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Membrane attack complex deposition in experimental glomerular injury.

D T Perkinson, P J Baker, W G Couser

    The American Journal of Pathology
    |July 1, 1985
    PubMed
    Summary
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    The terminal complement system

    Area of Science:

    • Nephrology
    • Immunology
    • Pathology

    Background:

    • The complement system (C) significantly contributes to glomerular injury.
    • Terminal C components, forming the membrane attack complex (MAC), may mediate cell-independent injury.
    • Investigating MAC's role in various renal injury models is crucial.

    Purpose of the Study:

    • To investigate the role of the membrane attack complex (MAC) in mediating glomerular injury.
    • To determine the correlation between MAC deposition and complement's pathogenetic role in experimental renal diseases.

    Main Methods:

    • Utilized rat models of immunologic renal injury.
    • Employed immunofluorescence to detect MAC neoantigens in glomeruli.
    • Assessed proteinuria and glomerular deposits of IgG, C3, and MAC.

    Related Experiment Videos

  • Used complement depletion with cobra venom factor (CVF).

    • Main Results:

    • MAC deposits were found in passive and active Heymann nephritis, correlating with proteinuria.
    • Complement depletion (CVF) reduced proteinuria and MAC deposition in passive Heymann nephritis.
    • MAC was absent in anti-GBM nephritis and aminonucleoside-induced proteinuria.
    • MAC deposits were present in sclerotic areas of chronic passive Heymann nephritis.

    Conclusions:

    • Glomerular MAC deposition correlates with the pathogenetic role of complement in renal injury.
    • These findings support a role for the membrane attack complex in mediating various forms of glomerular injury.