Abstract: PUB485
Catch It or Lose It: Timely Recognition and Conservative Management of Thrombotic Microangiopathy in a Kidney Transplant Recipient
Session Information
Category: Transplantation
- 2102 Transplantation: Clinical
Authors
- Matarneh, Ahmad, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
- Sardar, Sundus, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
- Portela, Rafael, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
- Ghahramani, Nasrollah, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
- Kaur, Gurwant, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
Introduction
Thrombotic microangiopathy (TMA) is rare and potentially lethal complication in kidney transplant recipients, characterized by hemolytic anemia, thrombocytopenia, and kidney failure. TMA can be triggered by multiple factors including medications. Calcineurin inhibitors (CNIs) are associated with TMA. Prompt recognition and management are crucial to prevent severe outcomes, such as graft loss. This case highlights early TMA occurring two weeks after a kidney biopsy-proven chronic acute antibody-mediated rejection, where timely intervention led to a favorable prognosis and graft salvage.
Case Description
A 41-year-old man with end-stage kidney disease from adult polycystic kidney disease who received deceased donor kidney transplant six years ago. His immunosuppression included mycophenolate mofetil (1000mg twice daily) and extended-release tacrolimus (5mg daily). His kidney function declined over time, with creatinine rising from 2.2mg/dl to 3.5mg/dl, prompting a kidney biopsy. The biopsy showed acute T-cell-mediated rejection (grade 1A) and chronic active antibody-mediated rejection, treated with pulse steroids, IV immunoglobulin, and a tapering course of oral steroids.
He presented to the hospital with bruising, abdominal pain, nausea, and diarrhea for 3 days. Labs revealed thrombocytopenia (35K/μL from 130K/μL), anemia (7.1g/dL from 8.9g/dL), and elevated creatinine (5.25 mg/dL, baseline 2.2mg/dL). Suspecting TMA, especially with recent supratherapeutic tacrolimus level. Workup showed high LDH (572 U/L), low haptoglobin (<10mg/dL), normal bilirubin (0.5mg/dL), and rare schistocytes on a peripheral smear. ADAMTS13 and Coombs tests were negative. Tacrolimus was replaced with belatacept. Platelet count, Hb, and kidney function improved with stopping tacrolimus. Early inclusion of TMA in the differential diagnosis enabled prompt treatment and favorable outcomes.
Discussion
The timely diagnosis of TMA in a kidney transplant recipient is critical and delay in diagnosis can lead to severe complications including graft loss. TMA in transplant recipients can be triggered by medications such as CNIs and mTOR inhibitors, antibody mediated rejection, viral infections (Hepatits C, HIV, BK Virus), genetic abnormalities in complement cascade. Prompt recognition and management of TMA can reduce graft loss and improve outcomes.