[The renin-angiotensin-aldosterone system in liver cirrhosis]

The role of the RAA system in the genesis of ascites in liver cirrhosis patients is not yet perfectly clear. The present study was conducted on 176 cirrhosis patients in order to investigate RAA system function, to assess the changes taking place in the various stages of the disease and to correlate such changes with the various kidney function parameters. The patients were divided into 3 groups as follows: Group I: patients without ascites on admission and with no history of the condition; Group 2: patients with ascites of recent onset and/or response to diuretic treatment; Group 3: patients with ascites not responsive to diuretic treatment. In Group 1, 19 patients (38%) reveal a significant reduction in renin activity together with portal hypertension and increased hydrosaline retention. In Group 2 renin activity was reduced in 4 patients (6%), aldosterone activity in 3 (4%). Progressive deterioration in liver function parameters and progressive activation of the RAA system combined with reduced sodiuria content were found in over 50% of these patients. The presence or absence of portal hypertension in this group was not related to significant changes in diuresis or sodiuria. In Group 3 renin was activated in 54 patients (89%), aldosterone in 58 (95%) and there was also a distinct reduction in sodiuria (96% of patients) and chloruria (100%). A substantial increase was also noted in the incidence of low blood sodium (53%) while portal hypertension was found in 97% of patients. On the basis of those data it may be hypothesised that high pressure inside the liver creates the stimulus for primary sodium retention. The decrease in effective blood volume after vasodilation, accentuated by low blood albumin and splanchnic venous stagnation may the stimulate the sympathetic nervous system and RAA system. Hyperaldosteronism only becomes the dominant factor in renal imbalance when the cirrhosis reaches the resistant ascites phase.