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ANTICOAGULANT THERAPY IN “ACUTE PROGRESSIVE” GLOMERULONEPHRITIS

6 azotemic patients in whom renal biopsy showed crescent formation, focal necrosis and fibrin deposition (“acute progressive” glomerulonephritis), were examined by plasma fibrinogen chromatography, a technique for quantifying fibrinogen/fibrin complexes, monomeric fibrinogen, and smaller fibrinogen derivatives in plasma. Serially, pathological concentrations of fibrinogen/fibrin complexes (> 20%) were invariably demonstrated, a finding indicative of intravascular fibrin deposition, presumably intraglomerular. Heparin followed by phenindione/dipyridamole therapy resulted in return of plasma fibrinogen chromatographic findings to normal. Therapy was continued for 2 years until, on termination, chromatographic findings remained normal. Serial renal evaluation by CIN, CPAH, 24-hour protein excretion and urinary sediments demonstrated substantial improvement in all patients by two months. In all cases, CIN was normal at one year and 2-year repeat biopsies showed apparent absence of active disease. In contrast, 2 patients with similar renal biopsy pathology did not demonstrate increased levels of fibrinogen complexes: these patients failed to respond to anticoagulant therapy. Our results suggest that “positive” plasma fibrinogen chromatographic findings are indicative of intrarenal fibrin deposition and that control of this process by long-term anticoagulant therapy is of clinical benefit.