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Related Experiment Videos

Localization of the membrane attack complex (MAC) in experimental immune complex glomerulonephritis.

D Koffler, G Biesecker, B Noble

    The Journal of Experimental Medicine
    |June 1, 1983
    PubMed
    Summary

    The membrane attack complex (MAC) contributes to kidney damage in immune complex glomerulonephritis by injuring the glomerular basement membrane and podocyte membranes. Its role in tubular basement membrane injury also suggests broader involvement in renal pathology.

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    Area of Science:

    • Nephrology
    • Immunology
    • Pathology

    Background:

    • Immune complex glomerulonephritis involves complement system activation.
    • The membrane attack complex (MAC) is a terminal product of complement activation.
    • Its precise role in mediating renal tissue injury is not fully elucidated.

    Purpose of the Study:

    • To evaluate the role of the MAC in mediating renal tissue injury in a rat model of bovine serum albumin (BSA)-induced immune complex glomerulonephritis.
    • To investigate the localization and distribution of the MAC within the glomerulus and tubulointerstitium.

    Main Methods:

    • Immunofluorescence microscopy to detect IgG, BSA, C3, and MAC deposits.
    • Immunoelectron microscopy to visualize ultrastructural localization of immune deposits and MAC.

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  • Morphological assessment of glomerular and tubular basement membranes and podocytes.

    • Main Results:

    • Concurrent deposits of IgG, BSA, C3, and MAC were found along glomerular capillary walls, with MAC showing a more restricted distribution.
    • MAC was localized within subepithelial and subendothelial dense deposits, and co-localized with fused podocyte foot processes.
    • IgG and C3 were found in tubulointerstitial regions, with C3 prominent in the tubular basement membrane (TBM) and scant MAC deposits.

    Conclusions:

    • The MAC is implicated as a mediator of glomerular basement membrane (GBM) and podocyte membrane injury, disrupting the glomerular filtration barrier.
    • Evidence suggests the MAC is associated with injury to the GBM, visceral epithelial foot process membranes, and the TBM.
    • Both immune and non-immune processes may contribute to extraglomerular lesions, with the MAC potentially playing a role.