Calcineurin inhibitors (CNIs) are both the savior and Achilles' heel of kidney transplantation. Although CNIs have significantly reduced rates of acute rejection, their numerous toxicities can plague kidney transplant recipients. By 10 years, virtually all allografts will have evidence of CNI nephrotoxicity. CNIs have been strongly associated with hypertension, dyslipidemia, and new onset of diabetes after transplantation—significantly contributing to cardiovascular risk in the kidney transplant recipient. Multiple electrolyte derangements including hyperkalemia, hypomagnesemia, hypercalciuria, metabolic acidosis, and hyperuricemia may be challenging to manage for the clinician. Finally, CNI-associated tremor, gingival hyperplasia, and defects in hair growth can have a significant impact on the transplant recipient’s quality of life. In this review, the authors briefly discuss the pharmacokinetics of CNI and discuss the numerous clinically relevant toxicities of commonly used CNIs, cyclosporine and tacrolimus.

钙调磷酸酶抑制剂（CNIs）既是肾脏移植的救星，也是跟腱的后跟。尽管CNI的急性排斥反应率显着降低，但其众多毒性会困扰肾移植接受者。到10年时，几乎所有同种异体移植都将具有CNI肾毒性的证据。CNIs与高血压，血脂异常和移植后新发糖尿病有很强的联系-大大增加了肾脏移植受者的心血管风险。包括高血钾，低镁血症，高钙尿症，代谢性酸中毒和高尿酸血症在内的多种电解质紊乱可能对临床医生来说是挑战性的。最后，与CNI相关的震颤，牙龈增生以及毛发生长的缺陷可能对移植接受者的生活质量产生重大影响。