The Central Role of Renal Microcirculatory Dysfunction in the Pathogenesis of Acute Kidney Injury

被引:27
作者
Ince, Can [1 ]
机构
[1] Univ Amsterdam, Acad Med Ctr, Dept Translat Physiol, NL-1105 AZ Amsterdam, Netherlands
来源
NEPHRON CLINICAL PRACTICE | 2014年 / 127卷 / 1-4期
关键词
Renal failure; Microcirculation; Oxygenation; Reactive oxygen species; Nitric oxide; SUPEROXIDE-DISMUTASE; ISCHEMIA-REPERFUSION; FLUID RESUSCITATION; OXYGEN-CONSUMPTION; OXIDATIVE STRESS; NITRIC-OXIDE; SEPSIS; FAILURE; HYPOXIA; PATHOPHYSIOLOGY;
D O I
10.1159/000363203
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
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. (C) 2014 S. Karger AG, Basel
引用
收藏
页码:124 / 128
页数:5
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