脓毒症相关性急性肾损伤
Sepsis-Associated Acute Kidney Injury.
作者信息
Manrique-Caballero Carlos L, Del Rio-Pertuz Gaspar, Gomez Hernando
机构信息
Department of Critical Care Medicine, Center for Critical Care Nephrology, University of Pittsburgh School of Medicine, 3347 Forbes Avenue, Suite 220, Room 207, Pittsburgh, PA 15213, USA; Department of Critical Care Medicine, The CRISMA (Clinical Research, Investigation and Systems Modeling of Acute Illness) Center, University of Pittsburgh School of Medicine, 3347 Forbes Avenue, Suite 220, Room 207, Pittsburgh, PA 15213, USA.
Department of Critical Care Medicine, Center for Critical Care Nephrology, University of Pittsburgh School of Medicine, 3347 Forbes Avenue, Suite 220, Room 207, Pittsburgh, PA 15213, USA; Department of Critical Care Medicine, The CRISMA (Clinical Research, Investigation and Systems Modeling of Acute Illness) Center, University of Pittsburgh School of Medicine, 3347 Forbes Avenue, Suite 220, Room 207, Pittsburgh, PA 15213, USA; Department of Internal Medicine, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430, USA.
出版信息
Crit Care Clin. 2021 Apr;37(2):279-301. doi: 10.1016/j.ccc.2020.11.010. Epub 2021 Feb 13.
Sepsis-associated acute kidney injury (S-AKI) is a common and life-threatening complication in hospitalized and critically ill patients. It is characterized by rapid deterioration of renal function associated with sepsis. The pathophysiology of S-AKI remains incompletely understood, so most therapies remain reactive and nonspecific. Possible pathogenic mechanisms to explain S-AKI include microcirculatory dysfunction, a dysregulated inflammatory response, and cellular metabolic reprogramming. In addition, several biomarkers have been developed in an attempt to improve diagnostic sensitivity and specificity of S-AKI. This article discusses the current understanding of S-AKI, recent advances in pathophysiology and biomarker development, and current preventive and therapeutic approaches.
脓毒症相关急性肾损伤（S-AKI）是住院患者和危重症患者中常见的、危及生命的并发症。其特征是与脓毒症相关的肾功能迅速恶化。S-AKI的病理生理学仍未完全阐明，因此大多数治疗方法仍具有反应性且缺乏特异性。解释S-AKI的可能致病机制包括微循环功能障碍、炎症反应失调和细胞代谢重编程。此外，已经开发了几种生物标志物，试图提高S-AKI的诊断敏感性和特异性。本文讨论了目前对S-AKI的认识、病理生理学和生物标志物开发的最新进展，以及当前的预防和治疗方法。
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