Zafrani Lara, Payen Didier, Azoulay Elie, Ince Can
Department of Translational Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Department of Anesthesiology and Critical Care, Lariboisière Hospital, Assistance Publique-Hôpitaux de Paris, University Paris Diderot, INSERM 1160, Paris, France.
Semin Nephrol. 2015 Jan;35(1):75-84. doi: 10.1016/j.semnephrol.2015.01.008.
The renal microcirculation plays a major role in the delivery of blood and oxygen to the kidney. In sepsis, alterations in renal microvascular perfusion, in conjunction with increased oxygen requirements, may contribute to renal failure even when renal macrovascular perfusion is preserved. In this review, we discuss the pathophysiology of the renal microcirculation during sepsis and how it contributes to acute kidney injury. Endothelial dysfunction largely is owing to inflammatory, oxidative, and nitrosative factors. Coagulative disorders and glycocalyx disruption also may contribute to the microcirculatory dysfunction. New technologies in experimental models and human beings are being developed to explore renal microcirculation in vivo. These technologies will allow a better understanding of the pathophysiopathology of the renal microcirculation and will help guide specific therapeutic strategies in sepsis-induced acute kidney injury.
肾微循环在向肾脏输送血液和氧气方面发挥着主要作用。在脓毒症中，即使肾大血管灌注得以维持，但肾微血管灌注的改变，再加上氧需求增加，可能会导致肾衰竭。在本综述中，我们讨论脓毒症期间肾微循环的病理生理学及其如何导致急性肾损伤。内皮功能障碍主要归因于炎症、氧化和亚硝化因素。凝血障碍和糖萼破坏也可能导致微循环功能障碍。正在开发实验模型和人体中的新技术，以在体内探索肾微循环。这些技术将有助于更好地理解肾微循环的病理生理学，并有助于指导脓毒症诱导的急性肾损伤的特定治疗策略。
