The pathogenesis of IgA nephropathy and implications for treatment.
A review outlining the multi-hit model of IgA nephropathy pathogenesis and how it is driving development of new targeted therapies against B cells, complement, and endothelin pathways.
Background
IgA nephropathy is a common form of primary glomerulonephritis and an important global cause of CKD, with most patients at risk of kidney failure over their lifetime.
Key findings
Disease pathogenesis follows a multi-hit model: increased circulating galactose-deficient IgA1, likely derived from the mucosal immune system, is bound by specific IgG/IgA antibodies to form immune complexes that deposit in the glomeruli, triggering inflammation and complement activation.
Clinical implications
New therapies targeting B cell priming in gut mucosa, the cytokines APRIL and BAFF, plasma cells, complement activation, and endothelin pathways are emerging, raising the realistic possibility of transforming long-term outcomes for patients with IgA nephropathy.
Category
Research
Source
Nature Reviews Nephrology
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