Department of Translational Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Curr Opin Crit Care. 2009 Dec;15(6):503-8. doi: 10.1097/MCC.0b013e328332f6cf.
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.
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.
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.
肾脏微循环的改变可通过肾缺氧和炎症途径的激活相互关联，促进急性肾损伤的发生。本综述重点介绍了这一领域的最新进展，并讨论了可能从这些研究结果中衍生出的治疗干预措施。
内皮损伤是导致肾缺氧的主要事件，一氧化氮途径的紊乱起着重要作用。一氧化氮、活性氧和肾脏氧合之间的失衡稳态构成了微循环功能障碍的主要组成部分。此外，损伤导致白细胞-内皮相互作用，加剧了微循环水平的肾缺氧。
急性肾损伤的病理生理机制的知识强调了微循环在其发生中的重要作用。预防和治疗方法应基于恢复一氧化氮、活性氧和肾脏氧合之间的稳态。
