Seminars in Immunopathology

, Volume 34, Issue 3, pp 365-382

First online:

Glycosylation of IgA1 and pathogenesis of IgA nephropathy

  • Jan NovakAffiliated withUniversity of Alabama at BirminghamDepartment of Microbiology, University of Alabama at Birmingham Email author 
  • , Bruce A. JulianAffiliated withUniversity of Alabama at Birmingham
  • , Jiri MesteckyAffiliated withUniversity of Alabama at Birmingham
  • , Matthew B. RenfrowAffiliated withUniversity of Alabama at Birmingham

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IgA nephropathy, described in 1968 as IgA-IgG immune-complex disease, is an autoimmune disease. Galactose-deficient IgA1 is recognized by unique autoantibodies, resulting in the formation of pathogenic immune complexes that ultimately induce glomerular injury. Thus, formation of the galactose-deficient IgA1-containing immune complexes is a critical factor in the pathogenesis of IgA nephropathy. Studies of molecular defects of IgA1 can define new biomarkers specific for IgA nephropathy that can be developed into clinical assays to aid in the diagnosis, assessment of prognosis, and monitoring of disease progression.


IgA nephropathy IgA1 O-glycans High-resolution mass spectrometry Measangial cells