Targeting oxidative stress in septic acute kidney injury: From theory to practice

CPC Ow; A Trask-Marino; AH Betrie; RG Evans; CN May; YR Lankadeva

Journal article

Targeting oxidative stress in septic acute kidney injury: From theory to practice

CPC Ow, A Trask-Marino, AH Betrie, RG Evans, CN May, YR Lankadeva

Journal of Clinical Medicine | MDPI | Published : 2021

DOI: 10.3390/jcm10173798

Download PDF

Abstract

Sepsis is the leading cause of acute kidney injury (AKI) and leads to increased morbidity and mortality in intensive care units. Current treatments for septic AKI are largely supportive and are not targeted towards its pathophysiology. Sepsis is commonly characterized by systemic inflammation and increased production of reactive oxygen species (ROS), particularly superoxide. Concomitantly released nitric oxide (NO) then reacts with superoxide, leading to the formation of reactive nitrogen species (RNS), predominantly peroxynitrite. Sepsis-induced ROS and RNS can reduce the bioavailability of NO, mediating renal microcirculatory abnormalities, localized tissue hypoxia and mitochondrial dysfun..

View full abstract

University of Melbourne Researchers

Clive May Author

Yugeesh Lankadeva Author

Related Projects (4)

What causes kidney failure in septic shock

Acute renal failure is a serious condition that affects up to 20% of patients in Intensive Care Units. Sepsis and septic shock remain the mo..

The pathophysiology of septic acute kidney injury

Septic shock is a common clinical problem; it is frequently associated with kidney failure that increases mortality. We aim to determine the..

Treatment of septic shock

Septic shock is a major cause of death in intensive care units. It is associated with large increases in sympathetic nerve activity to the h..

REVERSING RENAL MEDULLARY HYPOXIA AND ACUTE KIDNEY INJURY IN SEPSIS

Acute kidney injury is a major unresolved problem in patients with sepsis, which greatly increases their risk of death. We have shown that a..

Grants

Awarded by National Health and Medical Research Council

Funding Acknowledgements

The studies referred to from the C.N.M. and Y.R.L. laboratories have been funded by the National Health and Medical Research Council of Australia grants (NHMRC, 454615, 1009280, 1050672, 1122455, 1188514). Y.R.L. was supported by a Future Leader Postdoctoral Fellowship by the National Heart Foundation of Australia (NHF, 101853).