Abstract
In order to investigate the role of local fibrinolytic activity of the kidney in the pathogenesis of glomerulonephritis and to clarify the basis of fibrinolytic therapy in the renal disease, cortical tissue plasminogen activator was examined by histochemical method in 111 cases with renal disease. Materials examined in renal disease included glomerulonephritis, nephrotic syndrome, systemic disease, etc. Relationship between tissue plasminogen activator and several parameters in coagulation-fibrinolysis system were also studied. The results obtained were as follows: 1. Higher f ibrinolytic activity was observed around cortical vessels and cortico-medullary junction. Lower activity was found around glomeruli. No fibrinolytic activity was found over cortical tubules. 2. Stronger fibrinolytic activity was observed in advanced glomerulonephritis than mild prolifenative glomerulonephritis and benign recurrent hematuria. Normal kidney and focal glomerulonephritis demonstrated weaker fibrinolytic activity than other glomerulonephritis. "Hemp-dialysis kidney" showedd the strongest fibrinolytic activity. 3. In the nephrotic syndrome, proliferativc change group and M. P. G. N. demonstrated stronger fibrinolytic activity than minimal change and membranous nephropathy. Cases with intra-glomerular fibrin deposit showed higher fibrinolytic activity than cases without it. 4. S. L. E, with nephrotic syndrome demonstrated stronger plasminogen activator than S. L. E without it. D. M nephropathy and E. P. H gestosis showed reduced plasminogen activator. 5. These results suggest that tissue plasminogen activator will increase in the glomerular proliferative lesion to remove the intra-glomerular fibrin deposit and play a role to reduce the glomerular injury. Thus, when plasminogen activator is in the process of consumption, glomerular injury willl progress by immunological mechanism and intra-glomerular coagulation. 6. In the treatment of renal disease, fibrinolytic therapy will be available for casee with persistent high plasminogen activator and declined tissue plasminogen activator. In practice, advanced glomerulonephritis, nephrotic syndrome with proliferative lesion, M. P. G. N and E. P. H gestosis will be a good indication for fibrinolytic therapy.
