ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: TH-PO0441

Enhanced Serum IgA Reactivity to Gut Microbiota in IgAN Supports a Mucosal Origin of Pathogenic IgA

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology

Authors

  • Arbez, Laure, GIMAP INSERM U1111 CIRI, Saint Etienne, France
  • Mariat, Christopher R., CHU Saint Etienne, Saint Etienne, France
  • Paul, Stéphane, CHU Saint Etienne, Saint Etienne, France
  • Maillard, Nicolas, CHU Saint Etienne, Saint Etienne, France
Background

IgA nephropathy (IgAN) is characterized by galactose-deficient IgA1 and immune complex deposition within glomeruli. Increasing evidence suggests a mucosal origin of pathogenic IgA linked to intestinal dysbiosis. We investigated serum IgA reactivity against gut bacterial antigens in patients with IgAN.

Methods

An ELISA-based assay was developed using lysates from intestinal bacterial species coated onto ELISA plates. Serum samples from patients with biopsy-proven IgAN at time of diagnosis and healthy controls were incubated with bacterial antigens, and bound IgA were detected using HRP-conjugated anti-human IgA antibodies. Serum secretory IgA (SIgA) concentrations and correlations with bacteria-specific IgA reactivity were analyzed.

Results

Patients with IgAN exhibited significantly increased serum IgA reactivity against Faecalibacterium prausnitzii, Flavonifractor plautii, Bifidobacterium longum, and Lactobacillus rhamnosus compared with healthy controls (all p<0.0001). Significant but less pronounced differences were also observed for Akkermansia muciniphila and Bacteroides thetaiotaomicron (p<0.05). Serum SIgA levels positively correlated with reactivity against Flavonifractor plautii (p=0.002), Bifidobacterium longum (p=0.003), and Akkermansia muciniphila (p=0.004).

Conclusion

These preliminary findings support a mucosal and microbiota-related origin of aberrant circulating IgA in IgAN. The association between SIgA and bacteria-specific serum IgA responses further supports the role of the gut–kidney axis in IgAN pathophysiology and provides rationale for mucosal-targeted therapeutic strategies.