Acyclovir is an important antiviral agent in the therapy of herpes simplex and varicella zoster virus infections . Although the drug is well tolerated, severe nephrotoxicity, which often leads to acute renal failure, has been observed in patients . Acyclovir-induced renal failure occurs in approximately 12–48 % of cases . The optimal usage of acyclovir is very important in order to avoid its potentially life-threatening complications. Acyclovir-induced nephrotoxicity is typically evident by an increase in the plasma creatinine level, abnormal urine sediment, or acute renal injury . Acyclovir is rapidly excreted in the urine via glomerular filtration and tubular secretion, and reaches high concentrations in the tubular lumen. Renal excretion of unchanged drug reaches approximately 60–90 % . Acyclovir is relatively insoluble in the urine, particularly in the distal tubular lumen . Rapid intravenous administration of high-dose acyclovir is associated with high luminal concentrations of this drug and the intratubular precipitation of crystals can cause renal injury . Typically, crystalluria develops within 24–48 h of the initiation of acyclovir therapy. Severe intraparenchymal precipitation of crystals can cause interstitial congestion and hemorrhage, leading to a decrease of renal blood flow .