Abstract
Chimeric antigen receptor (CAR) T-cell therapy represents a major advancement in the treatment of patients with acute lymphoblastic leukemia (ALL) and refractory non-Hodgkin lymphoma [1]. CAR T-cells are genetically engineered T-cells that express a surface receptor that contains a single-chain variable fragment (scFv) that can recognize tumor antigens and target tumor cells. The intracellular portion of the CAR includes T-cell receptor and costimulatory domains that result in T-cell activation and proliferation upon antigen binding. CAR T-cell activation is essential for their antineoplastic function, but involves the release of cytokines and chemokines, which in turn recruit other effector cells of the immune system, such as macrophages. A well-described complication of CAR T-cell therapy is cytokine release syndrome (CRS), an immunoinflammatory event associated with uncontrolled release of cytokines. The release of cytokines can lead to vasodilation, decreased cardiac output and intravascular volume depletion, which may potentiate renal injury. Kidney injury remains a less-recognized side effect of CRS and CAR T-cells. There are limited data regarding renal outcomes of patients treated with CAR T-cells [2, 3] but there is no information about outcomes after CAR T-cell therapy in patients with underlying chronic kidney disease (CKD). We aim to further elucidate outcomes in patients with CKD treated with CAR T-cell therapy at our institution.
Published Version
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