Department of Nephrology, Medical School University of Ioannina, Ioannina, Greece.
Division of nephrology and Hypertension, 1st Department of Internal Medicine, AHEPA Hospital, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Oxid Med Cell Longev. 2017;2017:6193694. doi: 10.1155/2017/6193694. Epub 2017 Sep 28.
Acute kidney injury (AKI) is a multifactorial entity that occurs in a variety of clinical settings. Although AKI is not a usual reason for intensive care unit (ICU) admission, it often complicates critically ill patients' clinical course requiring renal replacement therapy progressing sometimes to end-stage renal disease and increasing mortality. The causes of AKI in the group of ICU patients are further complicated from damaged metabolic state, systemic inflammation, sepsis, and hemodynamic dysregulations, leading to an imbalance that generates oxidative stress response. Abundant experimental and to a less extent clinical data support the important role of oxidative stress-related mechanisms in the injury phase of AKI. The purpose of this article is to present the main pathophysiologic mechanisms of AKI in ICU patients focusing on the different aspects of oxidative stress generation, the available evidence of interventional measures for AKI prevention, biomarkers used in a clinical setting, and future perspectives in oxidative stress regulation.
急性肾损伤（AKI）是一种多因素实体，发生在多种临床环境中。尽管 AKI 不是重症监护病房（ICU）入院的常见原因，但它经常使重症患者的临床病程复杂化，需要肾脏替代治疗，有时进展为终末期肾病并增加死亡率。ICU 患者 AKI 的病因因代谢状态受损、全身炎症、败血症和血流动力学失调而变得更加复杂，导致失衡产生氧化应激反应。大量的实验和在较小程度上的临床数据支持氧化应激相关机制在 AKI 损伤阶段的重要作用。本文的目的是介绍 ICU 患者 AKI 的主要病理生理机制，重点介绍氧化应激产生的不同方面、AKI 预防的干预措施的现有证据、临床环境中使用的生物标志物以及氧化应激调节的未来展望。
