Reply

Sir,

A. K. Ghosh and K. Ghosh are concerned about some aspects of our study [1]: they point out that baseline proteinuria levels were higher in the losartan group: 3.1 g/24 h (2.5–3.8) compared with 2.5 g/24 h (2–3.2) in the amlodipine group and that this difference could influence the greater antiproteinuric response of patients treated with losartan. However, we would like to stress that this difference in baseline proteinuria between groups was not significant and that the antiproteinuric response was independent of the level of proteinuria at baseline, when considering the whole group of 97 randomized patients and patients of the losartan and amlodipine groups separately. With respect to the randomization process, it followed the usual requirements, as itemized in the CONSORT statement [2]. Taking into account the objectives and the primary and secondary end points of our study (decrease in the level of proteinuria and changes in the plasma and urinary levels of TGF-ß), we think that the statistical approach proposed by A. K. Ghosh and K. Ghosh (NNT, number needed to treat) would not add useful information to the study. On the contrary, we think that the results of our study, showing a drastic proteinuria decrease (–50.4% at week 20) in our non-diabetic patients treated with losartan will be of great interest for any skilled nephrologist aware of the fundamental clinical importance that such antiproteinuric responses represent in terms of future renoprotection. Confirming preliminary studies [3], all the multicentre studies of the last years with angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs) or the combination of an ACEI plus ARB, in both diabetic and non-diabetic proteinuric diseases, have consistently demonstrated that the renoprotection induced by these drugs is predicted by and closely related to their antiproteinuric efficacy [49]. In fact, on the basis of this accumulated clinical experience [10], we and others believe that proteinuria decrease should be considered as a surrogate marker of renoprotection in proteinuric nephropathies.

Conflict of interest statement. None declared.

Manuel Praga

Hospital 12 de Octubre Madrid, Spain Email: mpragat{at}senefro.org

References

  1. Praga M, Fernández Andrade C, Luño J et al. Antiproteinuric efficacy of losartan in comparison with amlodipine in non-diabetic proteinuric renal diseases: a double-blind, randomized clinical trial. Nephrol Dial Transplant 2003; 18: 1806–1813[Abstract/Free Full Text]
  2. Altman DG, Schulz KF, Moher D et al. The revised CONSORT statement for reporting randomized trials: explanation and elaboration. Ann Intern Med 2001; 134: 663–694[Abstract/Free Full Text]
  3. Praga M, Hernández E, Montoyo C et al. Long-term beneficial effects of ACE inhibition in patients with nephrotic proteinuria. Am J Kidney Dis 1992; 20: 240–248[ISI][Medline]
  4. Lewis EJ, Hunsicker L, Bain RP, Rhode RP, for the Collaborative Study Group. The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. N Engl J Med 1993; 329: 1456–1462[Abstract/Free Full Text]
  5. Maschio G, Alberti D, Janin G et al. Effect of the angiotensin-converting-enzyme inhibitor benazepril on the progression of chronic renal insufficiency. N Engl J Med 1996; 334: 939–945[Abstract/Free Full Text]
  6. The GISEN Group. Randomised placebo-controlled trial of effect of ramipril on decline in glomerular filtration rate and risk of terminal renal failure in proteinuric, non-diabetic nephropathy. Lancet 1997; 349: 1857–1863[CrossRef][ISI][Medline]
  7. Lewis EJ, Hunsicker LG, Clarke WR et al. for the Collaborative Study Group. Renoprotective effect of the angiotensin-receptor antagonist irbersartan in patients with nephropathy due to type 2 diabetes. N Engl J Med 2001; 345: 851–860[Abstract/Free Full Text]
  8. Brenner BM, Cooper ME, De Zeeuw D et al. for the RENAAL Study Investigators. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med 2001; 345: 861–869[Abstract/Free Full Text]
  9. Nakao N, Yoshimura A, Morita H, Takada M, Kayano T, Ideura T. 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: 117–124[CrossRef][ISI][Medline]
  10. Jafar TH, Stark PC, Schmid CD et al. Proteinuria as a modifiable risk factor for the progression of non-diabetic renal diseases. Kidney Int 2001; 60: 1131–1140[CrossRef][ISI][Medline]




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