDifficulty achieving Bld sugar controlEstablished CKDEstablished CKDUraemiaUraemiaHeart failureHeart failureAnaemiaAnaemia
