Mechanisms and mediators of lung injury after acute kidney injury

被引：0
作者：
Sarah Faubel
Charles L. Edelstein
机构：
[1] University of Colorado Denver,Division of Renal Diseases and Hypertension
来源：
Nature Reviews Nephrology | 2016年 / 12卷
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摘要：
Respiratory complications are common after acute kidney injury (AKI) and are associated with increased mortalityCardiogenic (volume overload) and non-cardiogenic (lung injury with inflammation) pulmonary oedema can occur after AKIAnimal data indicate that lung inflammation and lung endothelial apoptosis mediate non-cardiogenic pulmonary oedema after AKIHuman and animal data suggest that IL-6, IL-8, TNF, NFκB, TNFR1 and caspase-3-mediated apoptosis, HMG-B1, and T cells mediate lung injury after AKIThe high mortality associated with AKI might be due to both traditional (for example, electrolyte abnormalities) and non-traditional (for example, lung injury) complications of AKI
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页码：48 / 60
页数：12
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