Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Curr Opin Crit Care. 2009 Dec;15(6):481-7. doi: 10.1097/MCC.0b013e328332f69e.
Acute kidney injury (AKI) continues to contribute significantly to morbidity and mortality in the ICU setting, especially when associated with distant organ dysfunction. There is increasing evidence that AKI directly contributes to organ dysfunction in lung, brain, liver, heart and other organs. This review will examine our current understanding of the deleterious organ crosstalk in the critically ill, which can provide a framework for developing novel therapeutics.
The majority of studies correlating AKI with distant organ dysfunction have demonstrated the pathophysiological importance of proinflammatory and proapoptotic pathways as well as oxidative stress and reactive oxygen species (ROS) production. Leukocyte activation and infiltration, changes in levels of soluble factors such as cytokines and chemokines, and regulation of cell death in extra-renal organs are potentially important mechanisms by which AKI modulates multiorgan dysfunction.
There is increasing knowledge of AKI and deleterious interorgan crosstalk that arises, at least in part, due to the imbalance of immune, inflammatory, and soluble mediator metabolism that attends severe insults to the kidney. Further studies can build on these new mechanistic observations to develop strategies to improve outcomes in the critically ill patient.
急性肾损伤（AKI）在 ICU 环境中仍然是发病率和死亡率的重要原因，尤其是当与远处器官功能障碍相关时。越来越多的证据表明 AKI 直接导致肺、脑、肝、心和其他器官的功能障碍。这篇综述将探讨我们目前对危重病患者中有害的器官串扰的理解，这可以为开发新的治疗方法提供框架。
大多数将 AKI 与远处器官功能障碍相关联的研究表明，促炎和促凋亡途径以及氧化应激和活性氧（ROS）产生具有病理生理重要性。白细胞的激活和浸润、细胞因子和趋化因子等可溶性因子水平的变化，以及肾脏外器官细胞死亡的调节，是 AKI 调节多器官功能障碍的潜在重要机制。
越来越多的知识表明 AKI 与有害的器官间串扰有关，这至少部分归因于严重肾损伤时免疫、炎症和可溶性介质代谢的失衡。进一步的研究可以在这些新的机制观察的基础上，制定改善危重病患者预后的策略。
