Schmidt Julius J, Ramazan Leyla, Bockemeyer Clemens, Günter Hans-Heinrich, Martens-Lobenhoffer Jens, Ganzenmüller Tina, Bode-Böger Stefanie M, Kielstein Jan T
Department of Nephrology and Hypertension Medical School Hannover, Carl-Neuberg-Strasse 1, 30625, Hannover, Germany.
Institute of Pathology, Medical School Hannover, Hannover, Germany.
BMC Nephrol. 2016 Mar 15;17:28. doi: 10.1186/s12882-016-0240-8.
Acute interstitial nephritis (AIN) represents a frequent cause of acute kidney injury. While many etiologies of AIN have been recognized, the majority (60-70 %) are due to allergic reactions or drug exposure. Many different classes of drugs and several agents within a class can cause drug induced AIN. Flecainide, a class Ic antiarrhythmic drug, had thus far not been associated with the occurrence of AIN.
Here we describe a case of biopsy proven AIN after flecainide therapy in a pregnant patient. The 24-year old Caucasian woman was admitted to our university hospital for a planned c-section. She had been put on flecainide at a dose of 200 mg/d for supraventricular tachyarrhythmia of the fetus ten days earlier. The only fleaainide drug level was obtained 24 h after the last dose. At this time point the serum level was still in the therapeutic range (392 ng/mL). After hospital admission the patient underwent uneventful c-section and delivered a 3095 g baby girl with mild insufficiency of the tricuspid valve. In the hours following the c-section, a single dose of the non-steroidal anti-inflammatory drug (NSAID) ibuprofen (600 mg) as well as single dose of diclofenac (100 mg) was administered. Within 5 days after c-section her baseline creatinine of 30 μmol/L increased to 277 μmol/L. The serum creatinine continued to rise to 411 μmol/L on hospital day # 7. On renal ultrasound kidneys were enlarged and swollen. Urinary sediment at this point only revealed slight proteinuria (506 mg/g creatinine). A renal biopsy was performed showing acute interstitial nephritis. Within four days the renal function improved after discontinuation of flecainide and NSAIDs even without steroid therapy and the patient was discharged with a creatinine of 88 μmol/L after 13 days in the hospital.
This case suggests that flecainide, at least in combination with NSAIDs, can cause AIN.
急性间质性肾炎(AIN)是急性肾损伤的常见原因。虽然已认识到AIN的多种病因,但大多数(60% - 70%)是由过敏反应或药物暴露引起的。许多不同种类的药物以及同一种类中的几种药物都可导致药物性AIN。氟卡尼,一种Ic类抗心律失常药物,迄今为止尚未发现与AIN的发生有关。
在此,我们描述一例经活检证实的孕妇在使用氟卡尼治疗后发生AIN的病例。这位24岁的白种女性因计划剖宫产入住我们的大学医院。十天前,她因胎儿室上性快速心律失常开始服用氟卡尼,剂量为200mg/天。最后一剂氟卡尼后24小时测得唯一一次氟卡尼血药浓度。此时血清浓度仍在治疗范围内(392ng/mL)。入院后患者顺利进行了剖宫产,产下一名3095g的女婴,其患有轻度三尖瓣功能不全。剖宫产术后数小时,给予了单剂量的非甾体抗炎药(NSAID)布洛芬(600mg)以及单剂量双氯芬酸(100mg)。剖宫产术后5天内,她的基线肌酐水平从30μmol/L升至277μmol/L。住院第7天时血清肌酐继续升至411μmol/L。肾脏超声显示肾脏增大、肿胀。此时尿沉渣仅显示轻度蛋白尿(506mg/g肌酐)。进行了肾活检,结果显示为急性间质性肾炎。停用氟卡尼和NSAIDs后,即使未使用类固醇治疗,肾功能在四天内也有所改善,患者住院13天后肌酐水平为88μmol/L时出院。
该病例表明,氟卡尼至少与NSAIDs联合使用时可导致AIN。