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The course of mercuric chloride-induced immune glomerulonephritis is characterized by complement activation, intensive proteinuria, linear and then granular IgG and C3 deposits in the glomeruli. To assess the role of complement activation in the occurrence of the disease, decomplementation was achieved by intravenous injections of cobra venom factor in rats injected with mercuric chloride. In these animals, proteinuria still appeared while rats were decomplemented by cobra venom factor through the alternative pathway. These rats exhibited linear IgG deposits without detectable C3 deposits. In the rats injected with cobra venom factor alone, no proteinuria, no classical pathway complement activation and no renal IgG or C3 deposits were observed. Therefore, in Brown-Norway rats intoxicated with mercuric chloride, proteinuria appears to be at least in part complement independent.
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