Studies of serum complement in the hypocomplementaemic nephritides.

摘要: The sera from forty patients with mesangiocapillary glomerulonephritis (MCGN), fifty-two acute (AGN) and twenty-five the nephritis of systemic lupus erythematosus (SLE) were examined for concentrations C1q, C4, C3, C5, C6, C7, glycine-rich beta glycoprotein (GBG) properdin, their ability to generate cobra factor-dependent convertase, presence C3 splitting activity. Two types activity found. first, which caused breakdown in normal human serum Mg2+–EGTA, was MCGN a minority AGN. second, failed break down either Mg2+–EGTA or EDTA, found SLE In AGN low values C1q C4 found, there significant correlation between these components, suggesting activation classical pathway. much greater reduction observed. Significant GBG each disease and, SLE, C3. overall reductions properdin levels good whereas MCGN, although five had no properdin. These data suggest that complement is activated via C3b-feedback pathways but do not provide evidence role causing hypocomplementaemia MCGN. The two histological variants differ concentrations; intramembranous deposits lower concentration those subendothelial concentration, different pathogenetic mechanisms MCGN.