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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
The association between IgA nephropathy (IgAN) and inflammatory bowel disease (IBD) has gained attention, yet the clinical and pathological characteristics of IgAN in patients with ulcerative colitis (UC) or Crohn's disease (CD) remain poorly defined. This study aimed to compare the clinicopathological features and kidney outcomes of IgAN across three groups: IgAN alone, UC-associated IgAN, and CD-associated IgAN.
We identified patients with kidney biopsy–proven IgAN and comorbid IBD diagnosed between April 1, 1995, and June 30, 2025, at the four affiliated hospitals of The Jikei University School of Medicine. For each IBD case, two control patients with IgAN without IBD (non-IBD-IgAN) were then selected by individual 1:2 matching on sex, date of kidney biopsy (±1 year), and age (±3 years). Patients were thus classified into three groups: non-IBD-IgAN (n = 32), UC-associated IgAN (n = 8), and CD-associated IgAN (n = 8). Clinical parameters, histological grading, and treatment patterns (including TNF-α inhibitor use) were compared across groups. One-year outcomes included the percent change in proteinuria, improvement of microscopic hematuria, and change in eGFR from the time of kidney biopsy.
At the time of IgAN diagnosis, the CD-associated IgAN group showed lower kidney function than the non-IBD-IgAN group (median eGFR 51.0 [36.3–63.3] vs 70.8 [59.6–86.8] mL/min/1.73 m²; p < 0.05), more frequent tubulointerstitial nephritis (50% vs 0%; p < 0.05), and more advanced interstitial fibrosis/tubular atrophy (30 [20–30]% vs 10 [5–17.5]%; p < 0.05). Relative to the UC-associated IgAN group (eGFR 85.4 [69.1–91.6] mL/min/1.73 m²; interstitial fibrosis/tubular atrophy 15 [6–28]%; tubulointerstitial nephritis 0%), the CD-associated IgAN group had significantly lower eGFR (p < 0.05), with nonsignificant trends toward higher interstitial fibrosis/tubular atrophy and tubulointerstitial nephritis. At one year, proteinuria decreased in all groups, while changes in eGFR and hematuria remission were comparable. Notably, TNF-α inhibitor use was significantly more common in the CD-associated IgAN group, and several cases showed IgAN reactivation during or after such therapy.
CD-associated IgAN is characterized by more severe clinical and pathological features at the time of diagnosis compared with UC-associated or IgAN alone. Clinicians should be aware of this high-risk phenotype, especially in the context of biologic therapy, and consider tailored monitoring strategies.
