Renal Kallikrein Excretion in Cirrhotics with Ascites: Relationship to Renal Hemodynamics

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 rena 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 E 2 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 E 2 (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 E 2 (0.15 ± 0.02 ng per min) than did normal subjects and cirrhotics without renal failure. Glomerular filtration rate correlated (p < 0.001) with urinary kallikrein (r = 0.53), urinary prostaglandin E 2 (r = 0.55), plasma renin (r = ‐0.41) and norepinephrine (r = –0.44). These results suggest that renal kallikrein‐kinin system may be involved in maintenance of renal blood flow in cirrhosis with ascites, and that functional renal failure in these patients could be a consequence of impaired renal production of kallikrein and prostaglandins in the setting of activation of the renin‐angiotensin and sympathetic nervous systems.