Acyclovir nephrotoxicity

☑️@acyclovir_nephrotoxi · 7511 subscribers · Content 18+ 🔞
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Actual: Fleischer R, Johnson M: Acyclovir nephrotoxicity: a case report highlighting the importance of prevention, detection, and treatment of acyclovir
4.6 rating 2025-04-26
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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.

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The case described in this vignette is an example of the clinical manifestation of acyclovir crystal obstructive nephrotoxicity. We will briefly discuss the pathophysiology, diagnosis, prevention, and management of patients that present with acyclovir nephrotoxicity.

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by P Gunness 2024 Cited by 63For decades, acyclovir-induced nephrotoxicity was believed to be secondary to crystalluria. Clinical evidence of nephrotoxicity in the absence of

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by A Aboelezz Cited by 3The risk factors associated with acyclovir nephrotoxicity are obesity and concomitant administration of nephrotoxic drugs.25 Because AKI is

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Dosing Uses. AdultPediatric. ADULT. Dosage Forms Strengths. injectable solution acyclovir. acyclovir and amikacin both increase nephrotoxicity and/or

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Nephrotoxicity is the AE related to acyclovir exposure that is most concerning. 12 Damage to the renal tubules is thought to occur when acyclovir crystals precipitate leading to an obstructive nephropathy. 12 A retrospective case-control study of 373 infants and children treated with intravenous acyclovir found that nephrotoxicity defined as

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by AM Al-Alawi 2024 Cited by 4IV hydration is essential to prevent IV acyclovir induced-nephrotoxicity. intravenous acyclovir induced nephrotoxicity'. Together they form a

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Acyclovir may increase the nephrotoxic activities of Tenofovir disoproxil. Drink plenty of fluids. Dehydration with acyclovir predisposes patients to

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For decades, acyclovir-induced nephrotoxicity was believed to be secondary to crystalluria. Clinical evidence of nephrotoxicity in the absence of crystalluria suggests that acyclovir induces direct insult to renal tubular cells. We postulated that acyclovir is metabolized by the alcohol dehydrogenas

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