Abstract: PO2149
De Novo Inflammatory Bowel Disease in Kidney Recipients: A Single-Center Experience
Session Information
- Transplantation: Clinical - Underrecognized Risk Factors, Traditional Considerations, and Outcomes
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 1902 Transplantation: Clinical
Authors
- Ogata, Masatomo, St. Marianna University School of Medicine, Kawasaki, Japan
- Miyauchi, Takamasa, St. Marianna University School of Medicine, Kawasaki, Japan
- Murata, Marie, St. Marianna University School of Medicine, Kawasaki, Japan
- Imai, Naohiko, St. Marianna University School of Medicine, Kawasaki, Japan
- Shinoda, Kazunobu, St. Marianna University School of Medicine, Kawasaki, Japan
- Shibagaki, Yugo, St. Marianna University School of Medicine, Kawasaki, Japan
- Yazawa, Masahiko, St. Marianna University School of Medicine, Kawasaki, Japan
Background
Recipients of solid organ transplantation (SOT) receive immunosuppressants (IM) such as calcineurin inhibitors and steroids, both of which are also used for inflammatory bowel disease (IBD). However, the incidence of IBD following SOT (de novo IBD) is 5 to 10 times higher than that among the general population. Although reports of de novo IBD have been mostly reported in liver transplants, and that after kidney transplantation (KT) remains scarce.
Methods
Of the patients who underwent KT from 1998 to 2021 at St. Marianna University Hospital (N=241), we included those diagnosed by colonoscopy with de novo IBD including ulcerative colitis (UC) or Chron’s Disease (CD). We retrospectively described the symptoms, time course, HLA typing, IM, and treatment of de novo IBD.
Results
Of 241 recipients, 6 developed de novo IBD posttransplant (incidence: 2.5%): 5 were diagnosed with UC and 1 with CD. The median time from KT to IBD diagnosis was 6 years (range, 2–12). Allograft function did not worsen after IBD in any recipients. The initial presentation was bloody stool in 5 recipients and mild diarrhea in 1. In the recipient with CD, severe and continuous abdominal pain, and bloody stool with moderately elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were present (3.53 mg/dL and 71 mm/h, respectively). In recipients with UC, bloody stool or mild diarrhea without abdominal pain, and mild to moderate inflammation markers such as median CRP [0.28 mg/dL (range: 0.07–6.38 mg/dL)] and median ESR [26.5 mm/h [range: 9–81 mm/h] were present. Three recipients with UC had HLA B52, DR2, or DR15, which are known to associate with UC. All recipients received a triple maintenance IM for KT including tacrolimus and steroids. Regarding treatment for de novo IBD, infliximab for the recipient with CD and 5-aminosalicylate for recipients with UC were used as a primary treatment. One recipient with UC affected the whole colon was resistant to prednisolone, infliximab, and vedolizumab. He eventually underwent total colectomy at 1-year after diagnosis. The others achieved the remission of IBD after initial therapy.
Conclusion
De novo IBD should be a differential diagnosis of bloody stool after KT in spite of low or only mildly elevated inflammation markers. De novo IBD can present even without bloody stool.