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Components of the renin‐angiotensin‐aldosterone system in plasma and ascites in hepatic cirrhosis
Author(s) -
Kuiper J. J.,
Boomsma F.,
Van Buren H.,
De Man R.,
Danser A. H. J.,
Van Den Meiracker A. H.
Publication year - 2008
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2008.02044.x
Subject(s) - ascites , medicine , plasma renin activity , renin–angiotensin system , endocrinology , aldosterone , cirrhosis , albumin , chemistry , in vitro , blood pressure , biochemistry
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.