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Abstract: FR-PO755

A Case of Self-Limited Thrombotic Microangiopathy (TMA) After an ABO Incompatible (ABOi) Kidney Transplant (KT)

Session Information

Category: Transplantation

  • 2102 Transplantation: Clinical


  • Pothula Venkata, Varsha Reddy, University of Virginia, Charlottesville, Virginia, United States
  • Warburton, Karen M., University of Virginia, Charlottesville, Virginia, United States
  • Kamal, Jeanne, University of Virginia, Charlottesville, Virginia, United States
  • Glass, William F., University of Virginia, Charlottesville, Virginia, United States
  • Doyle, Alden Michael, University of Virginia, Charlottesville, Virginia, United States

TMA is a potentially fatal complication that occurs after solid organ transplant. Post transplant TMA development most commonly triggered with antibody mediated rejection (AMR) and calcineurin inhibitors (CNI).

Case Description

A 44 year old male with CKD secondary to congenital anomalies of kidney and urinary tract who underwent a preemptive living donor ABOi KT (blood type A to O). Anti-A titers prior to transplant were 1:4, and had no donor specific antibodies. Was started on mycophenolate prior to transplant, did not need any further desensitization therapies. Intraop course was uncomplicated with immediate graft function. Induction regimen included thymoglobulin 6 mg/kg, received rituximab and was started on tacrolimus on POD 1. He had worsening anemia and thrombocytopenia on POD 2 with high LDH level and low haptoglobin concerning for TMA . He underwent one session of plasmapheresis on POD 4. His kidney function continued to improve since transplant. Hemolysis improved on POD 5, so further pheresis sessions were held. An allograft biopsy on POD 7 showed acute endothelial injury, diffusely enlarged endothelial cell with mitotic figures and entrapped RBC fragments but no fibrin thrombi. There was no concern for AMR with absence of glomerulitis and peritubular capillaritis. C4d was positive as excepted in ABOi KT.


TMA is encountered twice as much in ABOi KT compared to other KT. The rapid clinical improvement with minimal therapy and while remaining on tacrolimus, and the absence of pathological evidence makes AMR and CNI use as less likely triggers of TMA. Evidence of early onset TMA, with injury isolated to endothelial cell, likely from an immune mediated injury triggered by isohemaglutinins against endothelial cells bearing blood group A antigens. The self-limited nature of this insult is possibly similar to the accommodation phenomena which is seen in ABOi KT.