造影剂诱导的急性肾损伤的发病机制及干预靶点研究进展  

Research progress on the pathogenesis and intervention targets of contrast-induced acute kidney injury

作　　者：杜霞 马梦青 曹长春 Xia Du;Mengqing Ma;Changchun Cao(Department of Nephrology,Sir Run Run Hospital,Nanjing Medical University,Nanjing 211166;Department of Nephrology,Nanjing First Hospital,Nanjing Medical University,Nanjing 210006,Jiangsu Province,China)

机构地区：[1]南京医科大学附属逸夫医院肾内科,211166 [2]南京医科大学附属南京医院肾内科,210006

出　　处：《中华肾病研究电子杂志》2024年第5期279-282,共4页Chinese Journal of Kidney Disease Investigation（Electronic Edition）

基　　金：国家自然科学基金(82170698)。

摘　　要：随着造影剂在临床诊疗中应用增加,造影剂诱导的急性肾损伤已成为肾功能不全的主要原因之一。造影剂诱导的急性肾损伤表现为造影剂进入血管内导致肾功能突然下降,相关病理生理机制包括肾髓质缺血缺氧、造影剂直接毒性、氧化应激和炎症。迄今,除降低造影剂毒性策略外,尚无防治造影剂诱导的急性肾损伤的有效手段。本文综述了造影剂诱导急性肾损伤的分子机制,并介绍了细胞凋亡、炎症、氧化应激以及肾脏血流动力学相关靶点在防治造影剂诱导的急性肾损伤中的潜在价值,以期为降低造影剂诱导的急性肾损伤发生率和改善患者预后提供参考。With the increasing use of contrast media in clinical diagnosis and treatment,contrastinduced acute kidney injury(CIAKI)has become one of the main causes of renal insufficiency.CIAKI is characterized by a sudden decline in kidney function following contrast agent administration.The underlying pathophysiological mechanisms include renal medullary ischemia,direct contrast agent toxicity,oxidative stress,and inflammation.So far,except for the strategy of reducing the toxicity of contrast media,there is no effective means to prevent and treat CIAKI.This article reviewed the molecular mechanism of CIAKI,and introduced the potential value of targets related to apoptosis,inflammation,oxidative stress,and renal hemodynamic for the prevention and treatment of CIAKI,in order to provide reference for reducing the incidence of CIAKI,and improving the prognosis of the patients.

关 键 词：造影剂诱导的急性肾损伤 炎症 氧化应激 细胞凋亡 

分 类 号：R692[医药卫生—泌尿科学]