Effect of sodium depletion on urinary excretion of active and inactive kallikrein in glomerulonephritic patients.

To investigate the response of urinary active and inactive kallikrein excretion to sodium depletion in golmerulonephritic (GN) patients, we measured the excretion of urinary active and inactive kallikreins in 10 primary GN patients before and after a low sodium (17 mEq/day), constant potassium (40 mEq/day) diet. They ranged in age from 24 to 47 years with 7 men and 3 women. The etiology included 4 IgA nephropathy, 4 mesangial proliferative GN, 1 minimal change disease and 1 focal sclerosis. The active urinary kallikrein activity was measured by assay of its enzymatic activity on synthetic chromogenic substrate S-2266. The urinary inactive kallikrein excretion was determined indirectly by substracting active kallikrein activity from total kallikrein activity. The latter was measured after trypsin activation of inactive kallikrein. The results showed a significant increase in total and active urinary kallikrein excretion following a low salt diet. Yet, the inactive urinary kallikrein excretion and the ratio of active/total kallikrein excretion showed no significant change. There was no correlation between active and inactive urinary kallikrein excretion either before or after a low sodium, constant potassium diet. These findings suggest that the renal kallikrein-kinin system of GN patients responds normally to the stimulation of sodium depletion.