Bogdanova-Mihaylova Petya, Burke David, O'Dwyer John P, Bradley David, Williams Jennifer A, Cronin Simon J, Smyth Shane, Murphy Raymond P, Murphy Sinead M, Wall Catherine, McCabe Dominick J H
Department of Neurology, Adelaide & Meath Hospital, Dublin, incorporating the National Children's Hospital (AMNCH), Tallaght, Dublin 24, Ireland.
Department of Neurology, Imperial College Healthcare NHS Trust, London, UK.
Ir J Med Sci. 2018 Aug;187(3):777-780. doi: 10.1007/s11845-017-1728-3. Epub 2018 Jan 6.
Patients with 'suspected viral encephalitis' are frequently empirically treated with intravenous aciclovir. Increasing urea and creatinine are 'common', but rapidly progressive renal failure is reported to be 'very rare'.
To describe the clinical course and outcome of cases of aciclovir-induced acute kidney injury (AKI) encountered by the Liaison Neurology Service at AMNCH and to highlight the importance of surveillance and urgent treatment of this iatrogenic complication.
Retrospectively and prospectively collected data from the Liaison Neurology Service at AMNCH on patients who received IV aciclovir for suspected viral encephalitis and developed AKI were analysed. Aciclovir-induced AKI was defined by a consultant nephrologist in all cases as a rise in serum creatinine of > 26 μmol/L in 48 h or by ≥ 1.5 times the baseline value. Renal function, haematocrit, and fluid balance were monitored following AKI onset.
Data from 10 patients were analysed. Median time to AKI onset was 3.5 days (range: 1-6 days). Aciclovir was stopped or the dose adjusted. All patients recovered with IV normal saline, aiming for a urine output > 100-150 ml/h. The interval between first rise in creatinine and return to normal levels varied between 5 and 19 days.
Liaison neurologists and general physicians need to be aware that aciclovir may cause AKI attributed to distal intra-tubular crystal nephropathy. Daily fluid balance and renal function monitoring are essential because AKI may arise even with intensive pre-hydration. Prognosis is good if identified early and actively treated.
“疑似病毒性脑炎”患者常接受静脉注射阿昔洛韦的经验性治疗。尿素和肌酐升高很“常见”,但据报道快速进展性肾衰竭“非常罕见”。
描述AMNCH联络神经科遇到的阿昔洛韦所致急性肾损伤(AKI)病例的临床过程和结局,并强调对这种医源性并发症进行监测和紧急治疗的重要性。
对AMNCH联络神经科回顾性和前瞻性收集的、因疑似病毒性脑炎接受静脉注射阿昔洛韦并发生AKI的患者数据进行分析。所有病例均由肾内科顾问医生将阿昔洛韦所致AKI定义为血清肌酐在48小时内升高>26μmol/L或升高至基线值的≥1.5倍。AKI发生后监测肾功能、血细胞比容和液体平衡。
分析了10例患者的数据。AKI发病的中位时间为3.5天(范围:1 - 6天)。停用阿昔洛韦或调整剂量。所有患者通过静脉输注生理盐水恢复,目标尿量>100 - 150ml/h。肌酐首次升高至恢复正常水平的间隔时间在5至19天之间。
联络神经科医生和普通内科医生需要意识到阿昔洛韦可能导致因远端肾小管结晶性肾病引起的AKI。每日液体平衡和肾功能监测至关重要,因为即使进行充分的预先补液也可能发生AKI。如果早期识别并积极治疗,预后良好。