RETARDING PROGRESSION OF CHRONIC KIDNEY DISEASE (CKD)

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1 13 : 6 RETARDING PROGRESSION OF CHRONIC KIDNEY DISEASE (CKD) Abstract: Chronic Kidney Disease (CKD) is common, harmful and treatable. It is worldwide public health problem, with several adverse outcomes; progressive loss of kidney function and high risk of cardiovascular disease (CVD) and premature death. The asymptomatic nature of CKD needs early detection using laboratory tests. The laboratory approaches to detect CKD include urine examination for protein and urine albumin/creatinine ratio, S. creatinine estimation and measuring blood pressure. Screening is recommended for those who are at increased risk of CKD (diabetics, hypertensive, age above 50 years, family history of renal disease and patients with family history of diabetes, hypertension or coronary artery disease). Screening is useful only when a subject who has been found positive on such a screening can be offered effective treatment. We can slow down the progression of chronic kidney disease by early interventions and changing some of our living habits. Of importance, similar treatment help not only to prevent progressive renal function loss, they also contribute to prevent the progressive CVD encountered in patients with chronic kidney disease. Thus, all interventions (lowering blood pressure and lipids, blocking RAA system, cessation of smoking and life style modification) that are necessary to attenuate the progression of CKD are also beneficial for reducing cardiovascular diseases and mortality (what is good for kidney is also good for the heart). Introduction Chronic kidney disease (CKD) is a worldwide medical and public health challenge due to the high risk of progression to end-stagerenal-disease (ESRD), the increased cardiovascular burden and high management cost. Early detection of CKD followed by appropriate clinical management appears the only means by which the increasing burden on the health-care system and affected individual will be reduced. 1 The asymptomatic nature of CKD means that early detection can only occur through laboratory testing of individuals. CKD is defined as glomerular filtration rate <60 ml/minute/1.73m 2. The patient is not aware of having renal function impairment, because symptoms develop only if GFR decreases below 30 ml/minute/1.73m 2. Earlier identification of these patients is therefore warranted. 2 Jai Prakash, Varanasi This article will review options/interventions used to prevent the progression of CKD to end-stage-renal-disease. Of importance, similar interventions help not only to prevent progressive renal function loss, but they also contribute to prevent the progressive cardiovascular disease encountered in patients with CKD. 2 The following issues will be addressed- 1. Principles of Screening for CKD. 2. Who should be Screened? 3. How should CKD be Screened? 4. Retarding Progression of CKD. 5. Treating consequences of CKD. 6. Reducing risk of CVD. 7. Conclusion 8. Take Home Message 1. Principles of Screening for CKD The early recognition of CKD is made difficult by its largely asymptomatic nature. Stage 1-3 is known as Early CKD. The detection of CKD early in its course relies on the performance of tests on urine (albumin or protein) and blood (serum creatinine) together with blood pressure measurement. Glomerular filtration rate (GFR) is the best measure of overall renal function and in epidemiological studies this can be best performed using an estimated GFR (egfr). For this purpose the Cockraft-Gault formula and the Modification of Diet in Renal Disease (MDRD) formula are being used most frequently (Table I). 2. Who should be Screened? Whole population screening for CKD is impractical and is not cost-effective. Screening of those at increased risk of CKD (diabetes, hypertension, age > 55 years, persons with family history of diabetes, hypertension or chronic kidney disease) is cost-effective. Community screening programmes targeted at known diabetics, hypertensive and

2 Retarding Progression of Chronic Kidney Disease (Ckd) Table 1 : Formula to calculate egfr 1. Cockcroft-Gault formula: [(140 - age) x weight]/72 x (serum creatinine) (x 0.85 if female) 2. Simplified MDRD formula: 186 x (serum creatinine) x (age) x (0.742 if female) x (1.210 if black) Age in years, Wt. in Kg. and S. Creatinine in mg/dl Thus, tests for establishing the presence of CKD are simple, cheap and widely available. those over 55 years have been described to detect 93% of all CKD in the community. The prevalence of CKD stage 3-5 in general population has been found to vary from 10% to 20%. For practical point of view diabetics should be screened for the presence of microalbuminuria annually and the same should be advocated for hypertensive subjects as well. If microalbuminuria is diagnosed renal function should be monitored. 3. How should CKD be Screened? Urine dipstick for protein, urine albumin/creatinine ratio, serum creatinine measurement along with blood pressure measurement are the mainstay of any CKD Screening programme. Serum creatinine is used to calculate estimated Glomerular Filtration Rate (egfr) using formula as given in Table I. 4. Retarding Progression of CKD The two principal outcomes of CKD are progressive loss of renal function, and the development & progression of cardiovascular disease (CVD). 3 Although, the rate of progression of CKD is related to some non-modifiable characteristics such as race, baseline renal function, male gender, and increased age, there are a number of modifiable characteristics. It is important to note that three most widely studied interventions; lowering blood pressure (BP), proteinuria reduction and anti-hypertensive drugs are inextricably linked in their effects on glomerular filtration rate (egfr). Blood pressure (BP) Hypertension is both a cause and consequence of CKD. The prevalence of hypertension is inversely related to GFR. 4,5 Observational and interventional studies show that BP reduction slows the rate of progression of CKD. 6-9 In a metaanalysis of 11 RCT s including 1860 patients with non-diabetic kidney disease, the lowest risk of CKD progression was seen with systolic BPs of mmhg in patients with > 1 gm/day proteinuria (an effect not seen with lower grade of proteinuria). There was a significant increase in the risk of CKD progression at a systolic BP of > 130 mmhg. 8 The modification of diet in renal disease (MDRD) trial showed that there was a linear relation between increasing MAP and the rate of loss of GFR, the effect being greater in patients with higher degree of proteinuria. 10 In light of analysis of several studies; a BP target of < 130/80 mmhg for all patients with CKD and < 125/75 mmhg for those with > 1 gm/day of proteinuria is suggested. 11,12 Proteinuria Proteinuria is common in CKD and is a strong independent risk factor for CKD progression. 8,10 Reducing proteinuria reduces the risk of CKD progression. 13,14 BP reduction will reduce proteinuria. A meta-analysis of 84 studies demonstrated that proteinuria reduction was proportional to BP reduction in both diabetic and non-diabetic renal diseases. 6 However, some studies are able to show an effect of proteinuria reduction on CKD progression independent of BP control. Proteinuria reduction should be targeted to slow CKD progression. Anti-hypertensive drugs Specific anti-hypertensive drugs may reduce proteinuria and slow CKD progression independent of BP lowering effects, with the most rigorous data supporting the use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs). In non-diabetic CKD, meta-analysis demonstrate that ACEIs and ARBs can reduce proteinuria. In diabetic CKD, meta-analysis demonstrate that ACEIs in type-2 diabetics, and both ACEIs and ARBs in type-i diabetics regress microalbuminuria to normoalbuminuria. 15,16 ACEIs also reduce the rate of progression of microalbuminuria to macroalbuminuria in type-1 and 2 diabetics as do ARB in type-2 diabetics. Finally, two further meta-analyses demonstrate that ACEIs can reduce albuminuria in diabetics. Combination therapy significantly reduced proteinuria independent of BP lowering without causing clinically relevant change in serum potassium level or GFR. In terms of other agents, non-dihydropyridine CCBs significantly reduced proteinuria independent of BP control when compared with dihydropyridine CCBs. There are also RCTs supporting the use of thiazide diuretic indapamide in type-2 diabetics with hypertension resulting in reduction of microalbuminuria comparable to that achieved by ACEIs enalapril and captopril. In recent years complete blockade of the rennin-angiotensin-aldosterone (RAA) pathway is suggested to prevent progressive chronic kidney disease. Aldosterone antagonist reduces proteinuria in CKD patients already on ACEIs and ARBs, but increases the risk of hyperkalamia. Long-term effects of those agents on renal outcomes, mortality and safety need to be established. 17 At present use of complete RAA pathway blockade is not recommended in routine clinical practice

3 Medicine Update 2010 Vol. 20 ACEIs and/or ARBs should be used in all diabetics who tolerate them and in all non-diabetic CKD patients with > 0.5 gm/day proteinuria to reduce proteinuria and slow the rate of progression of CKD. Where RAAS-active drugs can not be tolerated, non-dihydropyridine CCBs or indapamide can be considered. Further research is needed to clarify the benefit of these drugs beyond BP control alone in patients without proteinuria. Complete blockade of the RAA-pathway to prevent progressive chronic kidney disease is not recommended because of risk of hyperkalamia, hypotension and even worsening of renal function. In theory, complete rennin-angiotensin-aldosterone blockade might be better than partial blockade, but we need more data. Role of other factors in slowing the progression of chronic kidney disease (CKD): 1. Strict glycemic control (for diabetics only) 2. Lipid-lowering therapy 3. Smoking cessation 4. Dietary modification 5. Regular exercise & weight loss Strict glycemic control Several trials (DCCT and UKPDS) suggested that glycemic control with target HbA 1 C level of 6.5% is helpful in preventing the onset and progression of diabetic microangiopathy. 19,20 The Joint British Society guidelines recommend that an HbA 1 C of 6.5% significantly reduce the risk of developing diabetic complications. 21 Lipid-lowering therapy Three analyses address the issue of lipid-lowering and CKD progression. 22,23 One suggested that current evidence for benefit was lacking, whilst another suggested that lipidlowering may reduce proteinuria and retard the progression of CKD. However, current evidence is insufficient to recommend lipid-lowering therapy to slow the progression of CKD. Smoking and alcohol Several observational studies highlighted the nephrotoxic nature of smoking. Chronic smoking increases the risk of proteinuria and accelerates the rate of decline of GFR. Observational studies showed that quiting smoking slowed down CKD progression. 24,25 The role of alcohol in the development and progression of CKD is less clear. Analysis of NHANES II data did not support a relationship between alcohol consumption and CKD. There are no data on the effects of reducing alcohol consumption on CKD progression. Smoking must be given up because smoking cessation slow CKD progression. However, there is insufficient evidence that alcohol moderation slows CKD progression. Dietary modification The evidence for dietary modification reducing CKD progression is limited to stage 1-3 CKD. Three small RCTs in diabetic patients with stages 2-3 CKD did not show any benefit of protein restriction on CKD progression (0.6 to 0.8 gm/kg/day). One small trial in non-diabetic patients with CKD stage 3 demonstrated a positive effect of protein restriction (0.6 gm/kg/day) on CKD progression, but this was at the expense of an overall deterioration in nutritional status. : There is insufficient evidence to recommend low protein diet to slow down the progression of early CKD. There is some evidence to support sodium restriction in order to reduce blood pressure. 5. Treating the consequences of CKD Additionally, anaemia, acidosis and disturbance of calcium and phosphate metabolism should be looked for and treated in patients with CKD stage 3 or above. Anaemia: Renal anaemia is common in CKD and is due to combination of factors; primarily erythropoietin (EPO) deficiency, iron deficiency, hemolysis, and ureamic inhibitors of erythropoiesis. 26 In the NHANES III Study, the prevalence of anaemia was 1% at an egfr of 60 ml/min/1.73m 2, 9% at an egfr of 30 ml/min/1.73m 2 and 33% (men) to 67% (women) at an egfr of 15 ml/min/1.73m 2. Whether, the early treatment of anaemia affects CKD progression and cardiovascular morbidity and mortality is currently not clear. 27 However, correction of anaemia predialysis can improve quality of life and exercise capacity. : CKD patients should maintain a target hemoglobin concentration of > 11 gm/dl using erythropoiesis-stimulating agents (ESA). Acidosis: The incidence of metabolic acidosis increases with declining renal function, but tends not to occur until CKD stage 4. The detrimental effects of acidosis include muscle wasting, loss of bone mass, exacerbation of β 2 -microglobulin accumulation, and impaired insulin sensitivity. 28,29 The correction of acidosis can result in beneficial effects in terms of bone and muscle metabolism, however, there have been no RCTs investigating acidosis correction on the clinical outcome. 710

4 Retarding Progression of Chronic Kidney Disease (Ckd) : There is insufficient evidence to make recommendation on the treatment of metabolic acidosis. However, maintenance of serum bicarbonate level at 22 mmol/l is reasonable. Calcium and Phosphate homeostasis: Disturbance in calcium and phosphate metabolism and secondary hyperparathyroidism occur with increasing frequency and severity as GFR declines. Serum phosphate level begins to rise below an egfr 60 ml/min/1.73m 2 due to phosphate retention, with serum calcium level falling due to reduced activity of vitamin D (reduced renal 1α-hydroxylation). Parathyroid hormone (PTH) level begins to rise as a consequence of both low calcium and high phosphate below an egfr 60 ml/min/1.73m 2. These changes not only affect bone integrity, but also promote soft tissue and vascular calcification over time increasing cardiovascular morbidity and mortality in later CKD stages. Observational data and experimental evidence suggest that early intervention is appropriate. The treatment targets in CKD stage 3 are currently more a matter of opinion than evidence. Initial therapy for hyperphosphatemia includes dietary phosphate restriction and the use of oral phosphate binders. Secondary, hyperparathyroidism is initially treated with the replacement of deficient 1α-calcidol. 6. Reducing risk of cardiovascular diseases (CVD) Independent of the etiology, the presence of CKD is a strong predictor of CVD. In fact, JNC-7 recognizes an estimated GFR below 60 ml/min as a major cardiovascular risk factor. The K/DOQI guideline suggests that all patients with CKD should be considered in the highest risk group for cardiovascular disease, irrespective of level of traditional CVD risk factor. Hypertension reduction reduces CVD risk in general population. In CKD population specifically, RAAS blockade may reduce cardiovascular risk. 30 Combination of lipid lowering agents and aspirin is beneficial in reducing cardiovascular event in patients with CKD. 31 The importance of lifestyle modification (diet, exercise, smoking cessation and alcohol moderation) must not be overlooked in CKD patients, because traditional CVD risk factors persist in Chronic Kidney Disease. Summary of interventions The current evidence would favor the following treatment goals in order to both slow the progression of CKD and reduce CVD risk: Lowering of Blood Pressure (BP) : Target BP <130/80 mm Hg (<125/75 mm Hg if > 1 gm/day proteinuria): BP reduction will reduce proteinuria, slow CKD progression and reduce CVD risk. Blocking RAA system : ACEIs and ARBs to reduce proteinuria and slow CKD progression. Glycemic control : HbAIc < 6.5% in diabetics to reduce microvascular complications. Smoking cessation : Smoking must be stopped. Lowering lipid : Total cholesterol < 4 mmol/l. Life style modification : Encourage regular exercise, weight reduction, alcohol and salt limitation, and avoidance of excess protein intake. Additionally, acidosis, anaemia, and disturbances of calcium and phosphate metabolism should be looked for and treated in patients with CKD stage 3 or above. 7. Conclusion: There exist strong evidence that CKD and its progression to ESRD are increasing worldwide. This pose a growing health-care and financial burden. Therefore, there is an urgent need to develop preventive strategies. The asymptomatic nature of CKD means that early detection can only occur through laboratory testing of individuals. Analysis of urine for albumin or protein, S. creatinine level in blood and measurement of blood pressure of individual at increased risk of CKD (diabetics, hypertensives, and aged > 50 yrs) are simple, cheap and easy ways to detect CKD. Institution of early intervention (antihypertensives, ACEI/ARB) will lead to reduction in cumulative incidence of ESRD. It has been observed that screening of population at risk and their treatment is cost effective. 8. Take Home Message: Early detection of chronic kidney disease (CKD) followed by appropriate clinical management appears the only means by which the increasing burden on the health-care system and affected individuals can be reduced. References: 1. Mathew T and Corso O. review article: Early detection of chronic kidney disease in Australia: Which way to go? Nephrology 2009; 14: John PD and Gansevoort RT. Prevention of chronic kidney disease (Review Article) : The next step forward. Nephrology 2006; 11: Levey AS, Eckardt K-U, Tsukamoto Y et al. Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2005; 67: Buckalew VM, Berg RL, Wang S-R et al. Prevalence of hypertension in 1,795 subjects with chronic renal disease: the modification of diet in renal disease study baseline cohort. Am K Kidney Dis 1996; 28: Coresh J, Wei GL, McQuillan G et al. Prevalence of high bleed pressure and elevated serum creatinine level in the United States: findings from the third national health and nutrition examination survey ( ). Arch Intern Med 2001; 161: Maki DD, Ma JZ, Louis TA et al. Long-term effects of antihypertensive agents on proteinuria and renal function. Arch Intern Med 1995; 155: Casas JP, Chua W, Loukogeorgakis S et al. Effect of inhibitors of the renal-angiotensin system and other antihypertensive drugs on renal outcomes: systematic review and meta-analysis. Lancet 2005; 366:

5 Medicine Update 2010 Vol Jafar TH, Stark PC, Schmid CH et al. Progression of chronic kidney disease: the role of blood pressure control, proteinuria, and angiotensincoverting enzyme inhibition: a patient-level meta-analysis. Ann Intern Med 2003; 139: He J, Whelton PK. Elevated systolic blood pressure and risk of cardiovascular and renal disease. Overview of evidence from observational epidemiologic studies and randomized controlled trials. Am Heart J 1999; 138: S211-S Peterson JC, Adler S, Burkart JM et al. Blood pressure control, proteinuria, and the progression of renal disease, the modification of diet in renal disease study. Am Intern Med 1995; 123: Chobanian AV, Bakris GL, Black HR et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report. JAMA 2003; 289: Williams B, Poulter NR, Brown MJ et al. Guidelines for management of hypertension: report of the fourth working party of the British Hypertension Society, 2004 (BHS IV). J Hum Hypertens 2004; 18; Ruggenenti P, Perna A, Remuzzi G. Retarding progression of chronic renal disease: the neglected issue of residual proteinuria. Kidney Int 2003; 63: Jafar T, Stark P, Schmid C et al. Proteinuria as a modifiable risk factor for the progression of non-diabetic renal disease. Kidney Int 2001; 60: The ACE Inhibitors in Diabetic Nephropathy Trialist Group. Should all patients with type 1 diabetes mellitus and micro-albuminuria receive angiotensin-converting enzyme inhibitors? A meta-analysis of individual patient data. Ann Intern Med 2001; 134: Strippoli GFM, Craig M, Deeks JJ et al. Effects of angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists on mortality and renal outcome in diabetic nephropathy: systematic review. Br Med J 2004; 329: Navaneethan SD, Nigwekar SU, Seghal AR, and Strippoli GFM. Aldosterone Antagonists for Preventing the Progression of Chronic Kidney Disease: A systemic review and meta-analysis. Clin J Am Soc Nephrol 2009; 4: Martin J and Schreiber Jr. Preventing renal disease progression: Can complete rennin-angiotensin-aldosterone blockade work? Cleveland Clin Jour Med 2008; 75: The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. New Engl J Med 1993; 329: United Kingdom Prospective Diabetes Study (UKPDS). Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998; 352: Okhubo Y, Kishikawa H, Araki E et al. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin-dependent diabetes mellitus: a randomized prospective 6-year study. Diabetes Res Clin Pract 1995; 28: Marisch NM, Pezzillo KK. HMG-CoA reductase inhibitors for the prevention of nephropathy. Ann Pharmacother 2004; 38: Tonelli M, Isles C, Craven T et al. Effect of pravastatin on rate os kidney function loss in people with or at risk for coronary disease. Circulation 2005; 112: Orth S. Smoking - a renal risk factor. Nephron 2000; 86: Taal M, Brenner B. Evolving strategies for renoprotection: non-diebatic chronic renal disease. Curr Opin Nephrol Hypertens 2001; 10: Fisher J. Mechanism of the anemia of chronic renal failure. Nephron 1980; 25: Rao M, Pereira B. Respective trials on anemia of chronic disease: the Trial to Reduce Cardiovascular Events with Aranesp Therapy (TREAT). Kidney Int 2003; 87[suppl]: S12-S Kraut J, Kurtz I. Metabolic Acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am J Kidney Dis 2005; 45: Bailey JL. Metabolic acidosis: an unrecognized cause of morbidity in the patient with chronic kidney disease. Kidney Int 2005; 68: S15-S Tokmakova MP, Skali H, Kenchaiah S et al. Chronic kidney disease, cardiovascular risk, and response to angiotensin-converting enzyme inhibition after myocardial infarction: the Survival And Ventricular Enlargement (SAVE) Study. Circulation 2004; 110: Ruilope LM, Salvetti A, Kamerson K et al. Renal function and intensive lowering of blood pressure in hypertensive participants of the hypertension optimal treatment (HOT) study. J Am Soc Nephrol 2001; 12:

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