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Abstract

Acute kidney injury (AKI) is a sudden decline in kidney function. AKI is at risk of progressing end-stage renal disease requiring hemodialysis. Increasing evidence suggests inflammation and oxidative stress important role in the pathogenesis of AKI. The purpose of this literature review is to investigate the role of inflammation and oxidative stress in AKI. Methods were conducted following the literature review guidelines. Inclusion criteria were reference sources less than 5 years old and data related to inflammation and oxidative stress in AKI. Exclusion criteria were manuscripts that were not fully accessible and unverified sources. AKI is commonly caused by reduced renal blood flow, structural damage to the kidney, and inflammation / obstruction. Cellular damage and molecular products are the main triggers of inflammation and the resulting ROS. Reperfusion increases ROS that activate various pathways causing cell membrane, cytoskeleton and DNA injury. The adaptive response after AKI is the repair of renal function and structure, but maladaptive responses can occur by inflammatory persistence, fibroblast proliferation and excessive extracellular matrix deposition. AKI involves complex interactions between the renal parenchyma and the immune system resulting in inflammation, apoptosis and oxidative stress leading to impaired renal function.

Keywords

AKI, Inflammation, oxidative stress, ischemia.

Article Details

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