Ergin Bülent, Akin Sakir, Ince Can
Department of Intensive Care, Laboratory of Translational Intensive Care, Erasmus MC, University Medical Center Rotterdam, 3015 GD Rotterdam, The Netherlands.
Department of Intensive Care, Haga Teaching Hospital, 2545 AA The Hague, The Netherlands.
J Clin Med. 2021 Sep 7;10(18):4041. doi: 10.3390/jcm10184041.
Acute kidney injury (AKI) is a serious multifactorial conditions accompanied by the loss of function and damage. The renal microcirculation plays a crucial role in maintaining the kidney's functional and structural integrity for oxygen and nutrient supply and waste product removal. However, alterations in microcirculation and oxygenation due to renal perfusion defects, hypoxia, renal tubular, and endothelial damage can result in AKI and the loss of renal function regardless of systemic hemodynamic changes. The unique structural organization of the renal microvasculature and the presence of autoregulation make it difficult to understand the mechanisms and the occurrence of AKI following disorders such as septic, hemorrhagic, or cardiogenic shock; ischemia/reperfusion; chronic heart failure; cardiorenal syndrome; and hemodilution. In this review, we describe the organization of microcirculation, autoregulation, and pathophysiological alterations leading to AKI. We then suggest innovative therapies focused on the protection of the renal microcirculation and oxygenation to prevent AKI.
急性肾损伤(AKI)是一种严重的多因素疾病,伴有功能丧失和损伤。肾微循环在维持肾脏的功能和结构完整性以供应氧气和营养物质以及清除废物方面起着至关重要的作用。然而,由于肾灌注缺陷、缺氧、肾小管和内皮损伤导致的微循环和氧合改变,无论全身血流动力学如何变化,都可能导致AKI和肾功能丧失。肾微血管独特的结构组织和自身调节的存在,使得理解诸如脓毒症、出血性或心源性休克、缺血/再灌注、慢性心力衰竭、心肾综合征和血液稀释等疾病后AKI的发生机制变得困难。在这篇综述中,我们描述了微循环的组织、自身调节以及导致AKI的病理生理改变。然后,我们提出了以保护肾微循环和氧合为重点的创新疗法,以预防AKI。