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. 2010 Apr 13;25(11):2257–2268. doi: 10.1007/s00467-010-1500-7

Fig. 3.

Fig. 3

The model of immunoglobulin A nephropathy (IgAN) pathogenesis in patients with high levels of galactose-deficient IgA1. Inherited defect of IgA1 glycosylation is not sufficient to cause the disease. Additional environmental or genetic factors are probably required for renal injury, which is likely mediated by antiglycan antibody production and immune complex formation