Conference Abstracts - 2025 Summit on Hematologic Cancers
Vol. 5, Issue Supplement 2, 2025 · S1-2
A rare case of large B-cell lymphoma presenting as acute liver failure one year after renal transplant.
Tasnim Rahman, Microbiology B.S (University of Michigan) Ann Arbor, MI 48109 Medical Doctorate M.D (Wayne State University School of Medicine) Detroit, MI 48201,Jamie Abad, Biological Sciences B.S (University of Nevada) Las Vegas, NV 89557 Medical Doctorate M.D (University of Nevada, Reno School of Medicine) Reno, NV 89557
Submission received: 2025-07-12 / Accepted: 2025-07-28 / Published: 2025-09-19
Background
Post-transplant lymphoproliferative disorder (PTLD) is a spectrum of abnormal lymphoid proliferations due to immunosuppression after organ transplant. It often involves impaired T-cell immunity, allowing for unchecked EBV-infected B cell proliferation. While 60-80% of PTLD causes are EBV-positive, 40% are EBV-negative with unclear etiology. PTLD risk is highest within the first-year post-transplant. About half of PTLD cases involve the abdomen. This case report presents a rare monomorphic B-cell lymphoma (a subtype of PTLD) one year after renal transplant.
Case Presentation
51-year-old female with history of IgA nephropathy s/p URKT renal transplant in July 2024 presented with acute liver failure and altered mental status. On presentation, labs revealed ALT of 396 U/L, AST of 607 U/L, ALP of 300 U/L, total bilirubin of 4.5 mg/dL and Cr of 3.2 mg/dL. Liver function showed hypoalbuminemia and an INR of 2.8. Further evaluation of acute liver failure including viral hepatitis serology, autoimmune markers, and thorough medication review was unremarkable. CT and MRI revealed a suspicious splenic mass. Infectious work-up revealed EBV of 478,621. Given her recent kidney transplant and subsequent immunosuppression and EBV reactivation, PTLD was suspected. Liver biopsy showed positive lymphoid markers and biopsy of the splenic mass confirmed CD20-positive, CD3- and PAX5-negative large B-cell lymphoma. The patient's liver failure was attributed to hepatic infiltration by the lymphoma. She was initiated on high-dose corticosteroids and Rituximab. Despite treatment, her liver function declined and she died from septic shock.
Conclusion
This case highlights the potential for PTLD to cause severe hepatic complications, even in non-hepatic solid organ transplant recipients. PTLD is most common after intestinal transplant and rare after renal transplant, making this case particularly unusual. Diagnosis requires biopsy confirmation. Initial treatment involves reducing or stopping immunosuppression. Rituximab and chemotherapy are added for high-risk or refractory cases. This case highlights the importance of considering PTLD in transplant recipients presenting with acute liver failure, as early recognition and intervention are critical despite the rarity of hepatic involvement following renal transplantation.
References
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