Evidence that some mechanism other than the renin system causes sodium retention in nephrotic syndrome.
8 of 16 patients with nephrotic syndrome had normal or low plasma renin activity while spontaneously retaining sodium. The other 8 patients had a high plasma renin activity which may have caused the sodium retention. Oral captopril and albumin infusion given separately both suppressed the renin system in these patients. Despite this, urinary sodium excretion remained less than sodium intake and patients continued to retain sodium and gain weight. These results suggest that, even in patients with nephrotic syndrome who do have stimulation of the renin angiotensin system, some other overriding mechanism is responsible for sodium retention. Therefore it seems unlikely that angiotensin-converting enzyme inhibitors will be useful in the treatment of sodium retention in nephrotic syndrome.
D000293:Adolescent; D000328:Adult; D000368:Aged; D000418:Albumins / Q000008:administration & dosage; D001810:Blood Volume; D001834:Body Water / Q000378:metabolism; D001835:Body Weight; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use; D004487:Edema / Q000209:etiology*; D005260:Female; D006801:Humans; D007668:Kidney / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000378:metabolism* / Q000503:physiopathology; D010953:Plasma Volume; D012083:Renin / Q000097:blood*; D012084:Renin-Angiotensin System / Q000187:drug effects; D012964:Sodium / Q000378:metabolism*
D000418:Albumins; D002216:Captopril; D012964:Sodium; D012083:Renin