All ETDs from UAB

Advisory Committee Chair

Jan Novak

Advisory Committee Members

Susan Bellis

Rodney King

Matthew B Renfrow

Dana Rizk

Document Type


Date of Award


Degree Name by School

Doctor of Philosophy (PhD) College of Arts and Sciences


IgA nephropathy (IgAN) is an autoimmune disease that is the most common form of glomerulonephritis in the world, and results in end-stage renal disease in 40% of patients. In IgAN, human immunoglobulin A1 (IgA1) has reduced levels of galactose (Gal) in the IgA1 O-glycosylated hinge region (HR) known as Gal deficient IgA1 (Gd-IgA1). These Gd-IgA1 glycoforms, which are elevated in circulation of IgAN patients, are recognized by Gd-IgA1-specific IgG autoantibodies, resulting in the formation of pathogenic immune complexes (CICs). Some of these CICs accumulate in the mesangium of glomeruli and induce kidney injury. Although the link between these deposits and the clinical manifestations of IgAN are established, there remains a gap in knowledge about the which glycoforms of IgA1 contribute to IgAN pathogenesis. The exact molecular origin of these Gd-IgA1 glycoforms in pathogenic CICs remains unknown as IgA1 exist in three distinct molecular forms: monomeric (produced by bone marrow 80-90% of total serum IgA1) (mIgA1), polymeric (produced by mucosal tissues 10-20% of total IgA1) (pIgA1), IgA1 bound in CICs (

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