Cao Ya-Li, Tian Zhi-Gang, Wang Fang, Li Wen-Ge, Cheng Dan-Ying, Yang Yan-Fang, Gao Hong-Mei
Ya-Li Cao, Wen-Ge Li, Yan-Fang Yang, Hong-Mei Gao, Department of Nephrology, China-Japan Friendship Hospital, Beijing 100029, China.
World J Gastroenterol. 2014 Oct 14;20(38):13956-65. doi: 10.3748/wjg.v20.i38.13956.
To determine the clinicopathological characteristics of nonsteroidal anti-inflammatory drug (NSAID)-induced acute hepato-nephrotoxicity among Chinese patients.
We conducted a retrospective chart review of patients using the International Classification of Diseases, Ninth Revision diagnosis code for acute kidney injury (AKI) (584.5 or 584.9) and for acute liver injury (ALI) (570.0 or 573.3) from January 2004 to December 2013. Medical records were reviewed to confirm the diagnosis of AKI and ALI and to quantify NSAID administration.
Seven of 59 patients (11.8%) were identified with acute hepato-nephrotoxicity induced by NSAIDs. Five patients (71.4%) received over the recommended NSAIDs dose. Compared with NSAIDs-associated mere AKI, the risk factors of NSAIDs-induced acute hepato-nephrotoxicity are age older than 60 years (57.1%), a high prevalence of alcohol use (71.4%) and positive hepatitis B virus (HBV) markers (85.7%). Compared with NSAIDs-associated mere ALI, the risk factors of NSAIDs-induced acute hepato-nephrotoxicity are age older than 60 years (57.1%), increased extracellular volume depletion (71.4%), and renin-angiotensin-aldosterone system (RAAS) inhibitor combined use (57.1%). Acute interstitial nephritis and acute tubulointerstitial disease were apparent in three out of six (42.9%) kidney biopsy patients, respectively. Acute hepatitis was found in four out of six (66.7%) liver biopsy patients. Overall complete recovery occurred in four patients within a mean of 118.25 ± 55.42 d.
The injury typically occurred after an overdose of NSAIDs. The risk factors include age older than 60 years, alcohol use, positive HBV markers, extracellular volume depletion and RAAS inhibitor combined use.
确定中国患者中非甾体抗炎药（NSAID）所致急性肝-肾毒性的临床病理特征。
我们对2004年1月至2013年12月使用国际疾病分类第九版诊断编码诊断急性肾损伤（AKI）（584.5或584.9）和急性肝损伤（ALI）（570.0或573.3）的患者进行了回顾性病历审查。审查病历以确认AKI和ALI的诊断并量化NSAID的使用情况。
59例患者中有7例（11.8%）被确定为NSAIDs所致急性肝-肾毒性。5例患者（71.4%）接受的NSAIDs剂量超过推荐剂量。与NSAIDs相关的单纯AKI相比，NSAIDs所致急性肝-肾毒性的危险因素为年龄大于60岁（57.1%）、高酒精使用率（71.4%）和乙肝病毒（HBV）标志物阳性（85.7%）。与NSAIDs相关的单纯ALI相比，NSAIDs所致急性肝-肾毒性的危险因素为年龄大于60岁（57.1%）、细胞外液量减少增加（71.4%）和肾素-血管紧张素-醛固酮系统（RAAS）抑制剂联合使用（57.1%）。在6例肾活检患者中，分别有3例（42.9%）出现急性间质性肾炎和急性肾小管间质性疾病。在6例肝活检患者中，有4例（66.7%）发现急性肝炎。4例患者在平均118.25±55.42天内完全康复。
损伤通常发生在NSAIDs过量使用后。危险因素包括年龄大于60岁、饮酒、HBV标志物阳性、细胞外液量减少和RAAS抑制剂联合使用。
