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The major pathogenetic mechanism of glomerulonephritis in SLE and in EMC is complement activation caused by immune complexes deposited in glomeruli. l Hypocomplementaemia and biopsy evidence of significant deposition of complement in glomeruli strongly support this. We postulated that amelioration of glomerulonephritis should occur if harmful complement activation is effectively inhibited. The complement-activation process is made up of cascade reactions of complement serine proteases (Clr, Cls, C2, and factors B and D), and we and others have demonstrated that nafamostat mesilate (6-arnidino-2-naphthyl-p-guanidinobenzoate dirnethanesulfonate) inhibits complement serine proteases. 2-4

In this study, we investigated the effectiveness of nafamostat mesilate in 5 patients with glomerulonephritis diagnosed by renal biopsy and clinical features: 3 patients had SLE and 2 had EMC. With informed consent, nafamostat mesilate was continuously infused into a central vein at 0 1-02 mg/kg per h for 14 days, and the serum complement components concentrations and the daily amount of urinary protein excreted were measured. All patients completed the study without any serious complications. As shown in the figure, the administration of nafamostat mesilate promptly