ArticleBMC nephrology2025
Valacyclovir-induced neurotoxicity and nephrotoxicity in an elderly patient with a history of nephrectomy: a case report.
Article in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- How to interpret low-dose valacyclovir for postherpetic neuralgia in the Zoster Eye Disease Study-a randomized clinical trial.Annals of translational medicine · 2026Article
- Drug-induced adverse events in modern pharmacotherapy: mechanisms, clinical manifestations, and implications for risk assessment and management.Frontiers in pharmacology · 2026Review
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6 authors.
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Abstract
backgroundValacyclovir is a prodrug of acyclovir, both of which are commonly used in the treatment of varicella zoster and herpes simplex viruses. Its mechanism as a guanosine analog antiviral inhibits DNA polymerase via chain termination. It has selective action in infected cells with minimal effect on host cells, lending to fewer side effects, and is a well-tolerated medication often chosen for its better oral bioavailability over acyclovir. Its side effect profile includes thrombotic thrombocytopenic purpura (TTP), gastrointestinal symptoms such as nausea, and increased transaminases. Common adverse effects include headache, nausea, and vomiting. A rare adverse effect of valacyclovir is acute kidney injury (AKI) due to obstructive crystal-induced nephropathy, tubular dysfunction, or tubulointerstitial nephritis. To date, no case report has cited normal dosing of valacyclovir causing acute kidney injury in a patient status post nephrectomy. CASE PRESENT: We present a 71-year-old female with history of chronic kidney disease (CKD), left nephrectomy due to renal agenesis and nephrolithiasis, type 2 diabetes mellitus, hypertension, and hyperlipidemia who presented to the emergency department due to visual and auditory hallucinations after taking two days of valacyclovir for shingles. Laboratory work demonstrates elevated creatinine at 6.19 mg/dL. Patient was monitored throughout hospitalization with cessation of valacyclovir. Patient's creatinine down-trended.
conclusionThis case report demonstrates a rare case of acute kidney injury due to an exaggerated response to valacyclovir-induced crystal nephropathy, presenting in tandem with valacyclovir-induced neurotoxicity, which has only been described in three case reports. This case highlights the importance of careful history and physical exam to facilitate a more accurate and timely diagnosis, especially in patients with a history of nephrectomy.
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