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Abstract: PO2193

Immune Checkpoint Inhibitor Therapy-Related Graft Intolerance Syndrome in a Failed Kidney Transplant Recipient on Hemodialysis

Session Information

  • Onco-Nephrology - 2
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 1500 Onco-Nephrology

Authors

  • Mejia, Christina Irene, Thomas Jefferson University, Philadelphia, Pennsylvania, United States
  • Frank, Adam Mathias, Thomas Jefferson University, Philadelphia, Pennsylvania, United States
  • Singh, Pooja, Thomas Jefferson University, Philadelphia, Pennsylvania, United States
  • Yadav, Anju, Thomas Jefferson University, Philadelphia, Pennsylvania, United States
Introduction

Immune check-point inhibitors (ICPIs) are monoclonal antibodies against inhibitory receptors on T-cells resulting in anti-cancer activity. The use of ICPIs among kidney transplant (KT) recipients with cancer is controversial, as ICPIs counter immune tolerance and is associated with a higher risk of rejection in functioning allografts. In failed allografts, the effects of ICPIs are unknown. We present a unique case of a patient with a failed KT on maintenance hemodialysis (HD) who developed graft intolerance syndrome (GIS) after ICPI therapy for metastatic renal cell carcinoma (RCC).

Case Description

Our patient is a 66-year old male with a history of diabetes, RCC and left nephrectomy in 1996. He developed end-stage kidney disease and had a deceased donor KT in 2012. His graft failed 6 years post KT, due to biopsy-proven recurrent diabetic nephrosclerosis. He was started on HD in 2018 and immunosuppression was tapered off. In 2019, he was diagnosed with renal and urothelial cell cancer in the right native kidney and underwent nephrectomy. Ten months later, distant metastasis was detected, and he was started on Nivolumab and Ipilimumab. Twenty-eight days after his 1st cycle of immunotherapy, he had good oncological response, but developed gross hematuria, pain over his allograft, malaise, and anemia consistent with GIS. Urine culture and cystoscopy were normal. A computed tomography scan of the abdomen revealed an enlarged allograft with patchy enhancement and perinephric stranding consistent with GIS. After a multidisciplinary discussion, he underwent transplant nephrectomy. Histopathology revealed grade II chronic active T-cell mediated rejection (TCMR).

Discussion

Although acute graft rejection from ICPI therapy has been documented, this is the first known report of GIS developing with ICPI therapy in a failed allograft. GIS typically occurs within 6-12 months of graft failure. Meanwhile, in functioning allografts, rejection occurs around 24 days after ICPI initiation. The temporal relation of GIS to ICPI initiation in our patient suggests the potential role of the latter as a trigger for GIS. As ICPI use becomes more prevalent in cancer management, we need to be aware of the potential complications with its use among KT recipients even with failed allografts, which requires multidisciplinary management.