Clavé Stéphanie, Rousset-Rouvière Caroline, Daniel Laurent, Tsimaratos Michel
Department of Multidisciplinary Pediatrics, Pediatric Nephrology Unit, Assistance Publique des Hôpitaux de Marseille, Marseille, France.
Department of Anatomopathology, Assistance Publique des Hôpitaux de Marseille, Marseille, France.
Front Pediatr. 2019 Dec 17;7:520. doi: 10.3389/fped.2019.00520. eCollection 2019.
Non-steroidal anti-inflammatory drugs (NSAIDs) are often used as analgesic and antipyretic drugs. Nephrotoxicity is a common side effect and leads in 1-5% of pediatric cases to acute kidney injury (AKI). The nephrotoxic effects of NSAIDs arise mainly from two pathological mechanisms: (1) acute tubulo-interstitial nephritis (ATIN) following immune reaction and (2) prerenal failure because of reduced renal plasma flow. Histological examinations are required to confirm the pathomechanism of AKI after NSAID exposure. The aim of this study was to illustrate the risk of ATIN in children with AKI after NSAID exposure. The medical records of all 100 pediatric patients with biopsy-proven AKI treated between January 2006 and 2016 at La Timone Hospital, Marseille, France, were analyzed retrospectively. Twenty-five of these patients had ATIN, four of which were healthy children who had been treated with NSAIDs. In other words, NSAID side effects accounted for 4% of all cases of biopsy-proven AKI and 16% of all cases of ATIN. None of the patients had hypovolemia when they received NSAIDs. Clinical symptoms were non-specific. All patients had abdominal pain and vomiting but normal urine volume output. Maximum serum creatinine levels ranged from 300 to 512 μmol/l, with estimated minimum creatinine clearances of 12-26 ml/min/1.73 m. None of the patients had significant proteinuria. One child had hyperechogenic enlarged kidneys. Three patients were treated with steroids, one of whom also received intravenous methylprednisolone. Renal function improved gradually in all patients, but the patient who received methylprednisolone developed moderate chronic kidney disease (CKD). Biopsy proven-AKI secondary to NSAID use can be severe and be associated with ATIN. Since NSAID-induced ATIN can lead to CKD, clinicians using NSAIDs should focus on preventing AKI.
非甾体抗炎药（NSAIDs）常被用作止痛和解热药物。肾毒性是一种常见的副作用，在1%至5%的儿科病例中会导致急性肾损伤（AKI）。NSAIDs的肾毒性作用主要源于两种病理机制：（1）免疫反应后发生的急性肾小管间质性肾炎（ATIN），以及（2）肾血浆流量减少导致的肾前性肾衰竭。需要进行组织学检查以确认NSAIDs暴露后AKI的发病机制。本研究的目的是阐明NSAIDs暴露后儿童发生AKI时ATIN的风险。对2006年1月至2016年期间在法国马赛拉蒂莫内医院接受活检证实为AKI的100例儿科患者的病历进行了回顾性分析。其中25例患者患有ATIN，其中4例是接受过NSAIDs治疗的健康儿童。换句话说，NSAIDs副作用占所有活检证实的AKI病例的4%，占所有ATIN病例的16%。所有患者在接受NSAIDs治疗时均无血容量不足。临床症状不具有特异性。所有患者均有腹痛和呕吐，但尿量正常。血清肌酐最高水平在300至512μmol/l之间，估计肌酐清除率最低为12 - 26 ml/min/1.73 m²。所有患者均无明显蛋白尿。1名儿童肾脏回声增强且肿大。3例患者接受了类固醇治疗，其中1例还接受了静脉注射甲泼尼龙。所有患者的肾功能逐渐改善，但接受甲泼尼龙治疗的患者发展为中度慢性肾脏病（CKD）。活检证实由NSAIDs使用继发的AKI可能很严重，并与ATIN相关。由于NSAIDs诱导性ATIN可导致CKD，使用NSAIDs的临床医生应专注于预防AKI。
