Plasma renin levels are dependant on both the rate of production of renin by kidney and heaptic inactivation. Several lines of evidence have suggested that hepatic clearance of renin is reduced in liver disease, but although a diminished hepatic extraction of renin
ate.
contributes to the elevated renin levels in liver disease, evidences indicate that this is not the major determinant of hypereninemia.
This study was undertaken to evaluate the responsiveness of renin to manipulation of posture and saline infusion in the setting of advanced liver disease. 46 male and 8 female cases were selected for study. Their ages ranged from 26 to 65 years. Group A included 7 normal subjects, Group B included 5 patints with fatty liver, Group C included 11 patients
with acute viral hepatitis, Group D included 10 patients with chronic persistent hepatitis, Group E included 4 patients with chronic active hepatitis, Group F included 7 patients with compensated liver cirrhosis, and G: oap G included 10 patients with decompensated liver cirrhosis. All cases of the Group C.D.E and 3 cases of Group F were diagnosed by liver biopsy.
The experimental protocol was as follows:
For basal renin activity, blood samples were drawn at 7 A.M. after overnight in supine position (Group j ). Thereafter lasix 40mg/1V was done and subjects were ambulated for 2 hours and blood sample was drawn in stand up position (Group i[ ), and then 0.9% NaCl were infused at a constant rate of 500ml/hour for 2 hour and blood samples were obtained every one hour (Group E, Group IV). In all groups the decrement rate of renin activity
Group R Group I (or IV)
was calculated as Group II x100. This index might be influenced by both hepatic clearance of renin and the suppressibility of renin secretion from the kidney.. The results were as follows.
Basal renin level is higher in decompensated liver cirhosis group comparing with other groups, but there is no difference of the increment of renin activity after stimulation
(Group 1l ) between decompensated liver cirrhosis group and the others. The decrement rate of renin activity after one hour suppression is lower in decompensated liver cirrhosis group than all other groups except control group and compensated liver cirrhosis group.
The decrement rate of renin activity after two hour suppression is lower in decompensated liver cirrhosis group than all other groups except control group. In all groups, there
is no significant difference between basal and post suppression: two hour renin activity. The 3
decrement rate of renin activity in overall subjects has the correlationship with serum j
alvumin level and prothrombintime but not with serum GPT and bilirubin level. 1
Above findings suggest that in decompensated liver cirrhosis group, basal renin activity is increased by the intrinsic stimuli of renin secretion which is not suppressed easily by position change or saline infusion, rather than disturbance of hepatic clearance of renin.
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