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Abstract

Kidney transplant remains the best type of renal replacement therapy in most patients with end-stage kidney disease, even in those with high immunologic risk. Immunosuppression in these patients is regarded as more complex, owing to the higher risk of both acute and chronic rejection. The advent of induction immunosuppression has resulted in a lower incidence of acute rejection and consequently improved shortterm patient and allograft outcomes. Indeed, the use of these agents, especially in high-risk recipients, has become standard of care at most transplant centers. Transplant physicians are constantly faced with the challenge of estimating the recipients' immunologic risk and tailoring their immunosuppression ac cordingly. This review article aims to provide an up-to-date evaluation of the various studies available, which investigated the use of induction agents in kidney transplant, specifically in high-risk recipients. It evaluates the use of the most frequently used polyclonal antibody (rabbit antithymocyte globulin) versus the less commonly used monoclonal antibody alemtuzumab, superseded agents such as muromonab-CD3, and potentially emerging agents such as rituximab, bortezomib, and eculizumab. With this systematic review, we hope to inform the scientific community and facilitate this controversial decision through the implementation of robust scientific evidence.

Polyclonal anti T-lymphocyte antibody therapy monitoring in kidney transplant recipients: comparison of CD3+ T cell and total lymphocyte counts

“…In patients receiving kidneys from donors with acute injuries, these products can be used to avoid early administration of calcineurin inhibitors. ( 12 ) These agents can also be used in acute graft rejection, either as primary treatment or rescue therapy for steroid-resistant rejections. ( 13 ) Significant benefits derived from the use of ATG in renal transplantation include low rejection rates, enhanced graft survival and function, potentially facilitated development of regulatory T cells implicated in suppression mechanisms, such as CD4 + /CD25 + / FOXP3 + , and improved graft survival.…”