Increasing
evidence from animal studies support the hypothesis that progression of renal
failure in glomerular diseases is related by local complement activation.
Interstitial vascular C4d vascular deposits have been described in acute and
chronic antibody-mediated rejection (ABMR) . C4d is a surface-bound split
product of inactive C4b obtained from classical or lectin complement pathways.
To the date, receptor for C4d has not been identified and its biological
function is unknown. C4d positive staining (C4d+) has also been reported in normal
human kidneys, primary and secondary
nephropathies.
The weak segmental C4d+ glomerular staining observed in normal
kidney biopsies possibly results by local complement activation involved in the
physiological clearance of IgM-containing immune complexes . A study on
C4-deficient guinea-pig showed increased IgM glomerular deposits when compared
to non C4ddeficient mammalian kidneys. Human diseases studies suggest that C4d+
mesangial staining in patients with IgA nephropathy (IgAN) could identify
individuals with a worse long-term prognosis. Read more........................
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