*Purpose: From August 2018 until July 2019, an alarming 6% of kidney transplant recipients at this transplant center had biopsy-proven thrombotic microangiopathy (TMA) within 1 week of transplantation in the absence of any evidence of rejection. We reviewed each case to identify a common link with the goal of deterring future events

*Methods: All transplant recipients with biopsy-proven TMA within 1 week of transplantation at our center were reviewed for a large number of donor and recipient characteristics, including but not limited to: receipt of a cadaveric versus living donor kidney, donor kidney donor profile index (KDPI), cold ischemia time, induction agent, highest tacrolimus level prior to biopsy, presence of donor specific antibodies (DSAs), presence of anti-endothelial cell antibodies (AECAs), and presence of anti-angiotensin II type 1 receptor (AT1R) antibodies. These characteristics were compared against those of other transplant recipients at our institution during the same time frame without TMA in order to identify statistically significant differences.

*Results: Across all available measured variables, no statistically significant differences were found between patients with early biopsy-proven TMA and those without. AECAs and AT1R antibodies are not checked routinely on transplant recipients at this institution, so data is not available for comparison. Antibody titers for AECAs and AT1R were measured for 5 of 6 patients who met inclusion criteria. Among those 5 patients, 3 were positive for AECAs and 1 was positive for AT1R antibodies, with 1 patient being negative for both antibodies. The patient with AT1R antibodies developed immediate ischemic graft failure without recovery despite plasmapheresis and calcineurin-inhibitor (CNI) discontinuation. The remaining patients recovered graft function and remain dialysis-independent with an average creatinine of 1.4. 4 of 5 underwent plasmapheresis and transition to a CNI-free regimen with belatacept. The fifth patient had a mild case of TMA clinically improving by the time of biopsy and notably negative for both antibodies, for whom decision was made to transition from tacrolimus to cyclosporine only.

*Conclusions: We found a high percentage of AECAs among kidney transplant recipients at our institution with immediate post-transplant TMA in the absence of other statistically significant differences compared to control recipients. Additionally, all patients with a positive AECA demonstrated significant graft recovery after CNI discontinuation, suggesting CNI-related TMA may be influenced directly by the presence of AECAs. These findings support the need for additional research, including broader AECA monitoring in transplant recipients to determine whether a statistically significant difference exists among those who develop TMA and those who do not. If additional studies confirm a link, it may prompt consideration for CNI-free maintenance therapy in AECA-positive patients.

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