Acyclovir (ACV), a DNA polymerase inhibitor, is widely used for the treatment and prophylaxis of varicella zoster virus (VZV) infections [1]. Valacyclovir (VACV), a prodrug of ACV, offers significantly improved oral bioavailability compared to ACV [1]. However, administration of either ACV or VACV can result in reversible renal impairment [[2], [3], [4], [5]]. Additionally, elevated serum concentrations of ACV may cause drug-induced neuropsychiatric adverse effects—referred to as ACV-induced encephalopathy—which may present with symptoms such as disorientation and hallucinations [[2], [3], [4], [5]].

ACV is primarily eliminated via renal excretion [6]. It is also oxidized by alcohol dehydrogenase to form ACV aldehyde, which is subsequently converted to a neurotoxic metabolite, known as 9-carboxymethoxymethylguanine (CMMG) [7]. In individuals with normal renal function, approximately 62 %–91 % of intravenously administered ACV is excreted unchanged in the urine, while 8 %–14 % is excreted as CMMG [8]. Therefore, impaired renal function can lead to accumulation of ACV and its toxic metabolites.

Continuous hemodiafiltration (CHDF) is commonly employed in critically ill patients to manage acute renal failure and subsequent fluid overload. Although previous studies have demonstrated that ACV concentrations are reduced across the dialyzer membrane during CHDF [9], clinical data on serum ACV concentrations in patients undergoing CHDF are limited. Here, we report a case highlighting the effect of CHDF on serum ACV concentrations in a patient who developed encephalopathy during antiviral therapy.