Urinary kallikrein in experimental renal disease.

Urinary kallikrein excretion was studied in two types of experimentally induced renal disease: anti-glomerular basement membrane nephritis (20 rats) and aminonucleoside nephrosis (five rats) with appropriate controls (23 rats) for a period of 6 to 9 weeks following disease induction. In both models there was a prompt significant decrease (p less than 0.01 - 0.001) in urinary kallikrein excretion associated with proteinuria but unrelated to urinary sodium and potassium excretion and urinary volumes. In antiglomerular basement membrane nephritis the fall in kallikrein excretion occurred within the first 24 hours concurrent with the onset of proteinuria. In aminonucleoside nephrosis the decrease antedated the onset of proteinuria by 48 hours beginning within the first 24 hours following injection of the aminonucleoside. Kallikrein inhibitors were not demonstrable in the urines of diseased animals from either model. The mechanism of the decrease in kallikrein excretion in immune and nonimmune glomerular disease associated with proteinuria is unknown.