Keywords albuminuria, hypertension, nephropathy, proteinuria
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1 Should proteinuria reduction be the criterion for antihypertensive drug selection for patients with kidney disease? Rigas G. Kalaitzidis and George L. Bakris Department of Medicine, Hypertensive Diseases Unit, University of Chicago Pritzker School of Medicine, Chicago, Illinois, USA Correspondence to George L. Bakris, MD, Hypertension Diseases Unit, University of Chicago Pritzker School of Medicine, MC1027, Room #P-328A, 5841 S. Maryland Avenue, Chicago, IL 60637, USA Tel: ; fax: ; Current Opinion in Nephrology and Hypertension 2009, 18: Purpose of review Proteinuria, that is, more than 200 mg/day of urinary albumin, is associated with the presence of kidney disease. Its increase over time is strongly correlated with progression of nephropathy. Retrospective analyses of nephropathy outcome trials show that proteinuria reduction of 30% or more after initiation of blood pressure (BP)- lowering therapy is associated with slower nephropathy progression than lowering BP without its reduction. Recent findings Retrospective analyses of five large nephropathy outcome trials demonstrate that nephropathy progression slowed by an additional 28 39% over the control or placebo group when proteinuria was reduced in concert with BP. Two separate trials demonstrate that nephropathy progression was slowed to a lesser degree when BP was reduced to a similar degree, but proteinuria reduced less than 30%. These associations do not hold for those with microalbuminuria, in which BP reduction is the key element to slowing nephropathy progression. Recent cardiovascular outcome trials fail to show a relationship between reductions in proteinuria and nephropathy outcomes. This large cardiovascular endpoint trial, however, was not only powered for nephropathy outcomes but also failed to show a benefit between proteinuria reduction and cardiovascular events, a previously established observation. Summary All patients with a history of hypertension and either kidney disease or diabetes should have an annual check for albuminuria. If albumin is present in amounts of more than 200 mg/day, strategies for BP-lowering therapy should also focus on a reduction of more than 30% of urinary protein. Keywords albuminuria, hypertension, nephropathy, proteinuria Curr Opin Nephrol Hypertens 18: ß 2009 Wolters Kluwer Health Lippincott Williams & Wilkins Introduction Urine protein consists of 20% low-molecular-weight proteins, 40% Tamm Horsfall mucoprotein, derived from the loop of Henle, and 40% albumin [1]. In patients with normal kidney function, less than 30 mg/day of albumin is usually lost. Transient increases in albumin above 30 mg/day, that is, microalbuminuria, have been observed in a number of common conditions including upright posture, presence of fever from any cause, and underlying inflammatory conditions such as arthritis, infection, smoking, or exercise [2]. Several methods exist to assess the level of albuminuria and are reviewed elsewhere [3]. A quick and accurate way of measuring albuminuria is an albumin-to-creatinine ratio on a spot collection of morning urine in a fasting state. Screening for albuminuria has been recommended for hypertensive patients [4], especially those with concomitant diabetes [5] and early chronic kidney disease (CKD) [6]. Screening for microalbuminuria is recommended due to its association with increased cardiovascular risk. Microalbuminuria is defined as a urine albumin excretion (UAE) rate between 30 and 300 mg/day (0.03 and 0.3 g/day) if measured in a 24 h urine collection, 20 and 200 mg/min if measured in a timed urine collection, or mg/g (0.03 and 0.3 g/g) if measured with the use of the urinary albumin creatinine ratio in a spot urine collection. Microalbuminuria is an indication of higher cardiovascular risk and endothelial dysfunction [7]. Microalbuminuria is an independent risk factor for cardiovascular morbidity and mortality in individuals ß 2009 Wolters Kluwer Health Lippincott Williams & Wilkins DOI: /MNH.0b013e32832edc99
2 Proteinuria reduction and nephropathy outcomes Kalaitzidis and Bakris 387 Figure 1 Time to attainment of SBP and DBP goal (Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines) by albuminuria status Probability of failure to attain goal Macroalbuminuria: (>300 mg/dl) Microalbuminuria: ( mg/dl) Normal: (<30 mg/dl) Log-rank P < Wilcoxon P < Time to goal attainment (months) Reproduced with permission from [17]. with and without diabetes [8,9]. It occurs in 30% of middle-aged individuals with type 2 diabetes and in 10 15% of individuals without diabetes [10]. There are no data that support the presence of microalbuminuria as an indicator of kidney dysfunction per se. Increases in microalbuminuria over time in the presence of adequate blood pressure (BP) control do predict worsening of CKD [11]. This study will focus on macroalbuminuria (proteinuria), that is, more than 200 mg/day of albuminuria, and its association with CKD progression in the face of BP control. The prevalence of macroalbuminuria is about 1.3% in the United States and ranges from 1% in white individuals to 2.4% in African Americans [12]. It is more common with aging [12] and very common in patients with diabetes and hypertension [13]. Approximately 80% of those with type 1 diabetes and 20 40% of those with type 2 diabetes with microalbuminuria will progress to macroalbuminuria without medical management over a year period [5]. The presence of proteinuria is an indicator of kidney disease with an increased probability of progressive kidney loss even in a setting of relatively normal glomerular filtration rate (GFR). Proteinuria, however, is associated with faster loss of GFR compared with little to no proteinuria [14,15]. The question debated is whether proteinuria is truly an independent therapeutic target for reducing the risk of CKD progression [16]. Should proteinuria reduction be a mandatory variable in optimizing BP control to optimally slow nephropathy progression? There is a direct correlation between the level of proteinuria and the number of BP medications needed to achieve the BP goal [17]. In one study, the presence of the proteinuria predicted a blunted systolic blood pressure (SBP) reduction of 10.3 mmhg over time. In this study, patients with albuminuria were less likely to attain their SBP goal than patients without albuminuria [17] (Fig. 1). These data support the notion that presence of proteinuria requires more aggressive treatment to achieve the recommended BP goals to halt CKD progression [18]. Many investigators have assumed that changes in proteinuria are concordant with the levels of BP reduction. A growing body of evidence indicates that the level of proteinuria and not the current level of GFR is the most relevant variable to predict CKD progression in those with a GFR of at least 30 ml/min [19]. Data support the notion that CKD progression is linked to the degree of albuminuria reduction even in patients who reached the current BP targets [20] (Fig. 2). Clinical trial evidence There have been no prospective trials to test the hypothesis that greater proteinuria reductions in the presence of similar levels of BP control provide greater slowing of nephropathy. Post-hoc analyses of all CKD outcome trials, to date, demonstrate that at SBP between 136
3 388 Pharmacology and therapeutics Figure 2 Change from baseline proteinuria associated with risk of end-stage renal disease development in the African American Study of Kidney Disease trial Relative risk of ESRD and 140 mmhg, a 30 35% greater reduction in proteinuria was associated with greater slowing in CKD progression (Table 1 [21]) [3]. It should be noted that the patients in all these studies have more than 300 mg/day of proteinuria, a GFR of less than 50 ml/min, and were hypertensive. These observations cannot be extrapolated to people with low levels or no proteinuria or to patients in cardiovascular outcome trials, in which change in proteinuria was associated with a broad range of kidney function such as the ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) [22]. The first trial to evaluate changes in proteinuria in the context of CKD outcomes was the Modification of Diet in Renal Disease (MDRD) study. In this trial, those with Table 1 Summary of post-hoc analysis of trials powered for chronic kidney disease outcomes: focus on proteinuria reduction on primary outcome Trials with >30% reduction in proteinuria from baseline at trial end a Nondiabetic MDRD AIPRI REIN AASK Hou et al. [21] > 50 > >+100 to 20 to +25 to +100 Proportional change in UPCR (%) ESRD, end-stage renal disease; UPCR, urinary protein/creatinine ratio. Data from Lea et al. [19]. Diabetic Captopril trial IDNT RENAAL AASK, African American Study of Kidney Disease; ACE, angiotensinconverting enzyme; AIPRI, ACE Inhibition in Progressive Renal Insufficiency; GFR, glomerular filtration rate; IDNT, Irbesartan in Diabetic Nephropathy Trial; MDRD, Modification of Diet in Renal Disease; REIN, Ramipril Efficacy In Nephropathy; RENAAL, Reduction of Endpoints in Noninsulin-dependent diabetes mellitus with the Angiotensin II Antagonist Losartan. a Note all these trials have the following baseline characteristics in common: more than 300 mg/day proteinuria and GFR is less than 50 ml/min. greater than 1 g of proteinuria allocated to the low BP group (mean BP of 92 mmhg) had a significant decrease in proteinuria and rate of kidney disease progression after 12 years of follow-up [23]. This association of slowed CKD progression was most prominent among those with a protein excretion above 3 g/day [14]. These observations were further supported by the African American Study of Kidney Disease (AASK) trial. In this trial, the subgroup with greater than 1 g of proteinuria had slower declines in kidney function among those with randomized mean BP less than 92 mmhg and had more than 30% reduction in proteinuria from baseline [24]. It should be noted that both of these trials failed to show significant slowing of proteinuria if proteinuria was not reduced. Other trials will be discussed based on their study design and randomized drug class. Pharmacologic treatment Several lines of evidence indicate that, in patients with proteinuria, agents that block the renin angiotensin aldosterone system (RAAS) should be the drugs of choice [4,6,18,24 30]. Antihypertensive treatments that do not directly target the RAAS may reduce BP to the same degree but do not reduce proteinuria or slow progression of CKD beyond that predicted by BP lowering [31,32]. Angiotensin-converting enzyme inhibitor trials The Collaborative Study Group assigned 409 patients with type 1 diabetes with overt nephropathy (proteinuria >500 mg/day) and mild renal insufficiency (serum creatinine <2.2 mg/dl) to captopril or placebo. The treatment arm showed a 43% decrease in doubling of serum creatinine and a 30% decrease in albuminuria independent of BP control [33]. Similarly, the Ramipril Efficacy In Nephropathy (REIN) trial showed decreased proteinuria and preserved kidney function in nondiabetic patients with kidney disease. In this trial, the average creatinine was 2.4 mg/dl with a 24 h urine protein excretion greater than 3 g/day. When given 5 mg of ramipril versus placebo, patients had a 55% decrease in median urine protein excretion. There was also a significant reduction in GFR decline and doubling of serum creatinine. These findings were not totally predicted by BP lowering alone [34]. In the AASK trial, patients had an average creatinine of 2.2 mg/dl and 24 h urine protein excretion of 0.6 g/day. The ramipril group had a 36% risk reduction in doubling of creatinine, end-stage renal disease (ESRD), or death compared with the amlodipine group and 22% compared with the metoprolol group [24]. The greatest reduction in proteinuria was seen in the ramipril group. An additional Chinese study supports reductions in proteinuria as predictors of CKD events in advanced
4 Proteinuria reduction and nephropathy outcomes Kalaitzidis and Bakris 389 nephropathy. This trial involved 224 patients with serum creatinine levels of ml/dl ( mmol/l) and persistent proteinuria (1.6 g/day) who were randomly assigned to benazepril or placebo along with other antihypertensive therapy. Benazepril was associated with a 43% decrease in risk for the primary endpoint (doubling of serum creatinine levels, ESRD, or death) and a 23% decrease in the rate of decline in renal function. There was a 2.5-fold greater reduction in proteinuria in the benazepril group than in the placebo group after a mean follow-up of 3.4 years [21]. The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) [35] and a metaanalysis by Casas et al. [36] have highlighted the relationship that angiotensin-converting enzyme inhibitors (ACEIs) have no specific benefit other than BP lowering for patients with nondiabetic kidney disease. Patients in ALLHAT had mild (GFR ml/min/1.73 m 2 ) or moderate-to-severe (<60 ml/min/1.73 m 2 ) CKD. No difference in rates of ESRD or greater than 50% decrease in GFR was noted when randomized to chlorthalidone, amlodipine, or lisinopril. However, in the ALLHAT, urinary albumin excretion was not measured, making the true benefit of ACE inhibition difficult to quantify. Moreover, it was powered for CKD outcomes. Lastly, the mean age of the trial was 67 years, making estimated GFR (egfr) equations inappropriate for use in analyzing CKD outcomes in contrast to CKD outcome studies that actually measured GFR directly [37 ]. Also, the trial excluded patients with serum creatinine more than 2.0 mg/dl. The study by Casas et al. [36] did not show benefit on CKD slowing with the use of ACEI or angiotensin receptor blockers (ARBs) in patients with GFRs above 70 ml/min/1.73 m 2 or those with no proteinuria but did show benefit among all those with proteinuria. In nondiabetic patients, a benefit independent of BP control was noted. This meta-analysis placed a large magnitude of effect on the ALLHAT trial, thereby raising similar issues outlined above. Thus, ACE inhibitors slow CKD progression in patients with advanced proteinuric nephropathy as they relate to the magnitude of proteinuria reduction. This antiproteinuric effect cannot be totally explained by their effect on BP reduction. Angiotensin receptor blockers The Reduction of Endpoints in Noninsulin Dependent Diabetes Mellitus with the Angiotensin II Antagonist Losartan (RENAAL) trial enrolled 1513 patients with type 2 diabetes with a mean creatinine of 1.9 mg/dl and a median albumin-to-creatinine ratio of 1237 mg/g to losartan or placebo. After an average follow-up of 3.4 years, losartan reduced the doubling of creatinine, progression to ESRD, or death by 16%. Also, a 35% reduction in the albumin creatinine ratio and a 15% decrease in decline of loss in creatinine clearance were seen in the losartan arm. It was estimated that the ARB could delay the need for dialysis or transplantation by 2 years, and that this effect was not related to BP but to the reduction in proteinuria [26]. Furthermore, in the post-hoc analysis of this study, the risk of ESRD had a dependence clearly on albuminuria reduction regardless of change in SBP. The Irbesartan in Diabetic Nephropathy Trial (IDNT) randomized 1715 patients with type 2 diabetes and a mean creatinine of 1.7 mg/dl and median urinary protein excretion of 2.9 g/day to irbesartan, amlodipine, or placebo. Over a mean follow-up of 2.6 years, treatment with irbesartan resulted in a 20% risk reduction of CKD progression compared with placebo and 23% reduction compared with amlodipine in the primary outcome [29]. A relationship between amount of proteinuria and progression of CKD was seen, that is, for every two-fold increase in baseline proteinuria, there was a doubling of the primary endpoint. The irbesartan group had a greater than 50% decrease in proteinuria after the first year in 40% of the patients compared with 20% in the amlodipine and 25% in the placebo arms, respectively. The antiproteinuric effect of ACEIs and ARBs are equivalent. In a recent meta-analysis of randomized trials, the reduction in proteinuria after a year was similar between ACEIs and ARBs [38 ]. Calcium channel blockers Calcium channel blockers are effective antihypertensive agents in patients with kidney disease. Dihydropyridine calcium channel blockers have not demonstrated a beneficial effect on the progression of advanced proteinuric CKD in the absence of RAAS blockade and are specifically prohibited as first-line agents in such patients by guidelines [39]. Nondihydropyridine calcium channel blockers are superior to dihydropyridine calcium channel blockers for reducing proteinuria and are suggested for use in people with proteinuria as either an alternative to RAAS blockade for those who cannot tolerate it or as an adjunctive treatment to reduce proteinuria [6,40,41]. Current evidence shows that nondihydropyridine calcium channel blockers (verapamil and diltiazem) reduce proteinuria among patients with advanced proteinuric nephropathy [42,43], whereas dihydropyridine calcium channel blockers do not have this effect unless used in the presence of a RAAS blocker [44,45]. It should be noted that drug classes not mentioned have no data for proteinuria reduction in patients with advanced nephropathy, and hence do not contribute to this argument. Combination therapy Kidney protection with dual blockade of the RAAS using ACEIs and ARBs has not been extensively studied. A
5 390 Pharmacology and therapeutics recent meta-analysis of all trials that evaluated dual blockade clearly demonstrated a reduction in proteinuria of about 20% over either agent alone [38 ]. The recent Aliskiren in the Evaluation of Proteinuria in Diabetes trial also supports the notion of a renin inhibitor added to a maximally dosed ARB, which also reduces proteinuria by an additional 20 22% [30]. Although it is clear that further reducing proteinuria by combining an ACEI with an ARB should translate into further slowing of nephropathy, unfortunately there are no prospectively designed outcome trials to address this issue. The only trial, to date, to address this has been the combination treatment of angiotensin-ii receptor blocker (ARB) and angiotensin-converting-enzyme inhibitor (ACEI) in non-diabetic kidney disease trial. Unfortunately, data inconsistencies have been found in this study, and hence, no conclusion can be drawn from these data [38,46]. The ONTARGET study in which people were enrolled with vascular disease comparing the effects of ramipril with telmisartan versus the combination of telmisartan along with ramipril also provides little insight as to CKD progression and proteinuria reduction [47]. Although the combination group had a greater effect on BP, and least increase in proteinuria over time, it was not powered for CKD outcomes [48 ]. Specifically, only 300 of the people had proteinuria of more than 1 g/day, and the majority of the patients had GFR values above 50 ml/min, thus the cohort cannot be compared with those of other advanced nephropathy trials. There are no outcome studies that evaluate other dual RAAS-blocking strategies such as those involving aldosterone receptor antagonists in patients already on an ACEI or an ARB, although this combination further reduces proteinuria [49 51]. Conclusion Proteinuria is a well known risk marker for CKD progression as well as cardiovascular morbidity and mortality. It is known that more aggressive antihypertensive treatment is needed when proteinuria is present. Taken together the data presented strongly support the concept that SBP reduction to levels of 130 mmhg or less in those with proteinuria will maximally slow nephropathy progression compared with no change in proteinuria in spite of BP reductions. This association is true regardless of whether the cause of nephropathy is related to diabetes or nondiabetic causes [3]. In practical terms, proteinuria lowering needs a multifactorial approach with treatment individualized to halt CKD progression [18]. In order to do this, physicians must routinely measure urinary protein with a spot albumin creatinine ratio annually to assess for the presence of protein as well as change. References and recommended reading Papers of particular interest, published within the annual period of review, have been highlighted as: of special interest of outstanding interest Additional references related to this topic can also be found in the Current World Literature section in this issue (pp ). 1 Carroll MF, Temte JL. Proteinuria in adults: a diagnostic approach. Am Fam Physician 2000; 62: Bakris GL. Microalbuminuria. Marker of kidney and cardiovascular disease. London: Current Medicine Group; Khosla N, Bakris G. Lessons learned from recent hypertension trials about kidney disease. Clin J Am Soc Nephrol 2006; 1: Mancia G, De BG, Dominiczak A, et al Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2007; 25: American Diabetes Association. Nephropathy in diabetes. Diabetes Care 2009; 27:S79 S84. 6 Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis 2004; 43 (5 Suppl 1):S1 S Wachtell K, Olsen MH. Is it time to change the definition of normal urinary albumin excretion? Nat Clin Pract Nephrol 2008; 4: MacIsaac RJ, Jerums G, Cooper ME. New insights into the significance of microalbuminuria. Curr Opin Nephrol Hypertens 2004; 13: Hermans MM, Henry R, Dekker JM, et al. Estimated glomerular filtration rate and urinary albumin excretion are independently associated with greater arterial stiffness: the Hoorn Study. J Am Soc Nephrol 2007; 18: Rossi MC, Nicolucci A, Pellegrini F, et al. Identifying patients with type 2 diabetes at high risk of microalbuminuria: results of the DEMAND (Developing Education on Microalbuminuria for Awareness of renal and cardiovascular risk in Diabetes) Study. Nephrol Dial Transplant 2008; 23: Khosla N, Sarafidis PA, Bakris GL. Microalbuminuria. Clin Lab Med 2006; 26: Coresh J, Byrd-Holt D, Astor BC, et al. Chronic kidney disease awareness, prevalence, and trends among U.S. adults, 1999 to J Am Soc Nephrol 2005; 16: Atkins RC, Polkinghorne KR, Briganti EM, et al. Prevalence of albuminuria in Australia: the AusDiab Kidney Study. Kidney Int Suppl 2004; S22 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. Ann Intern Med 1995; 123: Jafar TH, Stark PC, Schmid CH, et al. Proteinuria as a modifiable risk factor for the progression of nondiabetic renal disease. Kidney Int 2001; 60: de Zeeuw D. Targeting proteinuria as a valid surrogate for individualized kidney protective therapy. Am J Kidney Dis 2008; 51: Flack JM, Duncan K, Ohmit SE, et al. Influence of albuminuria and glomerular filtration rate on blood pressure response to antihypertensive drug therapy. Vasc Health Risk Manag 2007; 3: de Jong PE, Navis G. Proteinuria lowering needs a multifactorial and individualized approach to halt progression of renal disease. Nat Clin Pract Nephrol 2008; 4: Lea J, Greene T, Hebert L, et al. The relationship between magnitude of proteinuria reduction and risk of end-stage renal disease: results of the African American study of kidney disease and hypertension. Arch Intern Med 2005; 165: Eijkelkamp WB, Zhang Z, Remuzzi G, et al. Albuminuria is a target for renoprotective therapy independent from blood pressure in patients with type 2 diabetic nephropathy: post hoc analysis from the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial. J Am Soc Nephrol 2007; 18: Hou FF, Zhang X, Zhang GH, et al. Efficacy and safety of benazepril for advanced chronic renal insufficiency. N Engl J Med 2006; 354: Sarafidis PA, Bakris GL. Renin-angiotensin blockade and kidney disease. Lancet 2008; 372: Sarnak MJ, Greene T, Wang X, et al. The effect of a lower target blood pressure on the progression of kidney disease: long-term follow-up of the modification of diet in renal disease study. Ann Intern Med 2005; 142:
6 Proteinuria reduction and nephropathy outcomes Kalaitzidis and Bakris Wright JT Jr, Bakris G, Greene T, et al. Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK trial. JAMA 2002; 288: Clinical Practice Recommendations. Diabetes Care 2009; 32 (Suppl 1):S1 S Brenner BM, Cooper ME, de ZD, et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med 2001; 345: Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42: Hou FF, Xie D, Zhang X, et al. Renoprotection of Optimal Antiproteinuric Doses (ROAD) Study: a randomized controlled study of benazepril and losartan in chronic renal insufficiency. J Am Soc Nephrol 2007; 18: Lewis EJ, Hunsicker LG, Clarke WR, et al. Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes. N Engl J Med 2001; 345: Parving HH, Persson F, Lewis JB, et al. Aliskiren combined with losartan in type 2 diabetes and nephropathy. N Engl J Med 2008; 358: Sato A, Saruta T, Funder JW. Combination therapy with aldosterone blockade and renin-angiotensin inhibitors confers organ protection. Hypertens Res 2006; 29: Samuelsson O, Wilhelmsen L, Pennert K, Berglund G. Prognostic factors in treated hypertension. J Hypertens Suppl 1985; 3:S497 S Lewis EJ, Hunsicker LG, Bain RP, Rohde RD, The Collaborative Study Group. The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. N Engl J Med 1993; 329: The GISEN Group (Gruppo Italiano di Studi Epidemiologici in Nefrologia). Randomised placebo-controlled trial of effect of ramipril on decline in glomerular filtration rate and risk of terminal renal failure in proteinuric, nondiabetic nephropathy. Lancet 1997; 349: ALLHAT Collaborative Research Group. Major cardiovascular events in hypertensive patients randomized to doxazosin vs chlorthalidone: the antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT). JAMA 2000; 283: Casas JP, Chua W, Loukogeorgakis S, et al. Effect of inhibitors of the renin-angiotensin system and other antihypertensive drugs on renal outcomes: systematic review and meta-analysis. Lancet 2005; 366: Glassock RJ, Winearls CG. egfr: Readjusting its rating. Clin J Am Soc Nephrol 2009; 4: This study presents arguments to reassess where and when to use the egfr equation, especially in the elderly and those with normal kidney function. 38 Kunz R, Friedrich C, Wolbers M, Mann JF. Meta-analysis: effect of monotherapy and combination therapy with inhibitors of the renin angiotensin system on proteinuria in renal disease. Ann Intern Med 2008; 148: A nice review and analysis of trials that evaluted BP control and proteinuria reduction. 39 Rahman M, Brown CD, Coresh J, et al. The prevalence of reduced glomerular filtration rate in older hypertensive patients and its association with cardiovascular disease: a report from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial. Arch Intern Med 2004; 164: Bakris GL, Weir MR, Secic M, et al. Differential effects of calcium antagonist subclasses on markers of nephropathy progression. Kidney Int 2004; 65: Sarafidis PA, Khosla N, Bakris GL. Antihypertensive therapy in the presence of proteinuria. Am J Kidney Dis 2007; 49: Bakris GL, Copley JB, Vicknair N, et al. Calcium channel blockers versus other antihypertensive therapies on progression of NIDDM associated nephropathy. Kidney Int 1996; 50: Bakris GL, Mangrum A, Copley JB, et al. Effect of calcium channel or betablockade on the progression of diabetic nephropathy in African Americans. Hypertension 1997; 29: Bakris GL, Weir MR, Shanifar S, et al. Effects of blood pressure level on progression of diabetic nephropathy: results from the RENAAL study. Arch Intern Med 2003; 163: Smith AC, Toto R, Bakris GL. Differential effects of calcium channel blockers on size selectivity of proteinuria in diabetic glomerulopathy. Kidney Int 1998; 54: Bidani A. Controversy about COOPERATE ABPM trial data. Am J Nephrol 2006; 26: Yusuf S, Teo KK, Pogue J, et al. Telmisartan, ramipril, or both in patients at high risk for vascular events. N Engl J Med 2008; 358: Mann JF, Schmieder RE, McQueen M, et al. Renal outcomes with telmisartan, ramipril, or both, in people at high vascular risk (the ONTARGET study): a multicentre, randomised, double-blind, controlled trial. Lancet 2008; 372: The substudy of ONTARGET that evaluates CKD progression. 49 Rossing K, Schjoedt KJ, Smidt UM, et al. Beneficial effects of adding spironolactone to recommended antihypertensive treatment in diabetic nephropathy: a randomized, double-masked, cross-over study. Diabetes Care 2005; 28: Chrysostomou A, Becker G. Spironolactone in addition to ACE inhibition to reduce proteinuria in patients with chronic renal disease. N Engl J Med 2001; 345: Epstein M, Williams GH, Weinberger M, et al. Selective aldosterone blockade with eplerenone reduces albuminuria in patients with type 2 diabetes. Clin J Am Soc Nephrol 2006; 1:
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