PARAMESANGIAL GLOMERULAR DEPOSITS IN MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS TYPE-II CORRELATE WITH HYPOCOMPLEMENTEMIA

To gain support for a previously proposed hypothesis that nephritic fa ctors predispose to chronic glomerulonephritis, the glomerular deposit s of patients with membranoproliferative glomerulonephritis type II ha ve been studied by electron microscopy and immunofluorescence and the results correlated with the C3 level at the time of biopsy. If, as hyp othesized, circulating convertase predisposes to nephritis, finding th at the glomeruli of patients hypocomplementemic at biopsy, presumably with nephritic factor-stabilized convertase in their circulation, diff er from those of patients normocomplementemic at biopsy would suggest that circulating convertase in some way alters the glomerulus. Among 2 5 biopsy specimens from 12 patients, hypocomplementemia did not correl ate with capillary loop deposits, but there was strong correlation wit h deposits in the paramesangial region as detected by electron microsc opy. Of 11 patients who were normocomplementemic at biopsy, none had p aramesangial deposits in their glomeruli. Of 14 patients who were hypo complementemic at biopsy, deposits were present in the paramesangium i n 12 patients (P <0.001). The deposits were either on both sides of th e paramesangial segment of the basement membrane (waist basement membr ane related) or in apposition to the paramesangial basement membrane i n a subepithelial position only. The detection of paramesangial deposi ts in the ultrastructure correlated with the detection of C3-containin g mesangial granules by immunofluorescence; immunoglobulin G, C5, prop erdin, and factor B could not be demonstrated in these granules. The s tudy identifies the mesangial deposits described by others in membrano proliferative glomerulonephritis type II as paramesangial deposits and , more importantly, demonstrates that their presence correlates closel y with hypocomplementemia. It is likely that these deposits in some wa y result from the presence in the circulation of convertase stabilized by the nephritic factor of the amplification loop. (C) 1995 by the Na tional Kidney Foundation, Inc.