In nephrologists' clinical experience, the overactivation of the complement alternative pathway (AP) is acquiring more and more importance in kidney failure etiopathogenesis. Indeed AP is involved in membranoproliferative glomerulonephritis, in atypical hemolytic uremic syndrome, in post-infectious glomerulonephritis, and now we are debating about a role of AP complement overactivation in ANCA associated vasculitis, in MGUS related nephrophaties.....Often patients with an AP dysregulation simulate Lupus without Lupus antibodies (SLE without SLE) and we observed some patients that overlaps with hypocomplementemic cutaneous vasculitis and/or cryoglobulinemic vasculitis
The AP amplifies complement activation initiated by any pathway through a positive feed-back loop. Thus, it is reasonable to expect that the AP contributes to the pathogenesis of most (if not all) diseases mediated by complement activation.
Yes it's true. But the question is about AP overactivation/dysregulation without any infectious or immunocomplexes trigger. This pathogenetic pathway was clearly showed in atypical haemolitic uremic syndrome, in dense deposit disease, in C3 glomerulonephritis. In ANCA associated vascultiis is described that ANCA primed neutrophils are able to activate the AP, and so on...
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