Components of the renin-angiotensin-aldosterone system in plasma and ascites in hepatic cirrhosis.
Eur J Clin Invest
; 38(12): 939-44, 2008 Dec.
Article
em En
| MEDLINE
| ID: mdl-19021719
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.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.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Ascite
/
Sistema Renina-Angiotensina
/
Líquido Ascítico
/
Angiotensinogênio
/
Renina
/
Aldosterona
/
Cirrose Hepática
Idioma:
En
Ano de publicação:
2008
Tipo de documento:
Article