Rodent models of AKI-CKD transition

被引:197
作者
Fu, Ying [1 ]
Tang, Chengyuan [1 ]
Cai, Juan [1 ]
Chen, Guochun [1 ]
Zhang, Dongshan [2 ]
Dong, Zheng [1 ,3 ,4 ]
机构
[1] Cent S Univ, Dept Nephrol, Xiangya Hosp 2, Changsha, Hunan, Peoples R China
[2] Cent S Univ, Dept Emergency Med, Xiangya Hosp 2, Changsha, Hunan, Peoples R China
[3] Augusta Univ, Med Coll Georgia, Dept Cellular Biol & Anat, Augusta, GA 30912 USA
[4] Charlie Norwood Vet Affairs Med Ctr, Augusta, GA 30912 USA
基金
美国国家卫生研究院; 中国国家自然科学基金;
关键词
acute kidney injury; chronic kidney disease; cisplatin; fibrosis; ischemia; model; nephrotoxicity; ACUTE KIDNEY INJURY; RENAL ISCHEMIA-REPERFUSION; CISPLATIN-INDUCED NEPHROTOXICITY; MOLECULAR-MECHANISMS; MURINE MODEL; MOUSE MODEL; FIBROSIS; DISEASE; PROGRESSION; ACTIVATION;
D O I
10.1152/ajprenal.00199.2018
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Acute kidney injury (AKI) is a contributing factor in the development and progression of chronic kidney disease (CKD). Despite rapid progresses, the mechanism underlying AKI-CKD transition remains largely unclear. Animal models recapitulating this process are crucial to the research of the pathophysiology of AKI-CKD transition and the development of effective therapeutics. In this review, we present the commonly used rodent models of AKI-CKD transition, including bilateral ischemia-reperfusion injury (IRI), unilateral IRI, unilateral IRI with contralateral nephrectomy, multiple episodes of IRI, and repeated treatment of low-dose cisplatin, diphtheria toxin, aristolochic acid, or folic acid. The main merits and pitfalls of these models are also discussed. This review provides helpful information for establishing reliable and clinically relevant models for studying post-AKI development of chronic renal pathologies and the progression to CKD.
引用
收藏
页码:F1098 / F1106
页数:9
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