"Don't Disregard the Duodenum!" Late-Onset Graft Pancreatitis Manifested as Tissue-Invasive Cytomegalovirus (CMV) Graft Duodenitis with Perforation

Introduction: Graft pancreatitis secondary to tissue-invasive CMV infection without systemic viremia is rare, and often missed due to challenges in obtaining a tissue sample, and its nonspecific presenting symptoms. We share a case of late occurrence tissue-invasive CMV infection, post simultaneous pancreas kidney (SPK) transplant, diagnosed by laparotomy finding of bowel perforation of the allograft. Case Description: A 39-year old woman with Type 1 Diabetes and end stage kidney disease, status-post SPK transplantation, with Thymoglobulin induction, CMV IgG donor positive/ IgG recipient negative, was evaluated for graft pancreatitis, 22 months post transplant. Post-transplant month 4 was complicated by CMV viremia, which resolved with Valgancyclovir and reduction of immunosuppression. Unfortunately, she developed an acute cellular rejection of the pancreas allograft at post-op month 7, treated with Thymoglobulin and increased maintenance immunosuppression. Most recently, she presented with vomiting and abdominal pain. Labs showed stable renal allograft function, and no donor specific antibodies but elevated pancreas allograft enzymes. Infectious workup was negative for BK and CMV PCR in blood. She clinically improved with treatmement of urine infection, and lipase normalized (90 U/L) at discharge. Labs one week after discharge showed lipase level of 1558 U/L with pancreatic graft site pain and diarrhea. Due to the acute rise in lipase and her prior history of cellular rejection of the pancreatic allograft, pulse steroids were initiated. However, her abdominal pain worsened, and CT abdomen pelvis showed pneumoperitoneum. Patient was emergently taken to the OR with findings of copious purulent fluid around the tail of the pancreas allograft, and densely adherent omentum to the allograft duodenum, consistent with perforation of donor duodenal graft requiring repair. Histology revealed CMV viral inclusions with acute and chronic inflammation, for which IV ganciclovir was promptly initiated. Patient clinically improved with resolution of graft pancreatitis. Discussion: CMV-involvement in the donor duodenal graft is uncommon, yet it can lead to serious bowel complications with high morbidity and mortality. Obtaining a tissue diagnosis will guide treatment interventions, and ultimately equate with better patient and allograft outcomes.

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Publication Details

Journal
Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.2025548zgc5z
Primary Topic
Cytomegalovirus and herpesvirus research
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article
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article

"Don't Disregard the Duodenum!" Late-Onset Graft Pancreatitis Manifested as Tissue-Invasive Cytomegalovirus (CMV) Graft Duodenitis with Perforation

Journal of the American Society of Nephrology
Cytomegalovirus and herpesvirus research
article

"Don't Disregard the Duodenum!" Late-Onset Graft Pancreatitis Manifested as Tissue-Invasive Cytomegalovirus (CMV) Graft Duodenitis with Perforation

article en

Abstract

Introduction: Graft pancreatitis secondary to tissue-invasive CMV infection without systemic viremia is rare, and often missed due to challenges in obtaining a tissue sample, and its nonspecific presenting symptoms. We share a case of late occurrence tissue-invasive CMV infection, post simultaneous pancreas kidney (SPK) transplant, diagnosed by laparotomy finding of bowel perforation of the allograft. Case Description: A 39-year old woman with Type 1 Diabetes and end stage kidney disease, status-post SPK transplantation, with Thymoglobulin induction, CMV IgG donor positive/ IgG recipient negative, was evaluated for graft pancreatitis, 22 months post transplant. Post-transplant month 4 was complicated by CMV viremia, which resolved with Valgancyclovir and reduction of immunosuppression. Unfortunately, she developed an acute cellular rejection of the pancreas allograft at post-op month 7, treated with Thymoglobulin and increased maintenance immunosuppression. Most recently, she presented with vomiting and abdominal pain. Labs showed stable renal allograft function, and no donor specific antibodies but elevated pancreas allograft enzymes. Infectious workup was negative for BK and CMV PCR in blood. She clinically improved with treatmement of urine infection, and lipase normalized (90 U/L) at discharge. Labs one week after discharge showed lipase level of 1558 U/L with pancreatic graft site pain and diarrhea. Due to the acute rise in lipase and her prior history of cellular rejection of the pancreatic allograft, pulse steroids were initiated. However, her abdominal pain worsened, and CT abdomen pelvis showed pneumoperitoneum. Patient was emergently taken to the OR with findings of copious purulent fluid around the tail of the pancreas allograft, and densely adherent omentum to the allograft duodenum, consistent with perforation of donor duodenal graft requiring repair. Histology revealed CMV viral inclusions with acute and chronic inflammation, for which IV ganciclovir was promptly initiated. Patient clinically improved with resolution of graft pancreatitis. Discussion: CMV-involvement in the donor duodenal graft is uncommon, yet it can lead to serious bowel complications with high morbidity and mortality. Obtaining a tissue diagnosis will guide treatment interventions, and ultimately equate with better patient and allograft outcomes.

Journal of the American Society of NephrologyVol. 36(10S)
Houston Methodist (US)
Good health and well-being, Gender equality
Openalex Percentile: Top 36%
Cytomegalovirus and herpesvirus research
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