Acute kidney injury due to acyclovir

Yıldız, Çiğdem; Özsürekçi, Yasemin; Güçer, Şafak; Cengiz, Ali Bülent; Topaloğlu, Rezan

doi:10.1007/s13730-012-0035-0

Cited by 46 publications

(44 citation statements)

References 20 publications

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“…2a ); by direct injury to the renal tubular epithelia causing tubular cell degeneration and sloughing. Indeed, renal biopsy findings of patients with acyclovir toxicity include bulging of tubular cells, dilated tubular lumens, loss of proximal-distal tubular differentiation, flattening and vacuolization of epithelial cells, and epithelial cells mitoses [ 5 ] (Fig. 2b ); and crystalluria , which usually develops 24–48 h after the initiation of acyclovir therapy due to its low solubility in urine.…”

Section: Discussionmentioning

confidence: 99%

“…Risk factors for developing acyclovir-induced nephrotoxicity include hypovolemia, rapid intravenous infusion, concurrent AKI prior to drug administration, excess medication dosage in relation to renal function, and concurrent use of other nephrotoxic agents [ 4 ]. Severe nephrotoxicity occurs in approximately 12–48% of the cases [ 5 ]. However, the potential damage induced by oral administration remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Oral acyclovir induced hypokalemia and acute tubular necrosis a case report

et al. 2018

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BackgroundAcyclovir is one of the most common prescribed antiviral drugs. Acyclovir nephrotoxicity occurs in approximately 12–48% of cases. It can present in clinical practice as acute kidney injury (AKI), crystal-induced nephropathy, acute tubulointerstitial nephritis, and rarely, as tubular dysfunction. Electrolytes abnormalities like hypokalemia, were previously described only when given intravenously.Case presentationA 54 year-old female presented with weakness and lower extremities paresis, nausea and vomiting after receiving oral acyclovir. Physical examination disclosed a decrease in the patellar osteotendinous reflexes (++ / ++++). Laboratory data showed a serum creatinine level of 2.1 mg/dL; serum potassium 2.1 mmol/L. Kidney biopsy was obtained; histological findings were consistent with acute tubular necrosis and acute tubulointerstitial nephritis. The patient was advised to stop the medications and to start with oral and intravenous potassium supplement, symptoms improved and continued until serum potassium levels were > 3.5 meq/L.ConclusionsThe case reported in this vignette is unique since it is the first one to describe hypokalemia associated to acute tubular necrosis induced by oral acyclovir.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Oral acyclovir induced hypokalemia and acute tubular necrosis a case report

et al. 2018

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“…(ii) Cases of drug resistance including escape mutants are frequently reported (8)(9)(10)(11)(12). (iii) Prolonged use of TFT can cause other ocular disorders (13)(14)(15), and prolonged use of ACV can cause nephrotoxicity (16)(17)(18). (iv) Nucleoside analogs have the potential to be a chromosomal mutagen and, therefore, often are not prescribed during pregnancy (19).…”

Section: Introductionmentioning

confidence: 99%

An off-target effect of BX795 blocks herpes simplex virus type 1 infection of the eye

et al. 2018

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Herpes simplex virus type 1 (HSV-1) causes recurrent mucocutaneous lesions in the eye that may advance to corneal blindness. Nucleoside analogs exemplified by acyclovir (ACV) form the primary class of antiherpetic drugs, but this class suffers limitations due to the emergence of viral resistance and other side effects. While studying the molecular basis of ocular HSV-1 infection, we observed that BX795, a commonly used inhibitor of TANK-binding kinase 1 (TBK1), strongly suppressed infection by multiple strains of HSV-1 in transformed and primary human cells, cultured human and animal corneas, and a murine model of ocular infection. Our investigations revealed that the antiviral activity of BX795 relies on targeting Akt phosphorylation in infected cells, leading to the blockage of viral protein synthesis. This small-molecule inhibitor, which was also effective against an ACV-resistant HSV-1 strain, shows promise as an alternative to existing drugs and as an effective topical therapy for ocular herpes infection. Collectively, our results obtained using multiple infection models and virus strains establish BX795 as a promising lead compound for broad-spectrum antiviral applications in humans.

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“…This nephrotoxicity can lead to AKI if it was not early identified and the patient may consequently require hemodialysis [4,14]. The fast increase in serum creatinine is an important indicator of acyclovir nephrotoxicity [15]. To lower the risk of acyclovir nephrotoxicity, hydration with isotonic fluids during the administration of the drug is imperative [14].…”

Section: Discussionmentioning

confidence: 99%