Ultrastructural Localization of the Membrane Attack Complex of Complement in Human Renal Tissues

Ronald J. Falk, Susan P. Sisson, Agustin P. Dalmasso, Youngki Kim, Alfred F. Michael, Robert L. Vernier

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Utilizing a monoclonal antibody (Poly C9-MA) to a neoantigen of the C9 portion of the membrane attack complex of complement (MAC), immunoelectron (IEM) and immunofluorescent (IF) microscopy were performed on kidney tissue from normal humans and patients with insulin-dependent diabetes mellitus (IDDM) and type II membranoproliferative glomerulonephritis (MPGN II). Comparative studies were conducted using polyclonal antibodies to human C3, C5, IgG, IgA, and IgM. In normal human tissue, there was a close correlation between increasing chronologic age and the quantity of MAC deposited in the mesangial stalk, along the interstitial aspect of and within tubular basement membranes (TBMs) and in arteriolar walls. IF of kidney tissues from 12 patients with IDDM with varying degrees of mesangial expansion and glomerulosclerosis demonstrated a direct relationship between the degree of tissue damage and the amount of MAC deposited in the mesangium. IEM of three normal and four diabetic specimens revealed reaction product of Poly C9-MA on linear and circular membranous structures within the mesangium, TBMs, and vessel walls, and within the glomerular basement membranes (GBMs) in diabetic subjects. Evidence is presented that these structures, which have been previously described by routine electron microscopy, represent cellular debris in these loci on which Poly C9-MA has been deposited. In MPGN II, Poly C9MA and C3 were distributed within subepithelial deposits, along either side of the dense deposits (DDs) within the GBMs and TBMs, and around circular masses of DDs within the mesangium. These studies document the ultrastructural distribution of Poly C9-MA in aging normal and diseased human kidney. With aging and in diabetes, we speculate that the MAC may participate in cellular turnover, a process accelerated by progressive renal disease.

Original languageEnglish (US)
Pages (from-to)121-128
Number of pages8
JournalAmerican Journal of Kidney Diseases
Issue number2
StatePublished - 1987

Bibliographical note

Funding Information:
From the Department of Pediatrics, Laboratory Medicine, alld Pathology, University of Minnesota Medical School, and Veterans Administration Hospital, Minneapolis. Supported by grants from the National Institutes of Health (All 0704, AM25518, AM26149), the Viking Children's Fund, and with the support of the lilriety Club of the Northwest. A portion of this manuscript was presented at the 1983 meetings of the Federation of American Societies for Experimental Biology Dr Falk is currently a member of the Division of Nephrology at the University of North Carolina, Chapel Hill. Address reprint requests to Robert L. Vernier, MD, Box 491, Department of Pediatrics, University of Minnesota, Minneapolis, MN 55455. © 1987 by the National Kidney Foundation, Inc. 0272-6386/87/0902-0005$03.00/0


  • Membrane attack complex
  • human kidney
  • immunoelectron microscopy


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