• Sadudee Peerapornratana, Carlos L Manrique-Caballero, Hernando Gómez, and John A Kellum.
• Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; The Clinical Research, Investigation and Systems Modeling of Acute Illness Center, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; Excellence Center for Critical Care Nephrology, Division of Nephrology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand; Department of Laboratory Medicine, Chulalongkorn University, Bangkok, Thailand.
• Kidney Int. 2019 Nov 1; 96 (5): 1083-1099.

AbstractSepsis-associated acute kidney injury (S-AKI) is a frequent complication of the critically ill patient and is associated with unacceptable morbidity and mortality. Prevention of S-AKI is difficult because by the time patients seek medical attention, most have already developed acute kidney injury. Thus, early recognition is crucial to provide supportive treatment and limit further insults. Current diagnostic criteria for acute kidney injury has limited early detection; however, novel biomarkers of kidney stress and damage have been recently validated for risk prediction and early diagnosis of acute kidney injury in the setting of sepsis. Recent evidence shows that microvascular dysfunction, inflammation, and metabolic reprogramming are 3 fundamental mechanisms that may play a role in the development of S-AKI. However, more mechanistic studies are needed to better understand the convoluted pathophysiology of S-AKI and to translate these findings into potential treatment strategies and add to the promising pharmacologic approaches being developed and tested in clinical trials.Copyright © 2019 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

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