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缺血性急性肾损伤的病理生理学

Pathophysiology of ischaemic acute kidney injury.

作者信息

Kanagasundaram Nigel Suren

机构信息

Renal Services, Newcastle upon Tyne Hospitals NHS Foundation Trust, Freeman Hospital, High Heaton, Newcastle upon Tyne, UK

出版信息

Ann Clin Biochem. 2015 Mar;52(Pt 2):193-205. doi: 10.1177/0004563214556820. Epub 2014 Oct 7.

DOI:10.1177/0004563214556820
PMID:25293591
Abstract

Acute kidney injury is common, dangerous and costly, affecting around one in five patients emergency admissions to hospital. Although survival decreases as disease worsens, it is now apparent that even modest degrees of dysfunction are not only associated with higher mortality but are an independent risk factor for death. This review focuses on the pathophysiology of acute kidney injury secondary to ischaemia - its commonest aetiology. The haemodynamic disturbances, endothelial injury, epithelial cell injury and immunological mechanisms underpinning its initiation and extension will be discussed along with the considerable and complex interplay between these factors that lead to an intense, pro-inflammatory state. Mechanisms of tubular recovery will be discussed but also the pathophysiology of abnormal repair with its direct consequences for long-term renal function. Finally, the concept of 'organ cross-talk' will be introduced as a potential explanation for the higher mortality observed with acute kidney injury that might be deemed modest in conventional biochemical terms.

摘要

急性肾损伤很常见、危险且代价高昂,约五分之一因急诊入院的患者会受到影响。尽管随着疾病恶化生存率会降低,但现在很明显,即使是轻度的功能障碍不仅与更高的死亡率相关,而且是死亡的独立危险因素。本综述聚焦于缺血性急性肾损伤的病理生理学——这是其最常见的病因。将讨论其起始和进展过程中所涉及的血流动力学紊乱、内皮细胞损伤、上皮细胞损伤及免疫机制,以及这些因素之间导致强烈促炎状态的大量复杂相互作用。还将讨论肾小管恢复的机制以及异常修复的病理生理学及其对长期肾功能的直接影响。最后,将引入“器官间相互作用”的概念,作为对急性肾损伤患者较高死亡率的一种潜在解释,而从传统生化指标来看,这些患者的急性肾损伤可能被认为程度较轻。

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