Acyclovir

Although aciclovir is a relatively safe drug it has important side effects. It is predominantly excreted by the kidneys, where it can cause renal impairment through crystalluria resulting in obstructive nephropathy. This reversible nephropathy usually manifests after 4 days of intravenous therapy and can affect up to 20% of patients. It is only rarely seen after oral valaciclovir, usually as an overdosage.7
Acute kidney injury secondary to acyclovir is characterized by a decrease in renal function that usually develops within 12–48 hours of drug administration as indicated by a rapid rise in the serum creatinine. Acyclovir, which is relatively insoluble in urine, is rapidly filtered by the glomeri and secreted by the renal tubules which can produce high urine concentrations, especially in patients with decreased urine flow rates. Oral acyclovir has poor bioavailability and usually only
Postulated that acyclovir is metabolized by the alcohol dehydrogenase (ADH) enzyme to acyclovir aldehyde, which is metabolized by the aldehyde dehydrognase 2 (ALDH2) enzyme to 9-carboxymethoxymethylguanine (CMMG). Hypothesized that acyclovir aldehyde plays a role in acyclovir-induced nephrotoxicity. Human renal proximal tubular (HK-2) cells were used as in vitro model. The results indicates that acyclovir aldehyde is produced in HK-2 cells and that inhibition of its production by 4-methylpyrazole offers significant protection from cell death in vitro, suggesting that acyclovir aldehyde may cause the direct renal tubular insult associated with acyclovir.18 Common laboratory findings other than an increase in serum creatinine include hematuria and pyuria on urinalysis, as well as birefringent needleshaped crystals seen on polarizing light microscopy. The risks of nephropathy can be reduced by maintaining adequate hydration and monitoring renal