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Kidney Week

Abstract: PO2444

Human Herpesvirus 8-Associated Kaposi Sarcoma Developing in a Kidney Allograft from a Hepatitis C-Positive Donor

Session Information

Category: Trainee Case Report

  • 1902 Transplantation: Clinical

Authors

  • Story, Maria T., The University of Iowa Roy J and Lucille A Carver College of Medicine, Iowa City, Iowa, United States
  • Sanders, M. Lee, The University of Iowa Roy J and Lucille A Carver College of Medicine, Iowa City, Iowa, United States
  • Jenigiri, Sreedevi koppisetti, The University of Iowa Roy J and Lucille A Carver College of Medicine, Iowa City, Iowa, United States
  • Bashir, Amani, The University of Iowa Roy J and Lucille A Carver College of Medicine, Iowa City, Iowa, United States
  • Longo, Jude, Iowa City VA Medical Center, Iowa City, Iowa, United States
  • Grodstein, Elliot, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Thomas, Christie P., The University of Iowa Roy J and Lucille A Carver College of Medicine, Iowa City, Iowa, United States
  • Katz, Daniel, The University of Iowa Roy J and Lucille A Carver College of Medicine, Iowa City, Iowa, United States
Introduction

Kaposi Sarcoma (KS) is an endothelial malignancy caused by the oncogenic virus Human Herpesvirus-8 (HHV-8) and transmission during kidney transplantation can occur. We describe two cases of donor-to-recipient transmission of HHV-8, with one recipient developing KS in the kidney allograft causing acute kidney injury (AKI).

Case Description

Donor: The donor died from complications of IV drug use and had known hepatitis C (HCV) at the time of organ donation.

Recipient 1: 64-year-old male with ESRD, induction with basiliximab. He tested positive for HCV on post-transplant day 2 and was treated with sofosbuvir/velpatasvir for 12 weeks. Two months post-transplant, he developed encephalopathy and was found to have HHV-8 viremia during his workup. Immunosuppression was decreased, HHV-8 PCR levels were monitored and eventually were undetectable. He did not develop KS.

Recipient 2: 71-year-old male with ESRD, induction with anti-thymocyte globulin. He was treated pre-emptively for HCV with glecaprevir/pibrentsvir. Five months post-transplant he was admitted for rising creatinine. Initial allograft biopsy was of poor quality but was suggestive of Banff IIA rejection; IV methylprednisone and anti-thymocyte globulin were administered. Repeat biopsy demonstrated extensive replacement of the allograft tissue with KS. PET scan revealed metastatic KS. Immunosuppression was discontinued and he underwent allograft nephrectomy. He died at home 2 months later.

Retroactive testing of samples prior to transplantation revealed the donor was HHV-8 PCR positive at the time of death and both recipients were HHV-8 antibody and PCR negative.

Discussion

We describe donor-to-recipient transmission of HHV-8 during kidney transplantation. HHV-8 associated post-transplant KS is well described but rare in the US. Post-transplant KS typically presents with classic skin lesions and kidney allograft involvement with KS is rare, with only 7 previously reported cases. Public Health Service (PHS) increased risk donors may represent a subset of donors at especially high risk for HHV-8 transmission. Future investigation is needed into this population to determine if post-transplant HHV-8 PCR monitoring or adjustments in immunosuppression are needed for kidney transplant recipients of PHS increased risk organs.