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Abstract: PO1447

Immune Complexes Containing Galactose-Deficient IgA1 Deposit on Mesangium Through Damage to Endothelial Cells

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Makita, Yuko, Juntendo University Faculty of Medicine, Bunkyo-ku, Tokyo, Japan
  • Suzuki, Hitoshi, Juntendo University Urayasu Hospital, Urayasu, Chiba, Japan
  • Nakano, Daisuke, Kagawa University, Kagawa, Japan
  • Kano, Toshiki, Juntendo University Faculty of Medicine, Bunkyo-ku, Tokyo, Japan
  • Nishiyama, Akira, Kagawa University, Kagawa, Japan
  • Suzuki, Yusuke, Juntendo University Faculty of Medicine, Bunkyo-ku, Tokyo, Japan

Galactose-deficient IgA1 (Gd-IgA1) plays a crucial role in the pathogenesis of IgA nephropathy (IgAN). However, the pathogenic role of mesangial Gd-IgA1-containing immune complexes (ICs) remains unclear. The endothelial surface glycocalyx modulates microvascular function. Loss of the glomerular endothelial glycocalyx is known to be involved in albuminuria. Here, we examined whether the deposition of Gd-IgA1-containing ICs in the mesangium may lead glomerular endothelial cell dysfunction in this disease.


Gd-IgA1 and recombinant anti-glycan IgG were used to form ICs to inject into nude mice. The renal microvascular endothelial glycocalyx removal of the injected nude mice was evaluated by real-time glycocalyx imaging. Human renal glomerular endothelial cells (HRGECs) were used to assess the potential capacity of Gd-IgA1-containing ICs to activate endothelial cells.


After co-culture of Gd-IgA1-containing ICs with HRGECs, mRNA expression levels of endothelial adhesion molecules (ICAM-1, VCAM-1 and E-selectin) were significantly upregulated (P<0.01). Expression levels of proinflammatory mediators (TNFα and IL-6) that are able to induce the expression of the adhesion molecules on endothelial cells were also increased (P<0.01). Nude mice injected with Gd-IgA1-containing ICs showed podocyte and endothelial injuries with IgA, IgG, and C3 co-deposition along the glomerular capillaries and in the mesangium. Moreover, albuminuria and hematuria were also induced. Real-time glycocalyx imaging showed that renal microvascular glycocalyx was decreased immediately after the injection of Gd-IgA1-containing ICs and then mesangial IgA deposition was increased.


Present data suggest that Gd-IgA1-containing ICs may induce glomerular endothelial injuries resulting in mesangial deposits.