Suppr超能文献

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.

Abstract

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.

摘要

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。

相似文献

1
Sepsis-Associated Acute Kidney Injury.脓毒症相关性急性肾损伤
Crit Care Clin. 2021 Apr;37(2):279-301. doi: 10.1016/j.ccc.2020.11.010. Epub 2021 Feb 13.
2
The Pathophysiology of Sepsis-Associated AKI.脓毒症相关性急性肾损伤的病理生理学。
Clin J Am Soc Nephrol. 2022 Jul;17(7):1050-1069. doi: 10.2215/CJN.00850122. Epub 2022 Jun 28.
5
The renal microcirculation in sepsis.脓毒症中的肾微循环。
Nephrol Dial Transplant. 2015 Feb;30(2):169-77. doi: 10.1093/ndt/gfu105. Epub 2014 May 21.

引用本文的文献

8
Review of research progress in sepsis-associated acute kidney injury.脓毒症相关性急性肾损伤的研究进展综述
Front Mol Biosci. 2025 Jul 11;12:1603392. doi: 10.3389/fmolb.2025.1603392. eCollection 2025.
10

本文引用的文献

2
Long-Term Outcomes in Patients with Acute Kidney Injury.急性肾损伤患者的长期预后。
Clin J Am Soc Nephrol. 2020 Mar 6;15(3):423-429. doi: 10.2215/CJN.10410919. Epub 2020 Feb 19.
3
The Role of Biomarkers in Acute Kidney Injury.生物标志物在急性肾损伤中的作用。
Crit Care Clin. 2020 Jan;36(1):125-140. doi: 10.1016/j.ccc.2019.08.010.
6
Mitochondria in Sepsis-Induced AKI.脓毒症诱导的急性肾损伤中的线粒体。
J Am Soc Nephrol. 2019 Jul;30(7):1151-1161. doi: 10.1681/ASN.2018111126. Epub 2019 May 10.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验