LACK OF EFFECT OF CAPTOPRIL ON THE SODIUM RETENTION OF THE NEPHROTIC SYNDROME

The mechanism of Na retention in the nephrotic syndrome remains controversial, though the classic pathophysiological explanation is stimulation of the renin-angiotensin-aldosterone system. Many patients with the nephrotic syndrome have a normal or low plasma renin activity suggesting that there might be an intrarenal cause for their Na retention. Captopril, an oral angiotensin-converting enzyme inhibitor, was given during 10 separate episodes of Na 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 Na and water and gain weight. This demonstrates that the sodium retention of nephrotic syndrome is not due to stimulation of the renin-anigotensin-aldosterone system, but must be due to some other mechanism, which is probably intrarenal.