Paramesangial glomerular deposits in membranoproliferative glomerulonephritis type II correlate with hypocomplementemia.

To gain support for a previously proposed hypothesis that nephritic factors predispose to chronic glomerulonephritis, the glomerular deposits of patients with membranoproliferative glomerulonephritis type II have been studied by electron microscopy and immunofluorescence and the results correlated with the C3 level at the time of biopsy. If, as hypothesized, circulating convertase predisposes to nephritis, finding that the glomeruli of patients hypocomplementemic at biopsy, presumably with nephritic factor-stabilized convertase in their circulation, differ from those of patients normocomplementemic at biopsy would suggest that circulating convertase in some way alters the glomerulus. Among 25 biopsy specimens from 12 patients, hypocomplementemia did not correlate with capillary loop deposits, but there was strong correlation with deposits in the paramesangial region as detected by electron microscopy. Of 11 patients who were normocomplementemic at biopsy, none had paramesangial deposits in their glomeruli. Of 14 patients who were hypocomplementemic at biopsy, deposits were present in the paramesangium in 12 patients (P < 0.001). The deposits were either on both sides of the paramesangial segment of the basement membrane (waist basement membrane related) or in apposition to the paramesangial basement membrane in a subepithelial position only. The detection of paramesangial deposits in the ultrastructure correlated with the detection of C3-containing mesangial granules by immunofluorescence; immunoglobulin G, C5, properdin, and factor B could not be demonstrated in these granules. The study identifies the mesangial deposits described by others in membranoproliferative glomerulonephritis type II as paramesangial deposits and, more importantly, demonstrates that their presence correlates closely with hypocomplementemia. It is likely that these deposits in some way result from the presence in the circulation of convertase stabilized by the nephritic factor of the amplification loop.