6/10/2014. Chronic Kidney Disease - General management and standard of care. Management of CKD according to stage (KDOQI 2002)

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Chronic Kidney Disease - General management and standard of care Dr Nathalie Demoulin, Prof Michel Jadoul Cliniques universitaires Saint-Luc Université Catholique de Louvain What should and can be

1 Chronic Kidney Disease - General management and standard of care Dr Nathalie Demoulin, Prof Michel Jadoul Cliniques universitaires Saint-Luc Université Catholique de Louvain What should and can be done when managing a CKD patient Above all, clinical care! Pathophysiology is presented only to explain why a practice is recommended The following topics will not be covered: - diagnosis of the cause of CKD (frequently crucial) - the methods to estimate GFR Management of CKD according to stage (KDOQI 2002) Stage Description GFR (ml/min./1,73m²) At increased risk >90 (with CKD risk factors) 1 Kidney damage With normal or GFR 2 Kidney damage With mild GFR Action Screening, CKD risk reduction >90 Diagnosis and treatment, Treatment of comorbid conditions, Slowing progression, CVD risk reduction Estimating progression 3 Moderate GFR Evaluating and treating complications 4 Severe GFR Preparation for kidney replacement therapy 5 Kidney failure < 15 (or dialysis) Replacement (if uremia present) 1

KDIGO CKD Guidelines 2012 Section 1: Definition and classification of

progression Section 3: Management of progression and complications of

patient safety, infections, hospitalizations, and caveats for

2 KDIGO CKD Guidelines 2012 Section 1: Definition and classification of CKD Section 2: Definition, identification and prediction of CKD progression Section 3: Management of progression and complications of CKD Section 4: Other Complications of CKD: CVD, medication dosing, patient safety, infections, hospitalizations, and caveats for investigating complications of CKD Section 5: Referral to specialists and models of care 2

with implications for health - this definition specifically excludes simple renal cysts,.

(CGA staging) Cause GFR Categories (ml/min/1.

3 Definition and Classification 1.1. Definition of CKD: CKD is defined as abnormalities of kidney structure or function for 3 months with implications for health - this definition specifically excludes simple renal cysts,.. - If duration < 3 months -> could be CKD or AKI or both Definition and Classification Staging of CKD (CGA staging) Cause GFR Categories (ml/min/1.73m 2 ) Diabetes G1 90 Hypertension G Glom Disease G3a Transplant G3b Albuminuria Categories (ACR, mg/g) A1 <30 N to midly increased A Moderately increased Unknown G etc G5 <15 A3 Tigette OK 300 Severly increased 3

4 Staging of CKD GFR and mortality 5,9 3,2 1,8 1 1,2 Go et al, NEJM 2004 Evaluation of Albuminuria The reference point= accurately timed 24h specimen Early morning urine preferred Protein dipstick grading Approx. amount Designation Concentration Daily Trace 5 20 mg/dl mg/dl < 0.5 g/day mg/dl g/day mg/dl 1 2 g/day 4+ > 2000 mg/dl >2 g/day 4

5 Relationship between categories of albuminuria and proteinuria Staging of CKD (CGA staging) Cause GFR Categories (ml/min/1.73m 2 ) Diabetes G1 90 Hypertension G Glom Disease G3a Transplant G3b Unknown G etc G5 <15 Albuminuria Categories (ACR, mg/g) A1 <30 A A3 N to midly increased Dipstick neg to trace Moderately increased Dipstick trace to Severely increased Dipstick > + Prognostic value of GFR and albuminuria: Cohorts and Subjects of CKD Consortium Community based populations With ACR data, 14 studies, n=105,872 With dipstick data, 10 studies, n=1,239,447 Populations at increased CVD risk (HTN, diab, CV) 10 studies, n=266,975 CKD cohorts 14 studies, n= 21, cohorts in total, >1.5 million subjects Collaborative meta-analysis Major publications: Lancet, KI, JAMA 5

Prognostic value of GFR and albuminuria: Cohorts and Subjects of CKD Consortium Community based populations With ACR data, 14 studies, n=105,872 With dipstick data, 10 studies,

5 million subjects Collaborative meta-analysis Major publications: Lancet, KI, JAMA Matsushita et al, Lancet 2010 Predictive ability of albuminuria at all categories of GFR:

6 Prognostic value of GFR and albuminuria: Cohorts and Subjects of CKD Consortium Community based populations With ACR data, 14 studies, n=105,872 With dipstick data, 10 studies, n=1,239,447 Populations at increased CVD risk (HTN, diab, CV) 10 studies, n=266,975 CKD cohorts 14 studies, n= 21, cohorts in total, >1.5 million subjects Collaborative meta-analysis Major publications: Lancet, KI, JAMA Matsushita et al, Lancet 2010 Predictive ability of albuminuria at all categories of GFR: Meta-analysis from General Population Cohorts - CKD Prognosis Consortium ACR>=300 ACR ACR <30 Levey, KI 2011 Predictive ability of albuminuria at all categories of GFR: General Population Cohorts ACR>=300 ACR ACR <30 Levey, KI

3: Management of progression and complications of CKD Section 4: Other Complications of CKD: CVD, medication dosing, patient safety,

7 Adjusted relative risk of renal and cardiovascular outcomes for GP cohorts with ACR Levey et al, Kidney Int 2011 KDIGO CKD Guidelines 2012 Section 1: Definition and classification of CKD Section 2: Definition, identification and prediction of CKD progression Section 3: Management of progression and complications of CKD Section 4: Other Complications of CKD: CVD, medication dosing, patient safety, infections, hospitalizations, and caveats for investigating complications of CKD Section 5: Referral to specialists and models of care 7

Definition of CKD progression Decline in GFR category (G1-G4) accompanied by 25% drop in egfr from baseline Rapid progression defined as sustained decline in egfr > 5ml/min/1,73m2/year Predictors of

8 Definition of CKD progression Decline in GFR category (G1-G4) accompanied by 25% drop in egfr from baseline Rapid progression defined as sustained decline in egfr > 5ml/min/1,73m2/year Predictors of progression of CKD Cause of CKD Level of GFR Level of albuminuria Age Gender Elevated BP Hyperglycemia Dyslipidemia Smoking Obesity History of CVD Ongoing exposure to nephrotoxic agents Anemia, acidosis, bone metabolism, hyperuricemia. Minimising CKD progression (and CV risk) BP control 8

Minimising CKD progression (and CV risk) BP control ACR <30mg/g 30-300 mg/g > 300 mg/g Diabetic 140/90 mmhg (1B) Non diabetic 140/90 mmhg (1B) 130/80 mmhg (2D) 130/80 mmhg (2D) 130/80 mmhg (2D)

9 Minimising CKD progression (and CV risk) BP control ACR <30mg/g mg/g > 300 mg/g Diabetic 140/90 mmhg (1B) Non diabetic 140/90 mmhg (1B) 130/80 mmhg (2D) 130/80 mmhg (2D) 130/80 mmhg (2D) 130/80 mmhg (2D) Minimising CKD progression Captopril protects against deterioration in renal function in insulindependent diabetic nephropathy independently of BP control Lewis et al. NEJM 1993; 329,

20 The angiotensin-ii-receptor blocker irbesartan is effective in protecting against progression in type 2 diabetes nephropathy, independently of BP control Irbesartan Amlodipine Placebo 1715

10 20 The angiotensin-ii-receptor blocker irbesartan is effective in protecting against progression in type 2 diabetes nephropathy, independently of BP control Irbesartan Amlodipine Placebo 1715 patients, Target BP 135/58 mmhg Lewis et al. N Engl J Med 2001; 345: Mean BP + 3,3 mmhg in placebo vs amlodipine and irbesartan (p=0,001) Lewis et al. N Engl J Med 2001; 345:

ACEi and ARBs are beneficial agents in CKD

perfusion pressure and efferent arteriole relaxation

2012 The anti-proteinuric effect of lisinopril is dose and time

11 ACEi and ARBs are beneficial agents in CKD Hemodynamic/antihypertensive actions capillary hypertension by perfusion pressure and efferent arteriole relaxation Anti-inflammatory/anti-fibrotic actions Turner et al, Kidney Int 2012 The anti-proteinuric effect of lisinopril is dose and time related, and strongly dependent on dietary sodium restriction Salt intake 50 and 200 mmol/day Heeg et al, Kidney Int

12 Salt restriction or diuretics : similar potentiation of ACE-I effect Addition of HCT -> 10% BP 40% proteinuria low= sodium 50 mmol/d high= sodium 200 mmol/d Buter et al, Nephrol Dial Transplant 1998 The optimal clinical use of diuretics egfr > 30 : thiazide ( Chlortalidone, «Co.», «Plus») egfr < 30 or poor response to thiazide: loop diuretic (furosemide / bumetanide) works for max 6-8h, thus if still poor response, give 2-3 times a day (8am, 12am and 5pm)! tolerance : cramps (volume related (not K, Ca, Mg)), pollakiuria ( prostate ) adapt timing of administration to daily activities 24 Estimating salt intake from 24 h urine sample? Prerequisite 1) Volume IN = Volume OUT (steady state) Thus not valid if diarrhea or vomiting, ileostomia or intense sweating or recent start or change of dosage or variable adherence to diuretics Prerequisite 2) Na IN = Cl IN Thus not valid if Vichy water or NaHCO3 taken orally 100 mmol Na = roughly 6g de salt Prerequisite 3) 24h urine collection is complete Estimated from creatininuria (10-25 mg/kg (depending on age, gender, ethnicity)) 25 12

13 ACE-I, ARB : should we stop them if creatinine rises? No if creatinine < 3 mg/dl and rising by less than < 30 % Treatment is associated +++ with preservation of GFR (if creatinine rises +++ (double or triple): look for renal artery stenosis or stenoses) Bakris et al. Arch Int Med 2000; 160: Example of a patient with diabetic nephropathy patient already under Irbesartan: loop diuretic increased progressively Hyperkalemia with ACE inhibitors / angiotensin II receptor antagonist / aliskiren (I) Is it true hyperkalemia? (to avoid stopping valuable drug because of a laboratory error) Time between blood sampling and analysis? Hemolysis? Confirmed (precautions), severe? (> 5.8 mmol/l) Dietary? Salt substitute (Dried) fruit, bananas, chocolate, instant coffee,

stop or reduce spironolactone ACE inhibitor or angiotensin II receptor or aliskiren monotherapy: dose - add Furosemide If persistence,

14 Hyperkalemia with ACE inhibitors / angiotensin II receptor antagonist / aliskiren (I) Correct any acidosis (Vichy 1-2 glasses/d) ACE inhibitor + angiotensin II receptor or aliskiren: stop or reduce 1 of the 2 ACE inhibitor (angiotensin II receptor ) + spironolactone: stop or reduce spironolactone ACE inhibitor or angiotensin II receptor or aliskiren monotherapy: dose - add Furosemide If persistence, add calcium kayexalate 15 g/2 days per os 29 Dual RAAS blockade in CKD? Similar results in «Altitude» with Aliskiren + ACEI or A2RB 14

15 Dual RAAS blockade? Nephro-protection : reducing proteinuria with medium to long-term renoprotective effect (dialysis later... or never) Nephro-risk: acute worsening of renal failure and hyperk if intercurrent disease (gastroenteritis ++, ) So block RAAS : YES but usually single agent (ACEi or ARB) + possibly microdose «cardio» spironolactone Association ACE inhibitor + ARB : only if heavy proteinuria («glomerular), close, careful nephrology follow-up in reliable patients 32 Protein intake Rationale: If BP and proteinuria are well controlled, the slope of CKD progression will not change much with lower protein intake In > 65 y old patients, potential for malnutrition! Glycemic control 15

Lifestyle measures KDIGO CKD Guidelines 2012 Section 1: Definition and classification of CKD Section 2: Definition, identification and prediction of CKD progression Section 3: Management of

16 Lifestyle measures KDIGO CKD Guidelines 2012 Section 1: Definition and classification of CKD Section 2: Definition, identification and prediction of CKD progression Section 3: Management of progression and complications of CKD Section 4: Other Complications of CKD: CVD, medication dosing, patient safety, infections, hospitalizations, and caveats for investigating complications of CKD Section 5: Referral to specialists and models of care Strong and independent associations between GFR and albuminuria categories and risk of CVD in people with CKD Cardiovascular risk in CKD is multifactorial Cardiovascular disease is more frequent and severe, often not recognised and undertreated in patients with CKD Patients with CKD should be viewed amongst the highest risk groups for CVD To prevent progression of CKD is to prevent CVD 16

The burden of cardiovascular disease: Causes of death per CKD stage (Canadian data) Gansevoort et al, Lancet 2013 Not modifiable Classical CV risk factors Modifiable but no proven benefit

17 The burden of cardiovascular disease: Causes of death per CKD stage (Canadian data) Gansevoort et al, Lancet 2013 Not modifiable Classical CV risk factors Modifiable but no proven benefit Modifiable with clinical benefit Older age Uric acid Smoking Male gender Homocysteine Obesity Ethnicity Lp (a) HDL cholesterol Hypertension Diabetes LDL cholesterol Physical activity

Lipid control and antiplatelet therapy No specific lipid targets are established in CKD patients -> treat in accordance with guidelines for other highrisk populations Antiplatelet therapy should be

18 Lipid control and antiplatelet therapy No specific lipid targets are established in CKD patients -> treat in accordance with guidelines for other highrisk populations Antiplatelet therapy should be offered to high risk patients unless bleeding risk outweighs CV benefits. Gansevoort et al, Lancet 2013 Chronic Kidney Disease - General management and standard of care Even if cause of CKD not treatable, much can and should be done for any CKD patient Treat BP to target and aggressively substantial albuminuria; both interventions delay CKD progression Underuse of salt restriction/diuretics!! Manage aggressively classical CV risk factors 18

CKDinform: A PCP s Guide to CKD Detection and Delaying Progression

CKDinform: A PCP s Guide to CKD Detection and Delaying Progression Learning Objectives Describe suitable screening tools, such as GFR and ACR, for proper utilization in clinical practice related to the