Proteinuria due to non-steroid-responsive renal disease may be harmful. Firstly, because it may cause a nephrotic syndrome, and, secondly, because it is, like hypertension, associated with an increased risk of progressive renal damage and loss of renal function over the years. Until recently, only non-steroidal antiinflammatory drugs (NSAIDs) were available to reduce proteinuria in such patients. Due to their potential side-effects, however, NSAIDs have never been widely used as antiproteinuric agents. In 1985 some studies were published showing that inhibition of angiotensin-converting enzyme (ACE) not only reduced the elevated blood pressure in rats with chronic renal failure (experimentally induced by renal ablation or by induced diabetic nephropathy), but also prevented the development of glomerular damage with proteinuria and loss of renal function in these animals. This beneficial effect of ACE inhibition was attributed to the prevention of glomerular hypertension. At the same time it was reported that ACE inhibition could reduce proteinuria in patients with advanced diabetic nephropathy. ACE inhibitors might thus be an attractive alternative for NSAIDs as antiproteinuric treatment, possibly being renoprotective, and being generally well-tolerated.