Role of terminal complement pathway in the heterologous phase of antiglomerular basement membrane nephritis

Groggel, Gerald C.; Salant, David J.; Darby, Christine; Rennke, Helmut G.; Couser, William G.
April 1985
Kidney International;Apr1985, Vol. 27 Issue 4, p643
Academic Journal
Terminal complement components, including the membrane attack complex, have been demonstrated in glomeruli of patients with immune complex and anti-GBM nephritis. We recently demonstrated the functional significance of C6 in the mediation of experimental membranous nephropathy in rabbits. In the present study, the role of C6 was examined in the heterologous phase of rabbit anti-GBM nephritis by studying normal and C6-deficient (C6D) rabbits. In C6D rabbits, C6 hemolytic activity was less than 0.01% of control. All control rabbits became heavily proteinuric in the first 24 hr following injection of a standard dose of sheep anti-rabbit GUM antibody (mean, 42.0 ± 26.3: range, 18.4 to 83.5 mg protein/mg creatinine, N = 5). In contrast, C6D rabbits excreted a mean of only 5.1 ± 5.5 mg/mg creatinine (range, 0.06 to 18.4, N = 6, P = 0.002). Protein excretion in normal rabbits was less than 0.06 mg/mg creatinine. Both control and C6D rabbits had similar deposits of sheep anti-rabbit GUM IgG in glomeruli when measured by radiolabeling techniques (control 15.8 ± 2.71, N = 5;C6D 18.7 ± 1.99 μg of sheep IgG/104 gomeruli, N = 6, P > 0.05). Control rabbits had a greater rise in serum creatinine in the first 24 hr (1.74 ± 1.15 vs. 0.53 ± 0.44 mg/dl, P < 0.05). Both groups had similar deposits of sheep IgG and rabbit C3 by IF. By light microscopy at 4 and 24 hr. both groups had qualitatively similar proliferative changes and similar numbers of neutrophils infiltrating glomeruli. C6 is critical in the mediation of proteinuria and decreased renal function in the heterologous phase of anti-GBM nephritis in rabbits thus demonstrating a requirement for this terminal complement component for full expression of this form of glomerular injury.


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