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A model of antiglomerular basement membrane nephritis in the rat was used to elucidate the origin of urinary fibrin-fibrinogen-related antigen (FRA). The intrarenal distribution and excretion of 125I-rat fibrinogen was examined to determine whether there was increased filtration of bibrinogen or fibrin degradation products (FDP) or lysis of intraglomerular fibrin. 125I-protein appeared in the urine immediately after injection of 125I-fibrinogen and fell in parallel with the fall in plasma 125I-fibrinogen. Renal retention of 125I-fibrin averaged less than 0.2 percent of the administered dose of 125I-fibrinogen. The infusion of epsilon aminocaproic acid (EACA) had no significant effect on either FRA excretion or 125I-protein excretion. Plasma FDP levels and the elution patteren of 125I-protein from the urine were not significantly changed by EACA infusion. These observations support the view that ruinary FRA excretion in glomerulonephritis is derived predominantly from increased filtration of plasma fibrinogen rather than from breakdown of intraglomerular fibrin.

Long-term anticoagulation therapy was evaluated in two patients with renal vein thrombosis and the nephrotic syndrome. Neither patient exhibited peripheral thromboemboli. Moreover, the renal vein thrombus resolved in both cases after eight months on a regimen of oral anticoagulant therapy. Glomerular filtration rate remained stable despite persistence of the nephrotic syndrome. These results suggest that long-term anticoagulation may be of distinct value in nephrotic patients with renal vein thrombosis.

The renal insufficiency which has been described in some of Legionnaires' Disease, has not been characterized. We describe a patient who developed severe oligoanuric renal failure associated with Legionnaires' Disease. Renal biopsy revealed acute tubular necrosis.

The effect of heparin on the development and progression of a form of antiglomerular basement membrane nephritis was examined in the rat. Animals which received heparin before and throughout the period of immunological insult developed lesions which were as severe, and perhaps more severe, than rats which did not receive heparin. Inulin clearances were lower in heparin-treated animals than in untreated rats. Animals in both groups exhibited renal fibrin-fibrinogen deposition and had increased rates of urinary fibrin-fibrinogen related antigen excretion. These results indicate that heparin per se has no beneficial effect on the development of this form of glomerulonephritis in this species.

Idiopathic crescentic glomerulonephritis is associated with a 70% to 80% incidence of end-stage renal failure. Oral corticosteroid therapy in combination with immunosuppressive agents or anticoagulants has not altered the prognosis of this disease. We have seen five adults with idiopathic crescentic glomerulonephritis and treated them with intravenous methylprednisolone. Before therapy, the average serum creatinine concentration was 7.4 +/- 1.3 mg/dL (chi-square +/- SEM). This value declined to 2.0 +/- 0.48 mg/dL within 4 weeks. All patients continue to maintain stable renal function over an average follow-up period of 19 months (range 1.5 to 36 months). These data suggest that a prospective controlled trial of this therapy is warranted in the management of this entity.