The mechanism of sodium retention in the nephrotic syndrome remains controversial, though the classic pathophysiological explanation is stimulation of the renin-angiotensin-aldosterone system. Recent evidence has shown that many patients with the nephrotic syndrome have a normal or low plasma renin activity suggesting that there might be an intrarenal cause for their sodium retention. We gave captopril, an oral angiotensin-converting enzyme inhibitor, during 10 separate episodes of sodium retention in nephrotic syndrome. There was evidence of stimulation of the renin system in 7 of these episodes. Despite a marked fall in plasma aldosterone, all patients continued to retain sodium and water and gain weight. This demonstrates that the sodium retention of nephrotic syndrome is not due to stimulation of the renin-angiotensin-aldosterone system, but must be due to some other mechanism, which is probably intrarenal.