Abstract
Immunofluorescent studies have suggested that immune complex deposition is the pathogenetic mechanism responsible for MGN and diffuse PGN. Despite this common mechanism, both renal disorders show considerable differences in the rate of progression of renal functional deterioration. To examine whether differences in the amounts of circulating immune complexes may in part be responsible for these differences, such complexes were assayed for in the sera of the two patient populations by a 1251-C1q binding assay, which has a lower limit of sensitivity for 75 microgram of aggregated human gamma globulin per milliliter of serum. Circulating complexes were found in sera from 11 of 14 patients with diffuse PGN but were undetectable in sera from 13 patients with MGN. Additional evidence for existing differences in the amounts of circulating immune complexes in the two groups was provided by serum C3 measurements. Serum C3 concentrations were below normal limits in nine of 14 sera from patients with diffuse PGN but were within normal limits for sera from all patients with MGN. Sucrose density gradient ultracentrifugation analysis of C1q reactive complexes showed them to have sedimentation coefficients ranging from 14.6S to 18.2S. The sizes of the complexes are consistent with those analyzed in animal models as being capable of inducing nephritis.