The renoprotective action of angiotensin-converting enzyme inhibitors in diabetes.

Chronic renal diseases evolve to terminal renal failure by a process leading to progressive parenchymal damage which appears relatively independent of the initial insult. When glomerular permselectivity is lost, proteins filtered through the glomerular capillary, via proximal tubular cell activation and upregulation of genes of inflammatory and vasoactive mediators, may give rise to an inflammatory reaction that in the long-term can contribute to renal scarring. If this interpretation is correct, the best approach to try to retard the progression of several renal diseases would be to limit the excessive traffic of macromolecules throughout the glomerular capillary by molecules such as the angiotensin-converting-enzyme (ACE) inhibitors, which may help restore permselective properties to normal. Thus, the present review addresses the mechanism(s) of the renal protective effect of ACE inhibitors and analyzes the evidence so far available of their salutary effect in human nephropathies, with particular focus on diabetic nephropathy.