Studies on experimental models of infections and observations in man indicate that immune complexes (IC) play an important role in the pathogenesis of nephropathies associated with malaria. All present evidence suggests that IC preformed in circulation localize in the glomeruli and initiate the lesions. In acute lesions, typical of falciparum infections in man, the depositions of IC are found quite soon after infection; glomerular injury is reversible, and these cases respond well to antimalarial therapy. Chronic lesions, typical for quartan malaria, are more progressive and do not respond to antimalarials. Deposits of IC in glomeruli have shown the presence of malarial antigens at the beginning, but the perpetuation of the lesions does not seem to be due to constant supply of malarial antigens. The possibility that malarial IC in these chronic lesions trigger a pathogenic sequence in which other mechanisms (perhaps autoimmune?) are later involved is discussed.
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