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See the DrugPatentWatch profile for acyclovir
Acyclovir, an antiviral used for herpes infections, is excreted primarily by the kidneys unchanged. High doses or rapid IV infusion cause it to precipitate in renal tubules, leading to acute kidney injury (AKI). This nephrotoxicity occurs in 5-12% of hospitalized patients on IV acyclovir, often within days of starting treatment.[1][2]
Acyclovir has low solubility in acidic urine (pH <7). IV administration overwhelms glomerular filtration, saturating tubules. Precipitation triggers inflammation and vasoconstriction, reducing glomerular filtration rate (GFR). Oral forms pose lower risk due to slower absorption.[1][4]
Patients with baseline CrCl <10 mL/min face 50% higher AKI risk; avoid IV use if possible, switch to oral valacyclovir (better tolerated). Dialysis clears acyclovir efficiently (half-life drops to 2 hours), aiding recovery in severe cases—most regain function within weeks.[3][6]
AKI is usually reversible if caught early; 80-90% recover fully within 1-2 weeks post-discontinuation. Persistent damage is rare but seen in elderly or those with comorbidities. No evidence of chronic kidney disease from short courses.[4] [1]: Lexicomp: Acyclovir Monograph [2]: NEJM: Acyclovir Nephrotoxicity [3]: AJKD: Antiviral Nephrotoxicity Review [4]: UpToDate: Acyclovir Dosing and Toxicity [5]: FDA Label: Zovirax (Acyclovir) [6]: Clinical Infectious Diseases: Acyclovir AKI Management
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