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A role for thromboxane in complement-mediated glomerular injury.

A V Cybulsky, W Lieberthal, R J Quigg

    The American Journal of Pathology
    |July 1, 1987
    PubMed
    Summary
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    The membrane attack complex (MAC) causes proteinuria in rat membranous nephropathy by damaging glomerular cells. This damage is partly mediated by thromboxane (Tx), a prostanoid synthesized in response to MAC.

    Area of Science:

    • Nephrology
    • Immunology
    • Complement System

    Background:

    • The membrane attack complex (MAC) of complement (C) activates prostaglandin (PG) and thromboxane (Tx) synthesis in nucleated cells.
    • Glomerular epithelial cell injury and altered permeability in rat membranous nephropathy are mediated by the MAC.

    Purpose of the Study:

    • To investigate whether MAC-induced proteinuria is linked to glomerular prostanoid synthesis.
    • To determine the role of thromboxane in MAC-mediated proteinuria.

    Main Methods:

    • Rat kidneys with planted antigen were perfused with C-fixing antibodies and human plasma to induce proteinuria.
    • The effects of cyclooxygenase blockade (indomethacin) and thromboxane synthetase inhibition (OKY-046) on proteinuria and prostanoid excretion were examined.
    • Inulin clearance was measured to assess renal hemodynamic changes.

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    Main Results:

    • MAC activation led to heavy proteinuria.
    • Indomethacin inhibited urinary PGE2 and reduced proteinuria, but also decreased inulin clearance.
    • OKY-046 significantly reduced proteinuria and urinary TxB2 excretion without affecting inulin clearance.

    Conclusions:

    • Proteinuria in rat membranous nephropathy is caused by MAC-dependent glomerular epithelial injury.
    • Thromboxane plays a significant role in mediating this proteinuria, independent of renal hemodynamic changes.