L. G. Hunsicker, F.A.C.P.; S. Ruddy, M.D.; C. B. Carpenter, M.D.; J. P. Merrill, F.A.C.P.; H. J. Muller-Eberhard, M.D.; K. F. Austen, F.A.C.P.
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Observations of circulating factors that destroy the third component of complement (C3) and of circulating split products of C3 suggest the depressions of serum C3 found in membranoproliferative glomerulonephritis are caused by activation with hypercatabolism. Complement (C3) can be activated either by the classical early complement components (Cl, C4, C2) or via the alternate complement pathway, utilizing the C3 proactivator (C3PA). Serum levels of C4 and C3PA have been measured by radial immunodiffusion in 18 patients with chronic hypocomplementemic (low C3) nephritis, to evaluate the participation of the classical and alternate pathways. Levels of C4 were uniformly normal. The C3PA
Hunsicker LG, Ruddy S, Carpenter CB, et al. Hypercatabolism of Third Complement Component (C3) in Chronic Glomerulonephritis: Role of the Alternate Complement Pathway.. Ann Intern Med. 1972;76:874. doi: https://doi.org/10.7326/0003-4819-76-5-874_3
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Published: Ann Intern Med. 1972;76(5):874.
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