Distant Organ Dysfunction in Acute Kidney Injury: A Review.

Distant Organ Dysfunction in Acute Kidney Injury: A Review.
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DOI:
10.1053/j.ajkd.2018.03.028
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发表时间:
2018-12
期刊:
American journal of kidney diseases : the official journal of the National Kidney Foundation
影响因子:
--
通讯作者:
Rabb H
Rabb H
中科院分区:
其他
文献类型:
--
作者:
Lee SA;Cozzi M;Bush EL;Rabb H

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急性肾损伤(AKI)在危重患者中很常见,并与发病率和死亡率增加有关。其他器官功能障碍是AKI预后不良的重要原因。大量的临床和流行病学数据表明,AKI与肺、心、脑和肝等远端器官功能障碍有关。基础和临床研究的最新进展已经证明了AKI中远端器官相互作用的生理和分子机制,包括白细胞活化和浸润、炎性细胞因子/趋化因子等可溶性因子的产生和内皮损伤。远端器官的氧化应激和活性氧(ROS)的产生以及细胞死亡的失调也是aki诱导远端器官功能障碍的重要机制。这篇综述将更新AKI中器官串扰的最新临床和实验发现,并强调潜在的分子机制和治疗靶点,以改善AKI的临床结果。
Acute kidney injury (AKI) is common in critically ill patients and associated with increased morbidity and mortality. Dysfunction of other organs is an important cause of poor outcomes from AKI. Ample clinical and epidemiological data show that AKI is associated with distant organ dysfunction in lung, heart, brain, and liver. Recent advancements in basic and clinical research have demonstrated physiologic and molecular mechanisms of distant organ interactions in AKI including leukocyte activation and infiltration, generation of soluble factors like inflammatory cytokines/chemokines, and endothelial injury. Oxidative stress and production of reactive oxygen species (ROS) as well as dysregulation of cell death in distant organs are also important mechanism of AKI-induced distant organ dysfunction. This review will update recent clinical and experimental findings on organ crosstalk in AKI and highlight potential molecular mechanisms and therapeutic targets to improve clinical outcomes during AKI.
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