Sympathetic nervous activity, renin‐angiotensin system and renal excretion of prostaglandin E₂ in cirrhosis. Relationship to functional renal failure and sodium and water excretion

To investigate if functional renal failure in cirrhosis could be related to disturbances of vasoactive systems, plasma renin activity, plasma catecholamines and urinary prostaglandin E 2 (PGE 2 ) were determined in twenty‐two normal subjects and sixty‐five cirrhotics. Furthermore, in thirty‐three of these subjects, the effect of lysine‐acetylsalicylate (450 mg i.v.) on renal function was studied. Patients with ascites without renal failure showed higher renin, noradrenalin and urinary PGE 2 than normal subjects (5.9±0.8 v. 1.1±0.1 ng ml ‐1 h ‐1 , P < 0.001; 512 ± 39 v. 224±17 pg/ml, P < 0.001; and 603 ± 71 v. 377±36 ng/day, P < 005, respectively). Patients with functional renal failure showed higher ( P < 0001) renin (13.5±1.9) and noradrenalin (1114±134) and lower ( P < 005) urinary PGE 2 (199 ± 36) than normal subjects and cirrhotics without renal failure. On the whole, patients glomerular filtration rate correlated ( P < 0001) with urinary PGE 2 ( r = 0.55), renin ( r =‐0.52) and noradrenalin ( r =‐0.52). Lysine‐acetylsalicylate did not alter renal function in normal subjects and cirrhotics without ascites. However, it reduced water diuresis (8.8 ± 0.9–2.7 ± 0.5 ml/min) and sodium excretion (from 57.1 ± 13.9 to 3.9 ± 11 μmol/min) in all the nineteen cirrhotics with ascites studied and the glomerular filtration rate (95.4 ± 11.8–46.7 ± 9.5 ml/min) in eleven of these patients. Urinary PGE 2 decreased in all patients (3.13 ± 0.65–0.54 ± 0.11 ng/min). The study suggests that: (a) functional renal failure in cirrhosis with ascites may be a consequence of an imbalance between vasoactive systems, (b) renal prostaglandins are involved in the tubular handling of sodium and water in these patients.