Components of the renin-angiotensin-aldosterone system in plasma and ascites in hepatic cirrhosis

Background: Decompensated liver cirrhosis is characterized by activation of the renin-angiotensin-aldosterone system (RAAS). We investigated whether compartmentalization of these components occurs in ascitic fluid. Methods: In 26 patients with cirrhosis RAAS components and albumin were quantified in simultaneously obtained plasma and ascitic fluid samples. Renin degradation was determined in vitro in plasma and ascites. Results: Plasma angiotensinogen was below normal reference values in all but two patients and correlated inversely with plasma renin (r = -0·73, P < 0·001). Plasma renin activity was elevated in most subjects. The plasma and ascites concentrations of renin, prorenin, angiotensinogen and aldosterone were closely (P < 0·001) correlated. Expressed as a percentage of plasma levels, the angiotensinogen level (18 ± 11%) was slightly lower than the albumin level (23 ± 8%), whereas the aldosterone level (43 ± 18%) was considerably higher (P < 0·0001). For renin and prorenin these percentages were much lower (P < 0·0001), despite the fact that their molecular weight is lower than that of albumin and angiotensinogen. This was not due to a more rapid degradation of renin in ascites fluid, since the in-vitro degradation rates of renin in plasma and ascitic fluid were identical. Conclusion: In hepatic cirrhosis ascites can be regarded as an ultrafiltrate of plasma RAAS components. Since differences in molecular weight or metabolic rate cannot explain the low ascites-to-plasma ratio of renin and prorenin, either their transcapillary transport is impaired and/or they selectively bind to (pro)renin binding sites.

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