To evaluate terminal
complement pathway activation in plasma from patients with
systemic lupus erythematosus (SLE) and primary glomerular diseases, we developed an
enzyme-linked
immunosorbent assay (ELISA) for measuring the terminal
complement complexes (TCC). The method is based on a sandwich technique using rabbit
antibodies against native human C5, C7 and C9. To avoid interference by native components, we equilibrated plasma specimens with 5%
polyethylene glycol buffer. The precipitates were measured by ELISA. TCC was detectable in all 14 normal controls (0.48 +/- 0.06 AU/ml; mean +/- s.e.m.). TCC levels were elevated in 18 of 54 patients with SLE (0.89 +/- 0.07 AU/ml; P less than 0.01) and in eight of 11 patients with
membranoproliferative glomerulonephritis (MPGN) (3.15 +/- 0.62 AU/ml; P less than 0.01). However, only one of six patients with
membranous nephropathy and none of 13 with mesangial proliferative
glomerulonephritis showed high values. In SLE, TCC was correlated with circulating
immune complexes and inversely with CH50, C3, C4, C5 and alternative complement pathway activity (AH50), and showed significantly high values even in normal CH50 cases (n = 34; P less than 0.01). In MPGN, TCC was inversely correlated with CH50, AH50, C3, C5 and C9. These results suggest that the classical pathway plays an important role for TCC generation in SLE and that the alternative pathway does in MPGN.