Abstract
Mesangial cell activation in response to deposition of pathogenic IgA-containing immune complexes is characterized by cellular proliferation and inflammatory cytokine secretion, and is considered the initiating intra-renal event in the pathogenesis of IgA nephropathy (IgAN). The molecular mechanisms have not been well defined. Endothelin (ET) pathway activation has been observed in kidney biopsies of IgAN patients and may be an important driver of disease progression by promoting proteinuria along with kidney inflammation and fibrosis via ETA receptor activation.
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