title: Components of the renin-angiotensin-aldosterone system in plasma and ascites in hepatic cirrhosis.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Dept of Gastroenterology & Hepatology, Division of Pharmacology, Vascular and Metabolic Diseases, Erasmus Medical Centre, Rotterdam, The Netherlands.
authors.forename: J J
authors.initials: JJ
authors.lastname: Kuiper
authors.forename: F
authors.initials: F
authors.lastname: Boomsma
authors.forename: H
authors.initials: H
authors.lastname: van Buren
authors.forename: R
authors.initials: R
authors.lastname: de Man
authors.forename: A H J
authors.initials: AH
authors.lastname: Danser
authors.forename: A H
authors.initials: AH
authors.lastname: van den Meiracker
mesh_terms: D000368:Aged; D000450:Aldosterone / Q000097:blood* / Q000378:metabolism; D000808:Angiotensinogen / Q000097:blood* / Q000378:metabolism; D000809:Angiotensins / Q000097:blood; D001201:Ascites / Q000378:metabolism*; D001202:Ascitic Fluid / Q000378:metabolism*; D005260:Female; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010949:Plasma; D012083:Renin / Q000097:blood* / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*
chemical_list: D000809:Angiotensins; D000808:Angiotensinogen; D000450:Aldosterone; D012083:Renin