Acyclovir-induced thrombotic microangiopathy

ObjectiveThe objective of this study was to describe the incidence of acute kidney injury (AKI) in children receiving intravenous acyclovir and determine risk factors that may be associated with it.DesignThis was a retrospective cohort study, conducted by chart review.SettingThe study was conducted across two paediatric hospitals.PatientsAll inpatients that received intravenous acyclovir in records from January 2015 to December 2015 were reviewed. Only patients with creatinine measurements taken before and after starting acyclovir were included in the study.Main outcome measuresThe main outcome measure was the development of AKI following intravenous acyclovir administration, with AKI defined according to change in serum creatinine.Results150 patients were included in the analysis. Patients’ ages ranged from 2 days to 18.6 years. 27 children (18%) developed at least stage 1 AKI. Children receiving cancer treatment developed AKI more frequently than children with other diagnoses; 29.3% vs 10.9% (OR 3.4, 95% CI 1.5 to 8.2, p=0.008). The baseline estimated glomerular filtration rate (eGFR) was higher in those children who developed AKI. 34% of children had an eGFR >120 mL/min/1.73 m2 prior to acyclovir use. 31% of these children developed AKI compared with only 11% of those with a normal baseline eGFR (OR 3.6, 95 CI 1.3 to 10.1, p=0.02). Baseline eGFR was a significant predictor of AKI in a multivariable analysis that included cumulative dose and treatment duration (OR 1.02, p=0.013).ConclusionAKI following intravenous acyclovir exposure is common in children. This study raises the possibility that glomerular hyperfiltration is a previously unrecognised risk factor for acyclovir-induced AKI.

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Drug-Induced Acute Kidney Injury

Zakharova

Остроумова

Klepikova

2021

Bezopasnost' i risk farmakoterapii

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Drug-induced nephrotoxicity is the third most common cause of acute kidney injury (AKI). The aim of the study was to analyse and summarise data on the factors and mechanisms responsible for increased risk of drug-induced AKI, to analyse potential methods of its prevention and treatment. At present, the following phenotypes of drug-induced AKI are distinguished: acute vascular disease, acute glomerular disease, acute tubular injury / necrosis, and acute interstitial nephritis. It was discovered that most often these complications occur following the use of antimicrobial drugs, renin-angiotensin-aldosterone system inhibitors, non-steroidal anti-inflammatory drugs, and anticancer drugs, including targeted therapy. Risk factors for drug-induced AKI include age >65, female gender, low body weight, pre-existing chronic kidney disease, hypovolemia, hypoalbuminemia, acute and chronic heart failure, diabetes, malignancies, liver cirrhosis, prolonged use of nephrotoxic drugs, and simultaneous use of two or more nephrotoxic drugs. Discontinuation of the drug which resulted in kidney failure is the first and foremost principle for managing not only drug-induced, but all AKI patients. The use of potentially nephrotoxic drugs should be avoided, especially in high-risk patients, in order to prevent drug-induced AKI. If a patient needs a drug that affects renal hemodynamics, the therapy should begin with a minimum effective dose, and combinations of two and more nephrotoxic drugs should be avoided. Close monitoring of kidney function is crucial for high-risk patients. They should also be informed about the importance of adequate water consumption schedule for prevention of hypovolemia.

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Acyclovir-induced thrombotic microangiopathy

Cited by 4 publications

References 5 publications

Aciclovir

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Acute kidney injury following intravenous acyclovir in children

Drug-Induced Acute Kidney Injury

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