Petya Bogdanova-Mihaylova1, David Burke1, John P O'Dwyer2, David Bradley3, Jennifer A Williams3,4, Simon J Cronin5, Shane Smyth6, Raymond P Murphy1, Sinead M Murphy1,4,7, Catherine Wall8, Dominick J H McCabe9,10,11,12,13. 1. Department of Neurology, Adelaide & Meath Hospital, Dublin, incorporating the National Children's Hospital (AMNCH), Tallaght, Dublin 24, Ireland. 2. Department of Neurology, Imperial College Healthcare NHS Trust, London, UK. 3. Department of Neurology, St James's Hospital, Dublin, Ireland. 4. Academic Unit of Neurology, School of Medicine, Trinity College Dublin, Dublin, Ireland. 5. Department of Neurology, Cork University Hospital, Cork, Ireland. 6. Department of Neurology, Mater Misericordiae University Hospital, Dublin, Ireland. 7. Stroke Service, AMNCH, Dublin, Ireland. 8. Department of Renal Medicine, Trinity Health Kidney Centre, AMNCH, Dublin, Ireland. 9. Department of Neurology, Adelaide & Meath Hospital, Dublin, incorporating the National Children's Hospital (AMNCH), Tallaght, Dublin 24, Ireland. dominick.mccabe@amnch.ie. 10. Academic Unit of Neurology, School of Medicine, Trinity College Dublin, Dublin, Ireland. dominick.mccabe@amnch.ie. 11. Stroke Service, AMNCH, Dublin, Ireland. dominick.mccabe@amnch.ie. 12. Department of Clinical Neurosciences, Royal Free Campus, UCL Institute of Neurology, London, UK. dominick.mccabe@amnch.ie. 13. Department of Neurology, Vascular Neurology Research Foundation, AMNCH, Dublin, Ireland. dominick.mccabe@amnch.ie.
Abstract
BACKGROUND: 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'. AIMS: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: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'. AIMS: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Authors: T Solomon; B D Michael; P E Smith; F Sanderson; N W S Davies; I J Hart; M Holland; A Easton; C Buckley; R Kneen; N J Beeching Journal: J Infect Date: 2011-11-18 Impact factor: 6.072
Authors: R J Whitley; C A Alford; M S Hirsch; R T Schooley; J P Luby; F Y Aoki; D Hanley; A J Nahmias; S J Soong Journal: N Engl J Med Date: 1986-01-16 Impact factor: 91.245