| 肝硬化并发急性肾损伤的非血管舒张机制的研究进展 |
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| 引用本文： | 李宇玫,周芳芳,罗群. 肝硬化并发急性肾损伤的非血管舒张机制的研究进展[J]. 中华全科医学, 2017, 15(8): 1407-1410. DOI: 10.16766/j.cnki.issn.1674-4152.2017.08.039 |
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| 作者姓名： | 李宇玫 周芳芳 罗群 |
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| 作者单位： | 宁波市第二医院肾内科, 浙江 宁波 315010 |
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| 基金项目： | 浙江省医药卫生科技项目（2013KYB236、2015KYA200）；宁波市自然科学基金（2013A610266） |
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| 摘 要： | 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。
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| 关 键 词： | 肝硬化 急性肾损伤 非血管舒张机制 |
| 收稿时间： | 2016-06-08 |
Research progress of non-vasomotor mechanism for cirrhosis complicated by kidney injury |
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| Affiliation: | Department of Nephrology, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, China |
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| Abstract: | Acute kidney injury (AKI) is a common complication of advanced cirrhosis with high mortality and high morbidity, often experience poor prognosis. It is characterized by a sudden drop in glomerular filtration rate, retention of metabolic waste products, water-electrolyte imbalance, and acid-base disturbance. The pathogenesis of advanced cirrhosis complicated by acute kidney injury is complicated and not completely understood, and the therapeutic approaches are limited.Therefore, to improve the understanding of the pathophysiological mechanisms involved in renal dysfunction occurring on a background of cirrhosis is the key to develop the effective treatment strategies, improve QOL and prognosis of patients, and reduce the economic burden of family. Traditionally, it is believed that the decreased effective circulating blood volume resulted in the renal artery hypoperfusion (vasomotor mechanism). The AKI is due to the combination of an impaired effective arterial blood volume secondary to arterial vasodilation and the effects of excessive activation of the rennin-angiotensin-aldosterone system, with increased intrarenal vasoconstriction and impaired renal autoregulation that predisposes to renal dysfunction. In recent years, more and more studies have found that the activation of different inflammatory factors, such as mediators of inflammation (tumor necrosis factor-α, Interleukin-6, Toll-like receptor 4, Interleukin-17A), increased the intra-abdominal pressure resulted by cirrhotic ascites, the increased the concentration of serum bilirubin and bile acids caused by the dysfunction of bilirubin uptake, combination and excretion, the relative adrenal insufficiency leaded by anomaly expression level of serum cortisol and the endotoxin play an important role in AKI in cirrhosis. This paper will summarize the recent advances in understanding the nonvasomotor mechanism of AKI in end-stage liver disease. |
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