ArticleClinical and experimental nephrology2026
Distinct clinicopathological features of IgA nephropathy associated with Crohn's disease: comparison with ulcerative colitis and non-IBD IgA nephropathy.
Article in Clinical and experimental nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Mechanistic remodeling and immunoregulatory functions of the B cell-humoral immunity axis in inflammatory bowel disease.Frontiers in immunology · 2026Review
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13 authors.
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Abstract
backgroundIgA nephropathy (IgAN) is increasingly recognized as a complication of inflammatory bowel disease (IBD), particularly Crohn's disease (CD). Recent studies suggest that mucosal immune dysregulation and biologic therapies, particularly tumor necrosis factor (TNF)-α inhibitors, may influence the onset and progression of IgAN in IBD. However, its clinicopathological characteristics in this context remain uncertain.
methodsWe conducted a retrospective, multicenter study of patients with biopsy-proven IgAN and concurrent CD. Patients with CD-associated IgAN (CD-IgAN) were compared with those with ulcerative colitis-associated IgAN (UC-IgAN) and with IgAN unassociated with IBD (non-IBD-IgAN). Clinical parameters at kidney biopsy, treatment history, and histopathological findings were evaluated. One-year outcomes included changes in proteinuria, hematuria status, and estimated glomerular filtration rate (eGFR).
resultsIn total, eight patients with CD-IgAN, eight patients with UC-IgAN, and 32 matched non-IBD-IgAN controls were included. Patients with CD-IgAN exhibited lower eGFR, higher serum IgA levels, and a higher prevalence of tubulointerstitial nephritis compared to non-IBD-IgAN controls. Moreover, CD-IgAN was characterized by significantly lower eGFR and a nonsignificant trend toward more advanced tubulointerstitial injury compared to UC-IgAN. The use of TNF-α inhibitors was more frequent in the CD-IgAN group. At 1 year, all groups exhibited reductions in proteinuria, with no significant differences in eGFR change or hematuria resolution.
conclusionsCD-IgAN represents a distinct clinicopathological phenotype characterized by lower kidney function and more severe tubulointerstitial injury. Although causality cannot be inferred, careful kidney monitoring should be considered in patients with CD, particularly those receiving TNF-α inhibitors.
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