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Related Experiment Video

Updated: May 30, 2026

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro
14:18

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro

Published on: October 13, 2023

Primary IgA nephropathy: new insights into pathogenesis.

Jonathan Barratt1, John Feehally

  • 1The John Walls Renal Unit, Leicester General Hospital and Department of Infection, Immunity & Inflammation, University of Leicester, Leicester, United Kingdom.

Seminars in Nephrology
|August 16, 2011
PubMed
Summary

IgA nephropathy, a common kidney disease, involves abnormal IgA1 O-glycoforms in patients. These altered proteins may trigger immune responses, leading to kidney damage and inflammation.

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Last Updated: May 30, 2026

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro
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Published on: October 13, 2023

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Published on: November 10, 2021

Area of Science:

  • Nephrology
  • Immunology
  • Pathogenesis of Kidney Disease

Background:

  • Immunoglobulin A (IgA) nephropathy is the most common primary glomerulonephritis worldwide.
  • Understanding its pathogenesis has advanced significantly, particularly in the last five years.

Purpose of the Study:

  • To review recent advances in understanding the pathogenesis of IgA nephropathy.
  • To focus on key findings from the past five years regarding IgA nephropathy.

Main Methods:

  • Review of scientific literature published within the last five years.
  • Analysis of studies investigating IgA1 O-glycoforms and their role in IgA nephropathy.

Main Results:

  • A consistent feature of IgA nephropathy is altered IgA1 O-glycoforms, with increased poorly galactosylated forms.
  • These glycoforms may act as autoantigens or antigens, forming immune complexes that activate kidney cells.
  • In vitro data support the role of these immune complexes in mesangial cell activation, podocyte injury, and proximal tubular epithelial cell activation.

Conclusions:

  • Altered IgA1 O-glycoforms and subsequent immune complex formation are central to IgA nephropathy pathogenesis.
  • While genetic factors are implicated, specific candidate genes remain unidentified.