*Purpose: A majority of kidney transplant recipients receive calcineurin inhibitor (CNI)-based immunosuppression. However, some do not tolerate CNIs and require other immunosuppressive strategies. Until recently, alternative approaches have been associated with inferior outcomes, but recent methods have effectively utilized belatacept in CNI intolerant patients. Though promising, belatacept uptake has been limited by higher acute rejection rates, unavailability due to production shortages, and logistical challenges as a result of intravenous infusion requirements. Interestingly, its predecessor abatacept is clinically available in subcutaneous formulation to treat autoimmune disorders but has not been used in clinical transplantation. In this study we aimed to determine the outcomes of CNI intolerant transplant recipients converted to abatacept as rescue immunosuppression.

*Methods: With institutional review board approval we reviewed our institutional database for kidney or simultaneous pancreas/kidney (SPK) transplant recipients that received abatacept after transplantation. We identified nine transplant recipients converted to abatacept as a result of CNI toxicity early after transplant during periods of belatacept unavailability. Retrospective chart review was performed on these nine patients.

*Results: Patients converted to abatacept were between the ages of 19 and 60 at the time of transplant. Five were first-time kidney transplant recipients, one a first-time SPK recipient, and three were re-transplants after prior renal allograft failures. CNI intolerance consisted of clinical toxicity, impaired renal function, prolonged delayed graft function and thrombotic microangiopathy. Patients received abatacept for a median duration of 82 months (range 3-116 months, mean 68 months). Four have remained on abatacept maintenance therapy and five have been converted to belatacept. Allograft salvage was achieved in all patients with 100% patient and graft survival at a median follow up of 115 months (range 14-145 months, mean 98 months) with stable, long-term renal allograft function (mean eGFR of 40.04 ±13.23 mL/min/1.73m²). A single cellular rejection episode occurred in one patient six weeks after conversion to abatacept. All recipients have exhibited stable PRA levels and none developed DSA. No clinically apparent protective immunity concerns were observed.

*Conclusions: Our findings in this small series of transplant recipients converted to abatacept introduce the concept of abatacept as a safe, effective and logistically viable alternative immunosuppressive option for long-term maintenance therapy following transplantation in the event of CNI intolerance, and suggest that future clinical studies utilizing abatacept either de novo or as conversion therapy in transplant recipients should be considered.

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