Glomerular C3 receptors in human renal disease.
The relationship between glomerular C3 receptor activity and intraglomerular C3 deposition was studied in 73 cases of various forms of renal disease. C3 receptor activity was measured by enumeration of complement-coated sheep red blood cells (IgM EAC) that adhered to glomeruli in frozen sections and expressed as a percentage of the mean number present in control kidneys. Adjacent sections were studied for the presence and distribution of C3 deposits. The precise location of corresponding dense deposits was determined through 1-mu sections or electron micrographs. Marked depression of C3 receptor activity was found in most cases in which there was accumulation of C3 along the glomerular basement membrane, irrespective of whether the deposits were in a subepithelial, intramembranous, or subendothelial location. In contrast, when C3 was not detectable or was found exclusively in the mesangium, C3 receptor activity was affected only moderately, if at all. These data are consistent with the hypothesis that the interaction of C3 with podocytes is a major determinant in the loss of C3 receptor activity in glomerular disease, but do not exclude the possibility that interaction with mesangial or endothelial cells may also influence C3 receptor activity.
D000230:Adenocarcinoma / Q000276:immunology* / Q000473:pathology; D001485:Basement Membrane / Q000276:immunology; D003176:Complement C3 / Q000378:metabolism; D006801:Humans; D007075:Immunoglobulin M / Q000032:analysis; D066298:In Vitro Techniques; D007674:Kidney Diseases / Q000276:immunology* / Q000473:pathology; D007678:Kidney Glomerulus / Q000276:immunology* / Q000473:pathology / Q000648:ultrastructure; D007680:Kidney Neoplasms / Q000276:immunology* / Q000473:pathology
D003176:Complement C3; D007075:Immunoglobulin M