Kidney Week

Abstract: PUB516

Kaposi Sarcoma in a Nonadherent Transplant Patient

Session Information

• Publication Only

Category: Transplantation

• 2102 Transplantation: Clinical

Authors

• Thomas, Dominik, University of Utah Health, Salt Lake City, Utah, United States

Dominik Thomas, MD

• Gilligan, Sarah, University of Utah Health, Salt Lake City, Utah, United States

Sarah Gilligan, MD, MS

• Oygen, Suayp, University of Utah Health, Salt Lake City, Utah, United States

Suayp Oygen, MD, DrMed

• Jweehan, Duha A., University of Utah Health, Salt Lake City, Utah, United States

Duha A. Jweehan, MD

• Hall, Isaac E., University of Utah Health, Salt Lake City, Utah, United States

Isaac E. Hall, MD, MS

• Molnar, Miklos Zsolt, University of Utah Health, Salt Lake City, Utah, United States

Miklos Zsolt Molnar, MD, PhD, FASN

• Raghavan, Divya, University of Utah Health, Salt Lake City, Utah, United States

Divya Raghavan, MD

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.