Is Acyclovir Treatment Associated With Kidney Issues?

Acyclovir is an antiviral medication that is available by prescription only. Acyclovir is commonly prescribed to treat the symptoms of genital herpes, cold sores, shingles, and chickenpox. Acyclovir medication is also used to prevent recurrent genital herpes infections. Additionally, Acyclovir is not a herpes cure however it relieves the associated pain, manages symptoms, and allows the infection to clear up rapidly.

Can Acyclovir Affect The Kidneys?

Acyclovir is among the most commonly prescribed antiviral drugs. Acyclovir nephrotoxicity happens in about 12 to 48% of patients. It can occur in clinical practice as acute kidney injury, acute tubulointerstitial nephritis, crystal-induced nephropathy, and a few times as tubular dysfunction.

Acyclovir may cause kidney failure through precipitation within the tubular lumen or from acute interstitial nephritis. Moreover, acute kidney injury is a well-explained side effect of Acyclovir therapy as crystal deposition may cause renal failure.

Let us understand the effect of Acyclovir on kidneys through various clinical trials and studies.

Case Report and Review to Examine Speedily Progressive Acute Renal Failure Because of Acyclovir

Acyclovir nephrotoxicity has been pronounced since the beginning of its use. Acute renal failure arbitrated by this compound is described by sudden elevations in serum creatinine and a steady return to baseline renal function after discontinuing the drug.

The formation of drug crystals in collecting tubules ensuing in an intraparenchymal form of obstructive nephropathy has been proposed as the mechanism for Acyclovir nephrotoxicity. The patient developed swiftly progressive acute renal failure with concomitant mental status modifications under the Acyclovir treatment with high-dose parenteral.

Acyclovir administration was stopped and an open renal biopsy was found to further examine the diminishing renal function of the patient. Pathologic examination of the biopsy specimen demonstrated loss of proximal tubule brush border and dilated proximal and distal tubules with focal nuclear loss and flattening of lining cells. No crystals were observed and these modifications were constant with acute tubular necrosis with regeneration.

In the next four days, the renal and neurologic levels of the patients recovered to their prehospitalization statuses. It seems that the patient was influenced by Acyclovir-mediated nephrotoxicity that showed on biopsy by acute tubular necrosis and the absence of crystal deposition.

Therefore intravenous Acyclovir administration can produce rapidly progressive acute neurologic and renal toxicity that is generally reversible. The pathologic variations of acute tubular necrosis must be comprised as part of the spectrum of renal damage allied to Acyclovir treatment.

A Case Report Concerning Oral Acyclovir-Induced Hypokalemia and Acute Tubular Necrosis

Acyclovir is a commonly used antiviral medication and Acyclovir nephrotoxicity develops in around 12 to 48% of patients. Electrolyte abnormalities such as hypokalemia were described earlier only when the drug was given intravenously.

A 54-year-old lady reported weakness, nausea, vomiting, and lower extremities paresis after taking oral Acyclovir. Physical examination revealed a reduction in the patellar osteotendinous reflexes. Laboratory reports demonstrated a serum creatinine level of 2.1 mg/dL and a serum potassium level of 2.1 mmol/L.

A kidney biopsy was attained, and histological discoveries were constant with acute tubular necrosis and acute tubulointerstitial nephritis. The patient was suggested to discontinue the medications and to begin with oral and intravenous potassium supplements. The symptoms improved well and serum potassium levels were > 3.5 meq/L.

The case reported here is unique as it is the initial one to pronounce hypokalemia linked to acute tubular necrosis induced by oral Acyclovir.


Drug-induced kidney injury is a common adverse effect observed during clinical practices. It can be due to various mechanisms that commonly cause acute kidney injury. As per a considerable cohort study of patients with community-acquired acute kidney injury, nephrotoxic medications were expected in 59.9% of the patients.

Antiviral medications including Acyclovir are known to cause acute kidney injury when the drug is administered intravenously. The risk factors associated with developing acyclovir-induced nephrotoxicity include concurrent intake of other nephrotoxic agents, excess dosage of medication concerning renal function, concurrent acute kidney injury before the drug administration, hypovolemia, and rapid intravenous infusion.

A study was performed to examine hospital admissions due to acute kidney injury within 30 days after they had been prescribed oral Acyclovir. The study found that neither the intake of Acyclovir nor Valacyclovir was linked to a higher risk of developing acute kidney injury as compared to Famacyclovir.

Potassium fluctuations are common consequences of drug intake. Drug-induced hypokalemia is usually caused by diuretic glucocorticoid and laxative administration. On the other hand, it can be a result of increased intracellular potassium influx induced by the use of insulin and sympathomimetic drugs.

This case report is an exclusive case of hypokalemia and community-acquired acute kidney injury because of acute tubular necrosis.

Clinical History and Laboratory Data

A 54-year-old woman reported nausea, vomiting, lower extremities paresis, and weakness after getting (to treat a dental abscess) oral Acyclovir, Dicloxacillin, and Clindamycin. Past medical history included smoking and allergy to penicillin.

Kidney Biopsy

Two fragments of kidney tissues were attained, and 11 glomeruli were observed by stereoscopic evaluation. 9 glomeruli were noticed by light microscopy, 3 were globally sclerosed and others were normal. Histological findings were constant with acute tubular necrosis and acute tubulointerstitial nephritis.

Clinical Follow-up

As a result of persistent hypokalemia, oral and IV potassium replacement was initiated with good tolerability without adverse events and symptoms improved. The patient was relieved from the hospital after 4 days and after a few days she resumed her normal life.


Intravenous administration of Acyclovir is most commonly given to treat herpes virus, it can lead to crystalluria and acute kidney injury. Drug-induced severe potassium fluctuations were noticed in 32.3% of patients and it was lethal in 23% of patients. Hypokalemia was noticed in 23.4% of life-threatening potassium instabilities.

In a study, hypokalemia was found in 46% of patients who were receiving intravenous Acyclovir as compared to 21% in the control group. Patients with normal potassium levels, modified estimated glomerular filtration rate, or previous use of diuretics were considered at greater risk of getting hypokalemia. It is assumed that intravenous acyclovir-induced hypokalemia by decreasing renal plasma flow and by crystal-induced distal tubular damage.


Acyclovir does not appear to impact the tubular handling of creatinine, demonstrating that the noticeable, transient elevation in plasma creatinine can be a result of decreased glomerular filtration rate due to renal dysfunction.

It is suggested to establish slow euvolemia, slow intravenous infusion regulating the dose depending on the renal function, and avoid the use of concomitant nephrotoxic compounds before Acyclovir administration to prevent possible adverse events of this drug.

Early detection of tubular and renal dysfunction of adverse drug reactions because of the administration of Acyclovir is crucial to offering safe, effective, and appropriate Acyclovir therapy.