Increased Serum IgA Reactivity to Gut Bacteria Observed in IgA Nephropathy
Patients with immunoglobulin A nephropathy (IgAN) exhibit increased serum IgA reactivity to several intestinal bacterial species compared with healthy individuals, according to a study being presented at the...
Patients with immunoglobulin A nephropathy (IgAN) exhibit increased serum IgA reactivity to several intestinal bacterial species compared with healthy individuals, according to a study being presented at the American Society of Nephrology (ASN) Kidney Week 2026. IgAN is characterized by the deposition of immune complexes containing galactose-deficient IgA1 in the glomeruli.
Previous research has suggested that alterations in the gut microbiota may contribute to the production of pathogenic IgA. Investigators sought to further explore this potential relationship by examining circulating IgA responses to intestinal bacterial antigens. Using an enzyme-linked immunosorbent assay, researchers measured serum IgA reactivity to bacterial antigens in patients with biopsy-confirmed IgAN at diagnosis and healthy controls.
They also assessed serum secretory IgA concentrations and their association with responses to individual bacterial species. Patients with IgAN demonstrated significantly greater serum IgA reactivity to Faecalibacterium prausnitzii , Flavonifractor plautii , Bifidobacterium longum , and Lactobacillus rhamnosus than healthy controls (all P <0.001).
Smaller but statistically significant differences were also observed for Akkermansia muciniphila and Bacteroides thetaiotaomicron (both P <0.05). Serum secretory IgA concentrations were positively correlated with IgA reactivity to Flavonifractor plautii ( P =0.002), Bifidobacterium longum ( P =0.003), and Akkermansia muciniphila ( P =0.004).
The investigators concluded that these preliminary findings support the hypothesis that abnormal circulating IgA in IgAN may originate from mucosal immune responses associated with the gut microbiota. They suggested that the findings provide further evidence for the involvement of the gut–kidney axis in IgAN and support continued investigation of therapies targeting mucosal immune pathways.
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