The fibrinolytic enzyme system of the rat: the effect of aminonucleoside-induced nephrotic syndrome.

Components of the fibrinolytic enzyme system were studied in rats rendered nephrotic by means of aminonucleoside of puromycin. At the peak of the disease fibrinolytic activity was greatly decreased and this was due to decreased plasminogen and increased plasma antiplasmins. Plasma fibrinogen was also increased. Plasma activator levels remained relatively constant but there was a marked increase in urokinase excretion. These changes could be explained from the loss of plasma proteins and abnormal protein metabolism associated with the nephrotic syndrome. Increases in plasma lipoproteins partly accounted for the increase in antiplasmins. Despite the profound alterations to fibrinolytic components there was no evidence of increased intravascular fibrin deposition. This evidence does not support the theory that fibrinolysis is essential in the maintenance of a fibrinfree vascular tree.