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• W3149271875 abstract "Juan Casas and colleagues' conclusion1Casas 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: 2026-2033Summary Full Text Full Text PDF PubMed Scopus (614) Google Scholar that angiotensin-converting-enzyme (ACE) inhibitors and angiotensin-receptor-blockers (ARBs) reduce the incidence of end-stage renal disease and double serum creatinine solely because of blood-pressure lowering is invalid. Their meta-analysis is grossly distorted by ALLHAT which did not define renal outcomes as a primary endpoint, and provides no data on proteinuria. Evidence from one conflicting trial with a post-hoc analysis of secondary outcomes should not guide clinical practice when homogeneous data from multiple randomised controlled trials with hard renal outcomes as primary endpoints and appropriate adjustment for proteinuria are available. The 12 studies in Casas and colleagues' paper besides ALLHAT show a beneficial effect of ACE inhibitors and ARBs on end-stage renal disease with substantial effect sizes (32% risk reduction [95% CI 4–52] in small studies; 24% risk reduction [5–39] in large studies). Despite ALLHAT contributing 90% of the data, the results for ACE inhibitors on end-stage renal disease remain significant. Casas and colleagues' meta-regression analysis on blood pressure and renal outcomes relates mean change in blood pressure within tertiles to occurrence of end-stage renal disease. However, associations between patients' averages across trials might not be the same as associations between patients within trials. There is a high risk of spurious associations caused by so-called ecological fallacy, which can only be investigated with individual patients' data. In their meta-analysis of individual patients' data,2Jafar TH Stark PC Schmid CH et al.Progression of kidney disease: the role of blood pressure control, proteinuria, and ACE inhibition: a patient-level metaanalysis.Ann Intern Med. 2003; 135: 73-87Crossref Scopus (886) Google Scholar Jafar and colleagues showed that ACE inhibitors reduce end-stage renal disease better when proteinuria is higher. What was the result of Casas and colleagues' meta-analysis if restricted to patients with proteinuria greater than 1 g/day? Klahr and colleagues showed no benefit of blood-pressure lowering if proteinuria was less than 1 g/day.3Klahr S Levey AS Beck GJ et al.The effects of dietary protein restriction and blood pressure control in the progression of chronic renal disease.N Engl J Med. 1994; 330: 877-884Crossref PubMed Scopus (2044) Google Scholar Proteinuria is a pivotal aspect of progression of renal disease. Casas and colleagues ignored its role. They suggest that blood-pressure lowering in normotension or mild hypertension reduces renal outcomes, contradicting randomised trials with active controls and different levels of target blood pressure that support renoprotection by ACE inhibitors.4Agodoa LY Appel L Bakris GL et al.Effect of ramipril vs amlodipine on renal outcomes in hypertensive nephrosclerosis: a randomized controlled trial.J Am Med Assoc. 2001; 285: 2719-2728Crossref Scopus (855) Google Scholar The MDRD study supports this view in patients with no major proteinuria.3Klahr S Levey AS Beck GJ et al.The effects of dietary protein restriction and blood pressure control in the progression of chronic renal disease.N Engl J Med. 1994; 330: 877-884Crossref PubMed Scopus (2044) Google Scholar Furthermore, the COOPERATE study5Nakao N Yoshimura A Morita H et al.Combination treatment of angiotensin-II receptor blocker and angiotensin-converting-enzyme inhibitor in non-diabetic renal disease (COOPERATE): a randomised controlled trial.Lancet. 2003; 361: 117-124Summary Full Text Full Text PDF PubMed Scopus (973) Google Scholar suggests that more intense renin inhibition reduces the incidence of end-stage renal disease independent of blood pressure. As well as stratification for proteinuria, we encourage Casas and colleagues to provide graphical displays of the results of the individual trials. This would reveal which trials are driving the aggregated results and permit independent judgment. Casas and colleagues omit any description of the primary studies, underlying populations, interventions, and methodological quality; the internet platform could easily have been used to disclose these essential data. Casas and colleagues claim that they did not find heterogeneity in their results on end-stage renal disease. The clinical heterogeneity of included studies casts doubt on the robustness of this statement. Again, graphical display of the data and an uncertainty interval around the I2 value of 0% would inform the reader. Soft endpoints (serum creatinine, albuminuria) are less important if unequivocal hard endpoints are available. Nevertheless, aggregation of those heterogeneous data without investigating sources of heterogeneity (trial quality, degree of proteinuria, or disease entity) questions this analysis. Most patients with renal disease need several antihypertensives to achieve target blood pressure. In the presence of proteinuria, ACE inhibitors and ARBs will achieve additional blood-pressure-independent protection of the kidney. JM and ER receive speaker fees from companies producing antihypertensive drugs. Renoprotective effects of renin-angiotensin-system inhibitors – Authors' replyThe results of ALLHAT challenged widely held beliefs about the renoprotective effect of renin-angiotensin-system (RAS) inhibition and so it is unsurprising that each of the correspondents raises this as an issue. However, it is the largest randomised double-blind trial with the longest follow-up of the effects of antihypertensive drugs on renal outcomes and it fulfilled our prespecified inclusion criteria. Exclusion of ALLHAT from our analysis would, quite rightly, have prompted great criticism since the trial provides around half the available evidence on renal outcomes. Full-Text PDF" @default.
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• W3149271875 title "Renoprotective effects of renin-angiotensin-system inhibitors" @default.
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