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Abstract: SA-PO1189

Progressive Donor-Derived Thrombotic Microangiopathy in Two Recipients from a Single Donor

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Arevalo Salazar, Dory E., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Kodali, Lavanya, Mayo Clinic Arizona, Scottsdale, Arizona, United States
  • Ryan, Margaret, Mayo Clinic Arizona, Scottsdale, Arizona, United States
  • Smith, Maxwell L., Mayo Clinic Arizona, Scottsdale, Arizona, United States
  • Fu, Liying, Mayo Clinic Arizona, Scottsdale, Arizona, United States
Introduction

Donor-derived thrombotic microangiopathy (TMA) is a rare cause of delayed graft function (DGF) in renal transplant patients, and donor kidneys are routinely screened for microthrombi on preimplantation biopsy. We report an unusual case of two kidney transplant recipients from a single deceased donor with chronic TMA on post-reperfusion biopsies, followed by DGF and progression to severe active chronic TMA on subsequent allograft biopsies.

Case Description

The donor was a 63 year old woman with brain death from subdural hematomas after a fall. Both kidneys were transplanted, and preimplant frozen section evaluation showed no intraglomerular or intravascular microthrombi.
The right kidney went to a 70 year old man with a cold ischemia time of 31 hours. The left kidney went to a 59 year old man with a cold ischemia time of 16 hours. Both recipients had end-stage kidney disease due to type 2 diabetes, no known donor specific antibodies (DSA) and 0% cPRA. Postreperfusion biopsies showed diffuse glomerular basement membrane (GBM) double contouring in both recipients. Both of the recipients had DGF. The first recipient underwent an allograft biopsy 41 days post-transplantation, and the second underwent an allograft biopsy 17 days posttransplantation. Both biopsies showed severe active chronic TMA with negative C4d in peritubular capillaries (Figure 1). No DSAs were detected. The immunosuppression was transitioned to belatacept with low-dose tacrolimus for both recipients, but they remained dialysis dependent.

Discussion

Both donor kidneys harbored chronic TMA without microthrombi, which was better recognized on postreperfusion biopsies with special stains. Despite early diagnosis and calcineurin inhibitor minimization with belatacept conversion, both recipients developed severe active chronic TMA and DGF, highlighting the importance of donor biopsy evaluation and diagnosis of subtle TMA.