Acute kidney injury (AKI) represents a significant clinical concern that is associated with high mortality rates and also represents a significant risk factor for the development of chronic kidney disease (CKD). This article will consider alterations in renal endothelial function in the setting of AKI that may underlie impairment in renal perfusion and how inefficient vascular repair may manifest post-AKI and contribute to the potential transition to CKD. We provide updated terminology for cells previously classified as 'endothelial progenitor' that may mediate vascular repair such as pro-angiogenic cells and endothelial colony-forming cells. We consider how endothelial repair may be mediated by these different cell types following vascular injury, particularly in models of AKI. We further summarize the potential ability of these different cells to mitigate the severity of AKI, improve perfusion and maintain vascular structure in pre-clinical studies.

译文

:急性肾损伤(AKI)代表了与高死亡率相关的重大临床问题,并且还代表了慢性肾脏疾病(CKD)发生的重要危险因素。本文将考虑在AKI的背景下肾内皮功能的改变,这可能是肾脏灌注受损的基础,以及AKI后的低效血管修复可能如何表现出来,并可能导致向CKD的转变。我们为以前被归类为“内皮祖细胞”的细胞提供了更新的术语,这些细胞可能介导血管修复,例如促血管生成细胞和内皮集落形成细胞。我们考虑血管损伤后这些不同细胞类型可能如何介导内皮修复,尤其是在AKI模型中。在临床前研究中,我们进一步总结了这些不同细胞减轻AKI严重性,改善灌注和维持血管结构的潜在能力。

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