[Terminal complement complex (TCC) levels in urine in patients with renal diseases]

The terminal complement complex (TCC) has been reported to play an important role in the pathogenesis of proteinuria not only in experimental nephritis but also in human glomerulonephritis. In order to clarify the clinical significance of TCC, the author investigated a total of 129 pediatric patients with the following glomerular diseases: idiopathic nephrotic syndrome (INS; 40 cases), IgA nephropathy (IgAN; 48 cases), mesangio-capillary glomerulonephritis (MPGN; 16 cases), lupus nephritis (LN; 16 cases), purpura nephritis (5 cases) and membranous nephritis (4 cases). Results were analyzed in relation to the responsiveness to steroid treatment in INS and the degree of proteinuria and histopathologic severity in glonerulonephritis groups. In 40 patients who underwent renal biopsy, the localizations of vitronectin and clusterin, both of which are regulatory proteins for TCC, were examined by immunofluorescence microscopy in conjunction with that of TCC for the study of the mechanism of local defense in glomerulonephritis. The urinary TCC levels were elevated in 9 (90%) of 10 patients with steroid-resistant INS, while they were elevated only in 2 of 30 steroid-responsive patients. In glomerulonephritis groups, urinary TCC levels were elevated in 13 of 48 patients with IgAN, 6 of 16 with MPGN, 8 of 16 with LN, 2 of 5 purpural nephritis and 1 of 4 with membranous nephritis. Urinary TCC levels correlated with histological severity in IgAN and showed a reciprocal relation to C3 levels in MPGN and LN. Immunofluorescence findings showed that localization of TCC was quite similar to that of C3 in glomerulonephritis groups. Vitronectin and clusterin were also demonstrated to deposit in similar pattern to TCC. These results suggest that in INS urinary TCC levels could predict the responsiveness to steroid therapy and might be useful as a non-invasive diagnostic method in differential diagnosis of INS. In IgAN, urinary TCC could be a useful marker of histologic severity. The deposition of vitronectin and clusterin together with TCC in glomerulus suggests the possibility that vitronectin and clusterin play a role in reducing the formation of TCC in glomerular tissues.