Korean J Transplant.  2023 Dec;37(4):299-305. 10.4285/kjt.23.0045.

T cell posttransplant lymphoproliferative disorder after kidney transplantation progressing to acute liver failure: a case report

Affiliations
  • 1Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea
  • 2Organ Transplantation Center, Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea
  • 3Department of Surgery, Seoul National University College of Medicine, Seoul, Korea

Abstract

Posttransplant lymphoproliferative disorder (PTLD) is a rare and serious complication of kidney transplantation (KT), with 85% of cases being of B cell lineage. We present a case of T cell PTLD (T-PTLD) that rapidly progressed to liver failure, septic shock, and death despite various therapeutic interventions. A 50-year-old woman underwent ABO- and human leukocyte antigen-compatible preemptive living donor KT for diabetic endstage kidney disease under basiliximab induction therapy. During routine monitoring, 2 months after KT, her Epstein-Barr (EB) viral load was found to be elevated to 318,443 copies/mL. Despite a reduction in maintenance immunosuppressants and preemptive rituximab treatment, the EB viremia continued to increase. Eight months after KT, abdominopelvic computed tomography revealed multifocal splenic lesions and nonspecific lymph node enlargement. Concurrently, the patient’s liver function tests began to deteriorate without evidence of viral hepatitis infection. A liver biopsy confirmed the di- agnosis of EB virus-associated T-PTLD with CD3 and CD56 expression. Only 2 months after the PTLD diagnosis, the patient developed acute and severe liver failure. She died 12 days after being hospitalized, despite the administration of rescue cytotoxic chemo-therapy. This case exemplifies the challenges of managing refractory EB virus-associated T-PTLD after KT, for which no specific treatment options are currently available. Further research into preventative and therapeutic methods for T-PTLD is warranted.

Keyword

Kidney transplantation; Lymphoproliferative disorders; Lymphoma T cell; Epstein-Barr virus infections

Figure

  • Fig. 1 Abdominopelvic computed tomography scan taken 8 months after kidney transplantation. The image reveals the new development of multifocal, wedge-shaped lesions with low enhancement, suggestive of splenic infarction (A, B: axial, C: coronal view).

  • Fig. 2 Positron emission tomography/computed tomography (PET/CT) indicative of posttransplant lymphoproliferative disorder (PTLD). (A) The PET/CT image reveals metabolic uptake in the spleen (arrow) and (B) the lymph nodes of the retroperitoneum and both iliac chains (arrow), suggesting the presence of PTLD.

  • Fig. 3 Pathologic findings of Epstein-Barr virus (EBV)-associated posttransplant lymphoproliferative disorder, characterized by T cell lineage of the liver. (A-C) Hematoxylin and eosin staining demonstrates infiltration of small lymphoid cells within the sinusoids, accompanied by occasional lobular necroinflammatory activity. The lymphoid cells were positive for (D) CD3, (F) Ki67, and (G) CD56 and negative for (E) CD20. (H, I) EBV in situ hybridization yielded positive results in scattered small T lymphocytes. The scale bar represents 100 μm. (A, B, D–H) ×200, (C, I) ×400 magnification.

  • Fig. 4 Abdominopelvic computed tomography findings revealing multiple hepatic nodules, indicating liver involvement of posttransplant lymphoproliferative disorder (PTLD). Multiple ill-defined nodules (<2 cm) are visible during (A) the arterial phase and (B) the venous phase. PTLD is combined with (C) multiple lymph node enlargement and (D) splenic involvement.


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