Sodium retention in nephrotic syndrome is due to an intrarenal defect: evidence from steroid-induced remission.

There is increasing evidence that the sodium retention of nephrotic syndrome is directly due to an intrarenal mechanism and not to a low blood volume stimulating the renin-angiotensin-aldosterone system. However the mechanism of the natriuresis that occurs during remission is not known. Patients with nephrotic syndrome were therefore studied during steroid-induced remission. At the onset of natriuresis, blood volume and plasma albumin were low and did not change. Plasma renin activity and plasma aldosterone were initially high and both fell during the natriuresis. At the end of the natriuresis when patients had lost their oedema, plasma renin activity and plasma aldosterone rose to high levels, plasma albumin and blood volume remained low, and yet the patients were no longer retaining sodium and were in sodium balance. These observations suggest that the natriuresis of remission is due to the correction of an intrarenal mechanism causing the sodium retention. This study raises two major unanswered questions. Firstly, when the presumed intrarenal mechanism is corrected, what tells the kidney to excrete large amounts of sodium when the blood volume remains low? Secondly, why do the patients come back into sodium balance when the blood volume is low, and plasma renin activity and plasma aldosterone are elevated?