Related Experiment Video
Updated: May 23, 2026

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
Beyond galactose-deficient IgA1: reconsidering IgA2 as a pathogenic driver in IgA nephropathy
Claudia Seikrit1, Jürgen Floege1
1Division of Nephrology, RWTH Aachen University, Aachen, Germany.
None:
IgA nephropathy (IgAN) has long been viewed as a disease driven almost exclusively by IgA1, in particular galactose-deficient IgA1. However, emerging evidence challenges this IgA1-centric paradigm. In this issue of Kidney International, Li et al. demonstrate that IgA2 is consistently deposited in IgAN glomeruli and actively promotes complement activation, macrophage infiltration, and tubulointerstitial injury. These findings could redefine IgA2 from a passive bystander to a pathogenic amplifier, linking mucosal immunity, complement biology, and progression of kidney disease in IgAN.
Related Concept Videos
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology
Transcytosis of IgG
IgG molecules from a mother undergo transcytosis starting around 13 weeks of gestation. The amount of IgG transferred and entering the fetal blood circulation increases with...
Type I Diabetes II: Pathophysiology
Chronic Pancreatitis II: Pathophysiology
Type I Diabetes I: Introduction

