De novo ulcerative colitis after kidney transplantation treated with infliximab

Abstract

Diarrhea is a common complication in kidney transplant recipients. Common causes of diarrhea include infection, side effect from medication, rejection, and malignancy. A less common but important cause of diarrhea is de novo inflammatory bowel disease (IBD). This is unexpected, as these patients are already immunosuppressed. Herein, we present the case of a 45-year-old man with end-stage kidney disease because of focal segmental glomerulosclerosis who underwent preemptive kidney transplantation, with his mother as donor. His immunosuppressive regimen included methylprednisolone, mycophenolate mofetil, and tacrolimus. He had no episodes of graft dysfunction, rejection, or infectious events. Two and a half years post-transplantation, he developed bloody diarrhea. After excluding infections, colonoscopy was performed and revealed edematous mucosa and erythema with pigmentation, which are typical findings in ulcerative colitis. Despite therapy with 5-aminosalicylate and granulocyte monocyte apheresis, he presented with massive bloody diarrhea. We initiated infliximab, an anti-tumor necrosis factor-α (TNF-α) agent. He responded very well and achieved remission within 6 months after initiation of infliximab, while administration of the other immunosuppressants was maintained. His course was uneventful and no complications developed. Management of immunosuppressants for de novo IBD after organ transplantation is complicated, because treatment of IBD, graft function protection, and prevention of infection must be considered. Therefore, cooperation between transplantation physicians and gastroenterologists is essential during therapy.

Keywords: De novo inflammatory bowel disease; Diarrhea; Infliximab; Kidney transplantation; Ulcerative colitis.

Fig. 1

Initial colonoscopy and colon biopsy findings. a Colonoscopy revealed edematous mucosa and erythema with pigmentation. b Light microscopic examination of colonic mucosa revealed severe inflammation with decreased goblet cells, and crypt abscesses, diffuse stromal lymphoplasmacytic infiltration, and irregular glands, which are consistent with UC (hematoxylin and eosin staining × 200)

Fig. 2

Colonoscopy finding 8 months after starting treatment with 5-ASA and apheresis. Colonoscopy showed mucosal erosion and spontaneous bleeding

Fig. 3

Follow-up colonoscopy 2 years after starting treatment with infliximab. Colonoscopy showed significant improvement of inflammation