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急性肾损伤(acute kidney injury,AKI)是终末期肝病患者最常见的并发症之一,以肾小球滤过率急剧下降,代谢废物血清肌酐、尿素氮等迅速升高,水电解质失平衡,酸碱平衡紊乱为特点,其发病率及病死率高,预后较差。肝硬化并发急性肾损伤的发病机制复杂,治疗方法有限,至今尚未完全阐明,了解肝硬化并发急性肾损伤的病理生理机制对其有效治疗,提高患者的生存率及生活质量,减轻经济负担和改善预后至关重要。目前传统的观点是内脏动脉血管扩张,全身有效循环血容量的减少,肾素-血管紧张素-醛固酮系统的进一步激活,肾自动调节功能受损导致肾脏动脉灌注不足等血管舒张机制,随着研究的不断深入,近年越来越多的研究发现各种炎症因子如肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、Toll样受体4(TLR4)和白细胞介素-17A(IL-17A)的激活,肝硬化合并腹水导致腹腔内压不断增高,胆红素摄取、结合和排泄功能发生障碍致血清胆红素和胆汁酸浓度增加,血皮质醇水平异常、内毒素导致相对肾上腺功能不全等非血管舒张机制也起着重要的作用。本文对肝硬化并发急性肾损伤非血管舒张机制方面的研究进展做一综述。
Acute kidney injury (AKI) is one of the most common complications in patients with end-stage liver disease. With the rapid decline of glomerular filtration rate, serum creatinine, urea nitrogen and other metabolic wastes rapidly increase, water and electrolyte imbalance, Acid-base balance disorders characterized by high morbidity and mortality, poor prognosis. The pathogenesis of cirrhosis complicated with acute kidney injury is complex and its treatment methods are limited. So far, it has not yet been completely elucidated, so as to understand the pathophysiological mechanism of cirrhosis complicated with acute kidney injury and to improve its survival rate and quality of life, reduce the economic burden and improve Prognosis is crucial. At present, the traditional viewpoints are vasodilatation of visceral arterial vasodilatation, reduction of systemic effective circulating blood volume, further activation of the renin-angiotensin-aldosterone system, impaired renal autoregulation, renal insufficiency, In recent years, more and more studies have found that various inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), Toll-like receptor 4 (TLR4) Activation of IL-17A (IL-17A), cirrhosis with ascites caused by increased intra-abdominal pressure, bilirubin uptake, binding and excretion dysfunction caused by serum bilirubin and bile acid concentration increased, abnormal cortisol levels, Endotoxin causes relative adrenal insufficiency and other non-vasodilation mechanisms also play an important role. This article reviews the research progress of the non-vasodilatation mechanism of cirrhosis complicated with acute renal injury.