急性肾损伤进展为慢性肾脏病的机制  

Chronic kidney disease after acute kidney injury

作　　者：杨茜[1] 谢红浪[1] 

机构地区：[1]南京军区南京总医院肾脏科国家肾脏疾病临床医学研究中心全军肾脏病研究所,南京210016

出　　处：《肾脏病与透析肾移植杂志》2016年第3期274-278,252,共6页Chinese Journal of Nephrology,Dialysis & Transplantation

摘　　要：肾脏具较强代偿能力,但急性肾损伤(AKI)后即使血清肌酐恢复至损伤前的基线水平,肾脏结构却未得到完全修复。AKI会造成血管内皮细胞损伤、微血管床减少,持续性的组织缺血缺氧,最终导致纤维组织增生和肾纤维化,从而增加发生慢性肾脏病(CKD)和终末期肾病的风险。此外,缺氧诱导因子、血管内皮生长因子、转化生长因子β1等细胞因子的慢性调节异常和相互间的复杂作用亦可引起并加重肾纤维化,最终导致AKI患者发生CKD,甚至进展至终末期肾病。The kidney has a strong compensatory ability,after acute kidney injury even if the serum creatinine returned to baseline,but the renal structure has not been fully restored. AKI can lead to tissue incomplete repair,resulting in the injury of vascular endothelial cells,microvascular reduce,ischemia and hypoxia leads to hyperplasia of fibrous tissue and renal fibrosis. AKI increase the risk of occurrence of CKD and ESRD. In addition,the chronic dysregulation of these factors（ such as hypoxia inducible factor,vascular endothelial growth factor,transforming growth factor beta 1） over time and their net interactions are likely to determine the extent of fibrotic responses and organ function,eventually leading to the occurrence of chronic kidney disease

关 键 词：急性肾损伤 慢性肾脏病 病理生理 分子机制 

分 类 号：R692[医药卫生—泌尿科学]