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J Am Soc Nephrol. 2019 May 10. pii: ASN.2018111126. doi: 10.1681/ASN.2018111126. [Epub ahead of print]

Mitochondria in Sepsis-Induced AKI.

Author information

1
Department of Emergency and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, China.
2
International Renal Research Institute of Vicenza, Vicenza, Italy.
3
Department of Nephrology, Dialysis and Transplantation, San Bortolo Hospital, Vicenza, Italy.
4
Molecular Biotechnology Center, Department of Medical Sciences, University of Turin, Italy.
5
Department of Nephrology, Dialysis and Transplantation, Virgen de la Salud Hospital, Toledo, Spain; and.
6
Department of Emergency and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, China; yinyongjie2003@sina.cn.
7
Division of Nephrology, University of Virginia Health System, Charlottesville, Virginia.

Abstract

AKI is a common clinical condition associated with the risk of developing CKD and ESKD. Sepsis is the leading cause of AKI in the intensive care unit (ICU) and accounts for nearly half of all AKI events. Patients with AKI who require dialysis have an unacceptably high mortality rate of 60%-80%. During sepsis, endothelial activation, increased microvascular permeability, changes in regional blood flow distribution with resulting areas of hypoperfusion, and hypoxemia can lead to AKI. No effective drugs to prevent or treat human sepsis-induced AKI are currently available. Recent research has identified dysfunction in energy metabolism as a critical contributor to the pathogenesis of AKI. Mitochondria, the center of energy metabolism, are increasingly recognized to be involved in the pathophysiology of sepsis-induced AKI and mitochondria could serve as a potential therapeutic target. In this review, we summarize the potential role of mitochondria in sepsis-induced AKI and identify future therapeutic approaches that target mitochondrial function in an effort to treat sepsis-induced AKI.

KEYWORDS:

Sepsis-induced AKI; biomarkers; metabolism; mitochondria; therapeutic targets

PMID:
31076465
DOI:
10.1681/ASN.2018111126

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