Renin-angiotensin-aldosterone system in cirrhosis.
According to traditional concepts, ascites formation and portal hypertension in cirrhosis lead to a deficit in the 'effective' extracellular fluid (ECF) and blood volumes respectively. The renin-angiotensin-aldosterone (RAA) system is thus stimulated and the kidneys retain fluid as a homeostatic mechanism to restore the ECF and blood volumes. Recent studies, however, show that approximately two-thirds of patients with ascites do not have a stimulated RAA system and in those without clinical evidence of fluid retention the RAA system is actually suppressed. These findings are incompatible with the concepts of reduced effective ECF and blood volumes. Despite the fact that most patients retaining sodim and accumulating ascites have a normal plasma aldosterone concentration, other evidence strongly suggests a dominant role for aldosterone in the regulation of renal sodium excretion. There might therefore be an increased renal tubular sensitivity to aldosterone in cirrhosis. For the one-third of patients with ascites  who do have a stimulated RAA system this may well be a response to reduced effective ECF and/or blood volumes in accord with traditional concepts.
D058186:Acute Kidney Injury / Q000209:etiology; D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000378:metabolism*; D001201:Ascites / Q000209:etiology; D001810:Blood Volume; D004487:Edema / Q000209:etiology; D005110:Extracellular Space / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D008103:Liver Cirrhosis / Q000150:complications / Q000378:metabolism*; D012083:Renin / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism
D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D012083:Renin