Abstract: PUB231
De Novo Post Kidney Transplantation Thrombotic Microangiopathy
Session Information
Category: Transplantation
- 1901 Transplantation: Basic
Authors
- Sabescumar, Janany Jansy, University of Rochester, Rochester, New York, United States
- Taylor, Jeremy G., University of Rochester, Rochester, New York, United States
- Shahbazov, Rauf, State University of New York Upstate Medical University, Syracuse, New York, United States
- Dewolfe, David M., University of Rochester, Rochester, New York, United States
Introduction
De novo post kidney transplantation thrombotic microangiopathy (TMA) is rare. We present two cases of post kidney transplant TMA acquired from the donor kidney
Case Description
A 26 year old male with a significant past medical history of end-stage kidney disease secondary to hereditary focal segmental glomerulosclerosis (FSGS) requiring initially presented for deceased donor kidney transplantation. The kidney donation was from a brain death donor with no significant medical history. The preliminary kidney biopsy of the donor kidney revealed focal patchy acute tubular necrosis (ATN). Induction immunosuppression included a total dose of 5 mg/kg of thymoglobulin and followed by initiation of tacrolimus for goal trough of 8 - 10 mg, prednisone 40 mg, and mycophenolate 1000 mg twice daily. The patient had delayed graft function with a creatinine initially at 18 mg/dL which only reduced to 17 mg/dL over the next couple of days. On postoperative day 5, the patient was dialyzed due to symptomatic uremia. In addition, he was noted to have developed worsening anemia and thrombocytopenia with a platelet count dropping from 208 to 47 per microliter of blood. A renal biopsy was pursued and the pathology results revealed post-transplant thrombotic microangiopathy (TMA) due to hemolytic uremic syndrome. In addition, the final donor kidney biopsy had later revealed thrombotic microangiopathy within approximately 60% of the glomeruli. The patient who received the second kidney had a similar clinical course. Both recipients received one dose of eculizumab with improvement in allograft function. They were both discharged without hemodialysis with close follow up.
Discussion
TMA was acquired by the donor TMA which was likely caused by ATN. It wasn't until later in the course that the final biopsy report of the donor kidney revealed TMA which confused the diagnosis of allograft kidney injury.