Abstract
New data from Kiryluk et al. show the importance of genetic factors in determining the profile of serum IgA1 O-glycoforms in IgA nephropathy and Henoch-Schönlein purpura nephritis. Elevated serum levels of poorly galactosylated IgA1 O-glycoforms do not, however, appear sufficient in themselves to cause nephritis in these two diseases, and a 'second hit' is necessary before changes in IgA1 glycosylation translate into clinical disease. The challenge now is to determine what these genetic factors are.
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