Varicella zoster virus reactivation often occurs in the setting of impaired immunity, which is generally present in patients with end-stage renal disease (ESRD). Therapy for variceIla zoster virus infection is well established. However, it is often been forgotten that acyclovir dosage should be adjusted to renal function. We point to the problem encountered in clinical practice when ESRD patient presents with cutaneous herpes zoster and neurological symptoms. Clinical findings alone may prove inadequate to determine whether neurological deficit is caused by infection of the central nervous system or is a consequence of acyclovir induced neurotoxicity.