Abstract
Over two decades have now passed since studies of bovine serum albumin (BSA) serum sickness in rabbits led to the hypothesis that glomerulonephritis associated with granular immune-complex deposits was mediated by glomerular trapping of circulating soluble immune complexes.1 , 2 This mechanism has since become widely accepted as the major process mediating immunologic renal disease in human beings.3 According to this theory, the presence in the circulation of an antigen complexed with specific antibody, coincident with the development in the glomerulus of granular deposits that contain the same antigen and antibody, demonstrates that passive entrapment of the circulating immune complexes caused the . . .