[Secondary hyperaldosteronism in patients with liver cirrhosis, frequently caused by therapy].
Plasma angiotensin II and plasma aldosterone was measured by radioimmunoassay in 78 patients with cirrhosis of the liver (group I: untreated, without ascites, n = 21; group II:untreated, with ascites, n = 25; group III: with ascites, during saluretic therapy, n = 32). From the obtained results it was concluded: (1) Excluding any pretreatment on the outpatient basis in most cirrhotics with or without ascites unaltered plasma levels of angiotensin II and aldosterone were found. (2) In contrast to previous suggestion secondary aldosteronism seems to be a minor determinant of hepatic ascites formation. (3) In untreated patients the 24-h-urinary excretion of electrolytes (Na+/K+ less than 1) represents an insufficient index of hyperaldosteronism. Obviously the kidney retains considerable amounts of sodium independent of circulating aldosterone levels. (4) Far above other mechanism hyperaldosteronism is most often induced by saluretic treatment of ascites and edema. The increased aldosterone secretion might indicate an adaptation phenomenon to restore total body sodium content. Certainly, the established concept of ascites therapy remains unimpaired by this physiological reaction.
D000450:Aldosterone / Q000097:blood / Q000652:urine; D000804:Angiotensin II / Q000097:blood; D004039:Diet, Sodium-Restricted; D004232:Diuretics / Q000009:adverse effects / Q000627:therapeutic use; D005965:Glucuronates / Q000652:urine; D006801:Humans; D006929:Hyperaldosteronism / Q000209:etiology*; D008103:Liver Cirrhosis / Q000150:complications* / Q000378:metabolism / Q000628:therapy; D011188:Potassium / Q000652:urine; D012964:Sodium / Q000652:urine
D004232:Diuretics; D005965:Glucuronates; D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D011188:Potassium
Seikundärer Hyperaldosteronismus bei Patienten mit Leberzirrhose häufig therapeutisch induziert.