Protection of Renal Function with ACE Inhibitors: Experience with Benazepril

Research into progressive renal scarring has been closely linked over the last two decades with angiotensin II (AII). This has led to a better understanding of the mechanisms underlying the development of glomerulosclerosis and tubulointerstitial scarring. AII appears to play an important role in the pathogenesis of both; this may be because of either a direct proliferative and fibrogenic effect of AII or an indirect effect mediated by growth factors such as platelet-derived growth factor (PDGF) and transforming growth factor (TGF(beta1)). These findings have led to significant therapeutic advances as ACE inhibition prevents the progression of experimental renal scarring and attenuates the progression of chronic renal failure in humans. Benazepril, through its metabolite benazeprilat, is a non-sulfhydryl orally active ACE inhibitor. The kinetics of benazeprilat are substantially affected by severe renal impairment; for patients with a creatinine clearance of <30 ml/min the initial recommended daily dose is 5mg. The angiotensin converting enzyme inhibition in a progressive renal insufficiency (AIPRI) study confirmed that benazepril provides protection against the progression of renal insufficiency in patients with various renal diseases and that this treatment is well tolerated.