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急性肾损伤的病理生理学。

Pathophysiology of acute kidney injury.

机构信息

Department of Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

出版信息

Compr Physiol. 2012 Apr;2(2):1303-53. doi: 10.1002/cphy.c110041.

DOI:10.1002/cphy.c110041
PMID:23798302
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3919808/
Abstract

Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high mortality rates. The primary causes of AKI include ischemia, hypoxia, or nephrotoxicity. An underlying feature is a rapid decline in glomerular filtration rate (GFR) usually associated with decreases in renal blood flow. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of renal injury appears to be impaired energetics of the highly metabolically active nephron segments (i.e., proximal tubules and thick ascending limb) in the renal outer medulla, which can trigger conversion from transient hypoxia to intrinsic renal failure. Injury to kidney cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or chronic kidney disease (CKD) patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future.

摘要

急性肾损伤 (AKI) 是肾脏科会诊的主要原因,与高死亡率相关。AKI 的主要原因包括缺血、缺氧或肾毒性。一个潜在的特征是肾小球滤过率 (GFR) 的快速下降,通常与肾血流量减少有关。炎症是 AKI 的一个重要的附加组成部分,导致损伤的扩展阶段,这可能与对血管扩张剂治疗的不敏感有关。有人认为,针对扩展阶段代表了一个具有最大治疗潜力的领域。肾脏损伤的潜在基础似乎是肾脏外髓质中高度代谢活跃的肾单位(即近端肾小管和厚升支)的能量供应受损,这可能导致短暂缺氧向内在肾功能衰竭的转化。肾脏细胞的损伤可能是致命的或亚致死的。亚致死性损伤是 AKI 的一个重要组成部分,因为它可能深刻地影响 GFR 和肾血流量。恢复反应的性质取决于亚致死细胞恢复正常功能和促进再生的程度。从 AKI 中成功恢复取决于这些修复过程的程度,而在老年或慢性肾脏病 (CKD) 患者中,这些过程可能会受到损害。最近的数据表明,AKI 代表了存活患者向 CKD 的潜在联系。最后,AKI 的早期诊断是治疗 AKI 患者的一个重要领域,这引发了人们对 AKI 生物标志物在未来可能发挥作用的认识。

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