Jump to main content
US EPA
United States Environmental Protection Agency
Search
Search
Main menu
Environmental Topics
Laws & Regulations
About EPA
Health & Environmental Research Online (HERO)
Contact Us
Print
Feedback
Export to File
Search:
This record has one attached file:
Add More Files
Attach File(s):
Display Name for File*:
Save
Citation
Tags
HERO ID
2836962
Reference Type
Journal Article
Title
The central role of renal microcirculatory dysfunction in the pathogenesis of acute kidney injury
Author(s)
Ince, C
Year
2014
Is Peer Reviewed?
1
Journal
Nephron Clinical Practice
ISSN:
1660-2110
Volume
127
Issue
1-4
Page Numbers
124-128
Language
English
PMID
25343835
DOI
10.1159/000363203
Web of Science Id
WOS:000343661900025
Abstract
Acute kidney injury (AKI) is a rapidly developing condition often associated with critical illness, with a high degree of morbidity and mortality, whose pathophysiology is ill understood. Recent investigations have identified the dysfunction of the renal microcirculation and its cellular and subcellular constituents as being central to the etiology of AKI. Injury is caused by inflammatory activation involving endothelial leucocyte interactions in combination with dysregulation of the homeostatis between oxygen, nitric oxide, and reactive oxygen species. Effective therapies expected to resolve AKI will have to control inflammation and restore this homeostasis. In order to apply and guide these therapies effectively, diagnostic tools aimed at physiological biomarkers of AKI for monitoring renal microcirculatory function in advance of changes in pharmacological biomarkers associated with structural damage of the kidney will need to be developed.
Keywords
Renal failure; Microcirculation; Oxygenation; Reactive oxygen species; Nitric oxide
Home
Learn about HERO
Using HERO
Search HERO
Projects in HERO
Risk Assessment
Transparency & Integrity