Ó hAinmhire Eoghainín, Humphreys Benjamin D
Division of Nephrology, Washington University School of Medicine, St. Louis, MO, USA.
Nephron. 2017;137(4):264-267. doi: 10.1159/000474960. Epub 2017 Jun 9.
End-stage renal disease (ESRD) is common, costly, and it results from progressive chronic kidney disease (CKD). ESRD claims many lives every year. It is increasingly recognized that episodes of acute kidney injury (AKI) predispose to the future development of CKD and ESRD. While our understanding of the pathophysiology of the AKI to CKD transition is improving, there are no validated therapeutic strategies to prevent this transition. In this review, we summarize the recent progress made in defining the cellular and molecular events underlying the AKI to CKD transition and highlight potential therapeutic targets and strategies to reduce the incidence of CKD following AKI.
终末期肾病（ESRD）很常见，治疗费用高昂，它是由进行性慢性肾病（CKD）导致的。ESRD每年致使许多人死亡。人们越来越认识到，急性肾损伤（AKI）发作会使未来发生CKD和ESRD的风险增加。虽然我们对AKI向CKD转变的病理生理学的理解正在不断加深，但目前尚无经过验证的预防这种转变的治疗策略。在本综述中，我们总结了在确定AKI向CKD转变背后的细胞和分子事件方面取得的最新进展，并强调了降低AKI后CKD发病率的潜在治疗靶点和策略。
