To investigate if the renal kallikrein-kinin system may be involved in the homeostasis of renal perfusion in cirrhosis, urinary kallikrein activity was measured in 11 normal subjects, 31 cirrhotics with ascites and preserved renal plasma flow (548.2 +/- 32.2 ml per min) and glomerular filtration rate (85.8 +/- 3.4 ml per min), and 18 cirrhotics with functional renal failure (renal plasma flow: 229.9 +/- 23.4 ml per min; glomerular filtration rate: 34.9 +/- 3.3 ml per min). Plasma renin activity, plasma norepinephrine concentration and the urinary excretion of prostaglandin E2 were also measured in these subjects. Cirrhotics without renal failure showed a significantly higher renin (4.9 +/- 1.1 ng per ml per hr), norepinephrine (458.2 +/- 50.4 pg per ml), urinary kallikrein (15.4 +/- 1.8 pkat per min) and urinary prostaglandin E2 (0.52 +/- 0.08 ng per min) than did normal subjects (1.08 +/- 0.1 ng per ml per hr, 218.1 +/- 18.2 pg per ml; 8.4 +/- 1.4 pkat per min and 0.24 +/- 0.02 ng per min, respectively). Cirrhotics with renal failure showed a significantly higher renin (16.1 +/- 3.4 ng per ml per hr) and norepinephrine (739.4 +/- 79.2 pg per ml), and a significantly lower urinary kallikrein (5.2 +/- 0.6 pkat per min) and urinary prostaglandin E2 (0.15 +/- 0.02 ng per min) than did normal subjects and cirrhotics without renal failure. Glomerular filtration rate correlated (p less than 0.001) with urinary kallikrein (r = 0.53), urinary prostaglandin E2 (r = 0.55), plasma renin (r = -0.41) and norepinephrine (r = -0.44).(ABSTRACT TRUNCATED AT 250 WORDS)