Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 124, Issue 6, Pages 2325-2332Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI74475
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Funding
- National Institute of Diabetes and Digestive and Kidney Diseases (NIH/NIDDK) [K23-DK090207, R03-DK099654]
- NIH/NIDDK [DK078244, DK082753]
- NIH/National Institute of General Medical Sciences (NIGMS) [GM098539]
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IgA nephropathy (IgAN) represents the leading cause of kidney failure among East Asian populations and the most frequent form of primary glomerulonephritis among Europeans. Patients with IgAN develop characteristic IgA1-containing immune complexes that deposit in the glomerular mesangium, producing progressive kidney injury. Recent studies define IgAN as an autoimmune trait of complex architecture with a strong genetic determination. This Review summarizes new insights into the role of the O-glycosylation pathway, anti-glycan immune response, mucosal immunity, antigen processing and presentation, and the alternative complement pathway in the pathogenesis of IgAN.
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