Posters
Not Every Focal Deficit Is a Stroke: A Case of Valacyclovir Neurotoxicity in End-Stage Renal Disease
Presenting Author Academic/Professional Position
Sikandar Zia
Academic Level (Author 1)
Resident
Discipline/Specialty (Author 1)
Internal Medicine
Academic Level (Author 2)
Resident
Discipline/Specialty (Author 2)
Internal Medicine
Academic Level (Author 3)
Resident
Discipline/Specialty (Author 3)
Internal Medicine
Academic Level (Author 4)
Resident
Discipline/Specialty (Author 4)
Internal Medicine
Academic Level (Author 5)
Faculty
Discipline/Specialty (Author 5)
Internal Medicine
Discipline Track
Patient Care
Abstract Type
Case Report
Abstract
Background: Valacyclovir is a widely used antiviral agent for herpesvirus infections. It is a prodrug of acyclovir, which is primarily excreted by the kidneys. In patients with normal renal function, it is well tolerated. However, in individuals with chronic kidney disease (CKD) or end-stage renal disease (ESRD), impaired clearance can lead to the accumulation of the drug and its metabolites, increasing the risk of neurotoxicity. Clinical manifestations include confusion, hallucinations, ataxia, and seizures—often mimicking stroke or viral encephalitis. This case highlights the importance of considering medication toxicity in patients with renal impairment presenting with neurological symptoms.
Presentation: A 57-year-old man with ESRD on thrice-weekly hemodialysis presented with a two-week history of slurred speech, unsteady gait, and intermittent confusion. On the day of admission, he experienced a fall and transient left upper extremity weakness, prompting the activation of a stroke alert. His spouse reported waxing and waning alertness, memory lapses, and visual hallucinations. Initial stroke workup, including a CT angiogram of the head and neck, was unremarkable. Labs confirmed advanced renal dysfunction (creatinine 6.5 mg/dL, BUN 69 mg/dL, GFR 9.3 mL/min). A urine drug screen and infectious workup were negative. No focal lesions or acute pathology were found to explain the neurological findings. The patient had been diagnosed with herpes zoster two weeks earlier and prescribed valacyclovir, initially 500 mg twice daily, later increased to 1 g twice daily—a dose significantly higher than that recommended for a dialysis-dependent patient. Given the presence of hallucinations, myoclonus, disorientation, and fluctuating mental status—atypical for stroke—and the timing relative to valacyclovir initiation, valacyclovir neurotoxicity was strongly suspected. The drug was discontinued, and the patient underwent two sessions of hemodialysis. Within 48 hours, his neurological status returned to baseline with full resolution of symptoms, including the transient focal weakness.
Conclusion: Valacyclovir-associated neurotoxicity is a well-documented but often underrecognized complication in patients with renal impairment. The majority of cases occur in those with kidney dysfunction, especially in patients on dialysis. Symptoms usually begin within days of starting therapy and tend to resolve after stopping the drug and initiating dialysis. The accumulation of a neurotoxic metabolite is believed to cause the central nervous system effects. Neurotoxicity can sometimes develop even when dosing follows guidelines, reflecting individual variability. This case underscores the importance of careful medication review and clinical vigilance—highlighting that not every focal neurological deficit in dialysis patients represents a stroke.
Presentation Type
Poster
Recommended Citation
Zia, Sikandar; Asif, Nida; Gonzalez, Elimar; Chouinard, Conrad; and Gutierrez, Cesar, "Not Every Focal Deficit Is a Stroke: A Case of Valacyclovir Neurotoxicity in End-Stage Renal Disease" (2025). Research Colloquium. 94.
https://scholarworks.utrgv.edu/colloquium/2025/posters/94
Included in
Not Every Focal Deficit Is a Stroke: A Case of Valacyclovir Neurotoxicity in End-Stage Renal Disease
Background: Valacyclovir is a widely used antiviral agent for herpesvirus infections. It is a prodrug of acyclovir, which is primarily excreted by the kidneys. In patients with normal renal function, it is well tolerated. However, in individuals with chronic kidney disease (CKD) or end-stage renal disease (ESRD), impaired clearance can lead to the accumulation of the drug and its metabolites, increasing the risk of neurotoxicity. Clinical manifestations include confusion, hallucinations, ataxia, and seizures—often mimicking stroke or viral encephalitis. This case highlights the importance of considering medication toxicity in patients with renal impairment presenting with neurological symptoms.
Presentation: A 57-year-old man with ESRD on thrice-weekly hemodialysis presented with a two-week history of slurred speech, unsteady gait, and intermittent confusion. On the day of admission, he experienced a fall and transient left upper extremity weakness, prompting the activation of a stroke alert. His spouse reported waxing and waning alertness, memory lapses, and visual hallucinations. Initial stroke workup, including a CT angiogram of the head and neck, was unremarkable. Labs confirmed advanced renal dysfunction (creatinine 6.5 mg/dL, BUN 69 mg/dL, GFR 9.3 mL/min). A urine drug screen and infectious workup were negative. No focal lesions or acute pathology were found to explain the neurological findings. The patient had been diagnosed with herpes zoster two weeks earlier and prescribed valacyclovir, initially 500 mg twice daily, later increased to 1 g twice daily—a dose significantly higher than that recommended for a dialysis-dependent patient. Given the presence of hallucinations, myoclonus, disorientation, and fluctuating mental status—atypical for stroke—and the timing relative to valacyclovir initiation, valacyclovir neurotoxicity was strongly suspected. The drug was discontinued, and the patient underwent two sessions of hemodialysis. Within 48 hours, his neurological status returned to baseline with full resolution of symptoms, including the transient focal weakness.
Conclusion: Valacyclovir-associated neurotoxicity is a well-documented but often underrecognized complication in patients with renal impairment. The majority of cases occur in those with kidney dysfunction, especially in patients on dialysis. Symptoms usually begin within days of starting therapy and tend to resolve after stopping the drug and initiating dialysis. The accumulation of a neurotoxic metabolite is believed to cause the central nervous system effects. Neurotoxicity can sometimes develop even when dosing follows guidelines, reflecting individual variability. This case underscores the importance of careful medication review and clinical vigilance—highlighting that not every focal neurological deficit in dialysis patients represents a stroke.
