期刊
CURRENT OPINION IN CRITICAL CARE
卷 15, 期 6, 页码 503-508出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCC.0b013e328332f6cf
关键词
acute kidney injury; acute renal failure; endothelium; microcirculation; nitric oxide; oxygenation; reactive oxygen species
Purpose of review Alterations of the renal microcirculation can promote the development of acute kidney injury through the interlinked occurrence of renal hypoxia and activation of inflammatory pathways. This review focuses on the recent advances in this area, and discusses the possible therapeutic interventions that might be derived from these insights. Recent findings Endothelial injury acts as a primary event leading to renal hypoxia with disturbances in nitric oxide pathways playing a major role. The unbalanced homeostasis between nitric oxide, reactive oxygen species and renal oxygenation forms a major component of the microcirculatory dysfunction. Furthermore, injury leads to leukocyte-endothelial interaction that exacerbates renal hypoxia at a microcirculatory level. Summary Knowledge of the pathophysiological mechanisms of acute kidney injury emphasizes the importance of the role of the microcirculation in its development. Preventive and therapeutic approach should be based on restoring the homeostasis between nitric oxide, reactive oxygen species and renal oxygenation.
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