[Role of secondary hyperaldosteronism in the pathomecanism of hydropic decompensation in the cirrhotic patient (author's transl)].

Plasma aldosterone levels before and after walking were compared in a series of 10 controls and 41 patients with cirrhosis of the liver. The latter were distributed in the following way: 8 had compensated cirrhosis, the remaining 33 were in a situación of hydropic decompensation, 10 with associated renal insufficiency, and 23 without. Basal aldosterone levels in compensated cirrhotics were similar to those of the controls, but these values increased significantly more than the controls following postural stimulation. Decompensated cirrhotics without renal insufficiency had significantly higher values than the controls, both in basal conditions and after stimulation. The highest values corresponded to the decompensated cirrhotic patients with renal insufficiency who were in advanced stages of liver disease. On the basis of the present findings and those of other authors, it is suggested that a certain reduction in the metabolic clearance of aldosterone appears to exist in hepatic cirrhosis. However, hormonal hyperproduction is the dominant factor in the pathogenic mechanism of secondary hyperaldosteronism. The pathogenesis of the excessive production of hormone is discussed. In conclusion, it appears that the scant affluence of sodium to the macula densa may be the primary factor in explaining this common situation in patients with cirrhosis of the liver.