药物性肾损害发病机制的研究进展

Research progress in mechanisms of drug-induced nephrotoxicity

儿童药物性肾损害的发病机制是由儿童肾组织解剖学、生理学特征和药物结构与功能特征所决定的。肾脏微血管网络和肾小管-肾间质的分布面积占绝对优势,因此间质性肾损害非常多见。药物性肾损害发病机制包括细胞毒性(坏死或凋亡)、缺血性损伤和免疫性损伤,但由于各种药物之间化学结构和药理学差异,具体的单个药物所致肾损害的发生机制也有所不同,该文回顾了几种常见抗生素(头孢类、氨基甙类、万古霉素、碳青霉素类、两性霉素B)、非甾体类抗炎药物和环孢素A相关性肾损害发病机制的主要特征,以期提高儿科医师对药物性肾损害的意识。

Drug-induced nephrotoxicity in children is dependent upon the histological, anatomical and physiological features of their kidneys and the structural and functional characteristics of drugs. The kidney is mainly composed of microvascular network and tubulointerstitial tissue, so drug-induced nephrotoxicity is usually manifested by interstitial nephropathy. The mechanisms of drug-induced nephrotoxicity include cytotoxicity （necrosis or apoptosis）, ischemic injury, and immunological injury. Individual drugs cause renal damage by various mechanisms due to differences in chemical structure and pharmacology. This article reviews the main features of nephrotoxicity induced by common antibiotics （cephalosporins, aminoglycosides, vancomycin, carbapenems and amphotericin B）, non-steroidal anti-inflammatory drugs, and cyclosporine A.