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To evaluate renal terminal complement activation in patients with glomerular diseases, we measured terminal complement complexes (TCCs) in plasma and urine with sandwich enzyme-linked immunosorbent assay (ELISA) using a monoclonal antibody against a C9 neoepitope expressed on TCC and a polyclonal antihuman C7 antibody. TCCs were detectable in plasma but not in urine in most of normal controls. In plasma, TCC levels were elevated in 4 of 22 patients with lupus nephritis and in 6 of 12 with membranoproliferative glomerulonephritis. However all patients with IgA nephritis, focal glomerulosclerosis, idiopathic membranous nephritis and idiopathic minimal change nephrotic syndrome (MC) showed normal values. In urine, TCCs were detectable in almost all patients with heavy proteinuria (greater than or equal to 100 mg/ml) except MC. The TCCs present in urine were partially purified by gel filtration using Sepharose 6B and were found to contain C5, C6, C7, C8, C9 and S protein by ELISA. Although the molecular weight of TCC is similar to that of IgM, the fractional excretion rate of TCC was about 100 times higher than that of IgM. These results suggest that TCCs detectable in urine contain SC5b-9 complexes and are mostly of renal origin.

1. Minute but appreciable amounts of d-amino acids were detected in normal human plasma. 2. The content was significantly higher in an elderly population (age 76 ± 6 years, mean ± sd, n = 41) than in a younger group (age 42 ± 4 years, n = 26), i.e. 6.9 ± 4.8 nmol/ml (mean ± sd, range 0–18.8 nmol/ml) and 2.5 ± 1.8 nmol/ml (range 0–6.3 nmol/ml) for the elderly and the younger groups, respectively. 3. Elevation of plasma d-amino acid level was observed in a group of patients with renal disease (3.6–52.6 nmol/ml), in proportion to the serum level of creatinine (n = 50, r = 0.726, P < 0.001), β2-microglobulin (n = 34, r = 0.551, P < 0.005), and to glomerular filtration rate (n = 39, r = 0.556, P < 0.001).

One hundred and four Japanese patients with IgA nephropathy were typed for HLA-A, HLA-B, and HLA-C antigens, and 75 of them were tested for HLA-D region antigens. A significant association was found only with HLA-DR4 (corrected P