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Background <p>IgA 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.</p> Methods <p>We 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).</p> Results <p>In 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&#xa0;year, all groups exhibited reductions in proteinuria, with no significant differences in eGFR change or hematuria resolution.</p> Conclusions <p>CD-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.</p>

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Distinct clinicopathological features of IgA nephropathy associated with Crohn’s disease: comparison with ulcerative colitis and non-IBD IgA nephropathy

  • 期刊论文

  • 发表日期：

    2026年3月23日

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  • Akihiro Shimizu,
  • Nobuo Tsuboi,
  • Saeko Hatanaka,
  • Shohei Fukunaga,
  • Takaya Sasaki,
  • Kotaro Haruhara,
  • Masahiro Okabe,
  • Shinya Yokote,
  • Hiroyuki Ueda,
  • Yuko Iwashita,
  • Kan Uchiyama,
  • Masato Ikeda,
  • Takashi Yokoo

摘要

Background

IgA 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.

Methods

We 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).

Results

In 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.

Conclusions

CD-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.