RESUMO
As a co-stimulatory blocker against CD28 receptor, belatacept has been approved and applied to the treatment of rejection in organ transplantation in Europe and America. Belatacept has been proven to outperform calcineurin inhibitor (CNI) in improving the long-term survival rate of recipients and grafts, and enhancing graft function. Nevertheless, it might cause a high incidence of rejection. To resolve this issue, transplant workers have attempted to optimize belatacept immunosuppressive regimen and achieved good clinical efficacy. Although belatacept has been proven to exert poor effect on memory T cells, it has potential value in exploring new co-stimulatory molecular targets to optimize immunosuppressive regimes due to its specificity for immune cells and mild adverse effects. In this article, the advent of co-stimulatory blocker, clinical efficacy and application of belatacept, and the causes of belatacept-resistant rejection were reviewed.
RESUMO
Thrombotic microangiopathy (TMA) is a serious complication of solid organ transplantation. Drug-induced TMA is typically caused by immunosuppressants, particularly calcineurin inhibitors. Withdrawing the causative drug can be one of the treatments for TMA. However, the more immunosuppressants are reduced, the more risk of rejection increases. Even if TMA is successfully resolved, the outcomes of patient and graft survival would be worse than expected. Therefore, it is necessary to maintain efficient and safe immunosuppression therapy. We report on a case of de novo TMA after kidney transplantation triggered by tacrolimus and reactivated by sirolimus. Belatacept, a novel CTLA4 Ig fusion protein, was administered for maintenance immunosuppressant with mycophenolate mofetil and prednisolon. The patient had excellent early graft outcome, and there have been no adverse events so far.