We examined 25 renal-biopsy specimens to determine whether there is a relation between immunologically mediated renal disease and the activity of complement receptors that selectively bind antigen-antibody complexes containing activated third component of complement (C3b). These receptors have been termed glomerular complement receptors. Renal lesions associated with in vivo deposition of C3 were associated with a loss of receptor sites as demonstrated by reduced or absent in vitro binding of C3b-coated test reagents by glomerular complement receptor. These findings suggest that binding of complement containing immune complexes to glomerular complement receptors in human subjects may participate in the immuno-pathologic processes of certain immune-complex-mediated renal diseases. (N Engl J Med 295:10-14, 1976). Many immunologically mediated renal diseases result from the deposition of antigen-antibodycomplement complexes within the glomerular capillary wall, frequently in a subepithelial position.12The precise mechanism whereby these immune complexes become deposited, however, remains unknown. Theories to date have generally ascribed a relatively nonspecific role to the glomerular capillary loop, suggesting that complexes arriving at the glomerulus via the renal circulation are coincidentally deposited in a passive fashion in the capillary wall by virtue of its filtering action. Other factors such as capillary-wall permeability and the structure, size and concentration of complexes in the renal circulation have been reported to contribute.
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