Kaposi Sarcoma in a Nonadherent Transplant Patient

Introduction: Kaposi Sarcoma (KS) is an angioproliferative cancer caused by human herpesvirus 8 (HHV-8). Most cases of post-transplant KS arise after HHV-8 reactivation triggered by immunosuppression with 60-times higher risk of KS in solid organ transplant recipients than the general population. We present a kidney transplant patient who develops KS shortly after transplant. Case Description: 53-year-old Somali man with end-stage renal disease due to diabetic nephropathy underwent kidney transplant with induction with thymoglobulin, and maintained on belatacept, mycophenolate sodium (MPS), and prednisone. Acute antibody-mediated rejection and Banff IIA acute cellular rejection is found four months after transplant due to non-adherence with belatacept infusions and treated with thymoglobulin, steroids, intravenous immunoglobulin, and therapeutic plasma exchange. Belatacept was subsequently switched to tacrolimus. He develops lymphadenopathy and a core biopsy of his axillary lymph nodes shows reactive lymphoid tissue. He has worsening disseminated rash two months later with initial rash noticed one month post-transplant. Biopsy of skin lesions shows KS. HHV-8 was checked and found to be 162,000 copies/ml. HIV was negative. Prior lymph node biopsy was found without features of KS and negative staining for HHV-8. MPS was switched to everolimus, a mammalian target of rapamycin inhibitor (mTORi), with regression of KS skin lesions. His graft function remained stable with serum creatinine around 1.5 mg/dL. Discussion: This patient developed progression KS despite nonadherence to immunosuppression which then worsened after treatment for rejection. Management of post-transplant KS focuses on reducing immunosuppression, switching to mTORi, and/or chemotherapy. In one study, conversion to mTORi and reducing immunosuppression induced response in over 80% of patients. Chemotherapy is usually reserved for cases of extensive KS and best understood in AIDS-related KS. We were able to control KS by switching to an mTORi.

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Journal
Journal of the American Society of Nephrology
Published
2024-10-01
DOI
https://doi.org/10.1681/asn.202496aae9y7
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1
Primary Topic
Polyomavirus and related diseases
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article
Field-Weighted Citation Impact
0.28
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article

Kaposi Sarcoma in a Nonadherent Transplant Patient

Isaac E. Hall, Dominik Thomas, Divya Raghavan, Miklos Zsolt Molnar et al.
1 citations
Journal of the American Society of Nephrology
Polyomavirus and related diseases
0.28
article

Kaposi Sarcoma in a Nonadherent Transplant Patient

Isaac E. Hall, Dominik Thomas, Divya Raghavan, Miklos Zsolt Molnar, Şuayp Oygen, Sarah Gilligan, Duha A. Jweehan
article en
1 citations

Abstract

Introduction: Kaposi Sarcoma (KS) is an angioproliferative cancer caused by human herpesvirus 8 (HHV-8). Most cases of post-transplant KS arise after HHV-8 reactivation triggered by immunosuppression with 60-times higher risk of KS in solid organ transplant recipients than the general population. We present a kidney transplant patient who develops KS shortly after transplant. Case Description: 53-year-old Somali man with end-stage renal disease due to diabetic nephropathy underwent kidney transplant with induction with thymoglobulin, and maintained on belatacept, mycophenolate sodium (MPS), and prednisone. Acute antibody-mediated rejection and Banff IIA acute cellular rejection is found four months after transplant due to non-adherence with belatacept infusions and treated with thymoglobulin, steroids, intravenous immunoglobulin, and therapeutic plasma exchange. Belatacept was subsequently switched to tacrolimus. He develops lymphadenopathy and a core biopsy of his axillary lymph nodes shows reactive lymphoid tissue. He has worsening disseminated rash two months later with initial rash noticed one month post-transplant. Biopsy of skin lesions shows KS. HHV-8 was checked and found to be 162,000 copies/ml. HIV was negative. Prior lymph node biopsy was found without features of KS and negative staining for HHV-8. MPS was switched to everolimus, a mammalian target of rapamycin inhibitor (mTORi), with regression of KS skin lesions. His graft function remained stable with serum creatinine around 1.5 mg/dL. Discussion: This patient developed progression KS despite nonadherence to immunosuppression which then worsened after treatment for rejection. Management of post-transplant KS focuses on reducing immunosuppression, switching to mTORi, and/or chemotherapy. In one study, conversion to mTORi and reducing immunosuppression induced response in over 80% of patients. Chemotherapy is usually reserved for cases of extensive KS and best understood in AIDS-related KS. We were able to control KS by switching to an mTORi.

Journal of the American Society of NephrologyVol. 35(10S)
University of Utah (US)
Zero hunger
Openalex Percentile: Top 35%
Polyomavirus and related diseases
0.28
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