*Purpose: Thrombotic Microangiopathy (TMA) in kidney transplant recipients is a serious complication that can cause graft loss. It can be associated with immunosuppressive medications such as calcineurin inhibitors (CNI). CNI-associated TMA can prove to be a therapeutic dilemma given the risks of rejection with CNI withdrawal. We report six cases of CNI-associated TMA that were converted to Belatacept therapy

*Methods: Retrospective review of the clinical course and outcomes in 6 kidney transplant recipients who developed CNI-associated TMA and were converted to Belatacept therapy. Outcomes of interest included eGFR pre- and post-conversion, patient and graft survival, and incidence of acute rejection

*Results: Patient and transplant characteristics are noted in Table 1. All patients were on a CNI (5 on tacrolimus, 1 on cyclosporine), an antimetabolite (5 on mycophenolate mofetil and 1 on azathioprine) and prednisone at the time of TMA diagnosis. The average time between kidney transplant and the diagnosis of TMA was 6.5 months. All patients except patient 6 were diagnosed based on a kidney allograft biopsy that showed acute TMA with concurrent allograft dysfunction. Patient 6 was presumed to have TMA based on concomitant evidence of MAHA and allograft dysfunction. The CNI was discontinued at the time of diagnosis in all patients. Patients 1 and 2 received Eculizumab at the time of diagnosis. Patient 3 received plasmapheresis and IVIG in view of positive C4d staining on biopsy but this was discontinued after confirming absence of donor specific antibodies. Patient 5 was switched to Sirolimus and patient 6 received a dose of basiliximab while awaiting insurance approval for Belatacept. Patient 3 had a negative EBV serology at the time of conversion to Belatacept and underwent monthly EBV PCR monitoring. He did not develop EBV viremia. None of the patients developed PTLD. Patient 2 required hemodialysis at the time of diagnosis and did not recover his allograft function. None of the other 5 patients developed episodes of rejection or had graft loss. Allograft function improved in all of these patients and the average GFR was 44.6, 30.2, and 57.4 mL/min/1.73 m² at baseline, time of TMA diagnosis, and at 6 months following conversion to Belatacept, respectively

*Conclusions: Conversion from CNI to Belatacept therapy was associated with an improvement in allograft function in all but one of the 6 patients in our report with no incidences of acute rejection. The effectiveness and safety of this approach warrant further evaluation in larger groups of patients

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