Abu Jawdeh Bassam G, Rabb Hamid
Contrib Nephrol. 2011;174:173-181. doi: 10.1159/000329395. Epub 2011 Sep 9.
Ischemia-reperfusion (IR) injury plays a significant role in the pathogenesis of both delayed graft function (DGF) in allografts and hemodynamic mediated acute kidney injury (AKI) of native kidneys. IR injury involves the interplay of several factors, including both the innate and adaptive immune systems. Though the final effector mechanisms causing injury are likely similar in both allograft and native kidneys, DGF is confounded by various donor, recipient and graft-handling factors. DGF is becoming increasingly important because of the growing number of patients awaiting kidney transplant. Identifying mediators, new diagnostics and therapeutics for DGF is important to provide more kidneys for transplant and improve outcomes. Furthermore, given that DGF occurs in a tightly controlled scenario, studying DGF is useful for early studies of proof of principle for biomarkers and therapeutics prior to launching into less wellcontrolled studies in large numbers of native kidney AKI patients.
缺血再灌注(IR)损伤在同种异体移植中延迟移植肾功能(DGF)以及自体肾血流动力学介导的急性肾损伤(AKI)的发病机制中均起重要作用。IR损伤涉及多种因素的相互作用,包括固有免疫系统和适应性免疫系统。尽管同种异体移植肾和自体肾中导致损伤的最终效应机制可能相似,但DGF会受到各种供体、受体和移植操作因素的影响。由于等待肾移植的患者数量不断增加,DGF变得越来越重要。识别DGF的介质、新的诊断方法和治疗方法对于提供更多可用于移植的肾脏并改善治疗结果至关重要。此外,鉴于DGF发生在一个严格控制的场景中,在对大量自体肾AKI患者进行较难控制的研究之前,研究DGF对于生物标志物和治疗方法的原理验证早期研究很有用。