Concurrent Nephrotoxicity and Neurotoxicity Induced by Oral Valacyclovir in a Patient With Previously Normal Kidney Function

Abstract

Drug-induced nephrotoxicity and neurotoxicity are commonly encountered problems in clinical practice. We describe a case of concurrent valacyclovir-induced nephrotoxicity and neurotoxicity in a 64-year-old man with no history of renal disease who developed acute renal injury and neurological symptoms after he received two weeks of the standard dose of oral valacyclovir for herpes zoster meningitis. His clinical condition improved significantly after the initiation of hemodialysis. Although nephrotoxicity due to intravenous infusion of valacyclovir and/or acyclovir is not uncommon, oral valacyclovir therapy is rarely associated with nephrotoxicity in patients with no history of renal insufficiency. Additionally, concurrent nephrotoxicity and neurotoxicity due to valacyclovir and/or acyclovir are rarely reported. Clinicians should be aware of these adverse events as immediate recognition and intervention are necessary to prevent morbidity.

A Case of Oral Valacyclovir–Induced Acute Kidney Injury

“…Oral valacyclovir-induced nephrotoxicity is rare, compared with more commonly encountered cases of nephrotoxicity caused by intravenous infusion of acyclovir. [1][2][3][4] In our case, as in other similar cases, AKI developed within 24 to 48 hours of valacyclovir administration, as indicated by the rapid rise in the patient's serum creatinine level. [1][2][3][4] After oral administration, valacyclovir is converted to acyclovir, and with the intratubular precipitation of acyclovir crystals, there is increased resistance to renal blood flow with subsequent elevation of serum creatinine.…”

“…[1][2][3][4] In our case, as in other similar cases, AKI developed within 24 to 48 hours of valacyclovir administration, as indicated by the rapid rise in the patient's serum creatinine level. [1][2][3][4] After oral administration, valacyclovir is converted to acyclovir, and with the intratubular precipitation of acyclovir crystals, there is increased resistance to renal blood flow with subsequent elevation of serum creatinine. 1,4,5 Because of the rapid speed of renal excretion, acyclovir can surpass the solubility, hence crystals can accumulate in the distal and collecting ducts.…”

“…6 The patient's history of valacyclovir intake just prior to the episode, along with laboratory correlation, made the diagnosis of crystal-induced nephrop-athy more likely. 1,3,4 Our case of an unexpected association between AKI and oral valacyclovir should serve as a wakeup call to physicians, particularly in the primary care setting, that care should be taken while prescribing valacyclovir to patients with underlying chronic renal insufficiency. Timely intervention with adequate hydration would contribute to a favorable prognosis.…”

“…[1][2][3][4] After oral administration, valacyclovir is converted to acyclovir, and with the intratubular precipitation of acyclovir crystals, there is increased resistance to renal blood flow with subsequent elevation of serum creatinine. 1,4,5 Because of the rapid speed of renal excretion, acyclovir can surpass the solubility, hence crystals can accumulate in the distal and collecting ducts. 6 The patient's history of valacyclovir intake just prior to the episode, along with laboratory correlation, made the diagnosis of crystal-induced nephrop-athy more likely.…”

“…Timely intervention with adequate hydration would contribute to a favorable prognosis. 1,4 Expert opinion from nephrology service can be helpful if there is no improvement in creatinine level with fluids.…”