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. Author manuscript; available in PMC: 2009 Jan 1.
Published in final edited form as: Semin Nephrol. 2008 Jan;28(1):78–87. doi: 10.1016/j.semnephrol.2007.10.009

Figure 3.

Figure 3

A model of pathogenesis of IgAN. Some polymeric IgA1 (pIgA1) produced by B cells and plasma cells in patients with IgAN is galactose-deficient and is recognized by anti-glycan IgG or IgA1 antibodies. The resultant immune complexes are too bulky to enter the space of Disse to reach the asialoglycoprotein receptor (ASGP-R) on hepatocytes, but are able to pass through the larger fenestrae in glomerular capillaries overlying the mesangium. These deposited complexes induce glomerular injury.