Abstract
Experimental studies have provided evidence that activation of the renin-angiotensin system plays a crucial role in the development and progression of glomerulosclerosis, i.e., the structural equivalent of progressive renal failure. Results of studies in animals, and later in patients with renal failure, documented that angiotensin converting enzyme (ACE) inhibitors exert a specific nephroprotective action: they decrease proteinuria and slow progression more than can be explained solely by their effect on blood pressure. These effects are observed even at doses that do not cause a decrease in systemic blood pressure. Recent controlled studies have shown that ACE inhibitors attenuate proteinuria and progression of renal disease in diabetic and non-diabetic renal disease to a greater extent than other antihypertensive drugs. Thus, ACE inhibitors should be regarded as the treatment of choice in diabetic nephropathy and chronic renal failure of non-diabetic origin, even for normotensive patients.