THE ROLE OF COAGULATION AND FIBRINOLYSIS IN THE DEVELOPMENT OF RABBIT MASUGI NEPHRITIS

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Abstract
Fibrinolytic activity of urine decreased rapidly to the minimum values at the peak of the disease. Histologic observations showed a severe proliferative glomerulonephritis. Immunofluorescent studies revealed localization of rabbit .gamma.-globulin along the glomerular basement membrane in a typical linear pattern. Fibrin was positive in glomeruli not only within fibrinoid deposits, but also often diffusely in the places where no obvious fibrin was detected in histologic sections. Bright strands of fibrin were present between the cells forming a crescent. EM indicated accumulation of fibrinoid materials beneath the endothelium. The basement membrane was damaged by the deposition of fibrinoid and followed by massive escape of intracapillary contents into the Bowman''s space. Abundant fibrin and fibrinoid were seen in newly formed monocytic-epithelial crescents. Todd''s fibrinolysis autography revealed diminished fibrinolytic activity in the severely affected glomeruli. Treatment with heparin prevented crescent formation and glomerular disorganization, while treatment with t-AMCHA [tranexamic acid] increased fibrin and fibrinoid deposition and aggravated the glomerular injuries. The coagulation-fibrinolysis system may play an important role in the course of rabbit Masugi nephritis.