Aberrant O-linked glycosylation of the IgA hinge segment resulting in galactose-deficient IgA1 (Gd-IgA1) is frequently observed in patients with IgA nephropathy (IgAN), and it is hypothesized to be pathogenic. Here, we genetically disrupted the expression of galactosyltransferase 1 (C1galt1) to elevate Gd-IgA1 levels in mice and examine its role in glomerular deposition.
Kidney International published a clinical update in Research Highlights on 27 Mar 2026.
The item focuses on Absence of glomerular IgA1 deposition despite overexpression of galactose-deficient IgA1 in the B cell c1galt1 knockout mouse.
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