Oral acyclovir induced hypokalemia and acute tubular necrosis a case report

A 54 year-old female presented to the outpatient clinic with weakness and lower extremities paresis, nausea and three times vomiting, after receiving clindamycin, dicloxaciline, and oral acyclovir 400 mg each 8 h were prescribed to treat a dental abscess. Relevant past medical history included allergy to penicillin and smoking for 20 years. Physical examination disclosed good hydration status, decrease in the patellar osteotendinous reflexes (++ / ++++). Initial laboratory data showed a serum creatinine level of 2.1 mg/dL; blood urea nitrogen 86.4 mg/dL; serum potassium 2.1 mmol/L, sodium 134 mmol/L, phosphorus 1.7 mg/dL, and magnesium 2.15 mg/dL. (Table 1).

The patient was advised to stop the medications and to start with oral potassium supplement. She noticed improvement of the weakness; however, due to persistent hypokalemia, the patient was admitted to the hospital for further evaluation; new blood test showed a serum creatinine level of 1.7 mg/dL and blood urea nitrogen 76.3 mg/dL; serum potassium 2.5 mmol/L, sodium 139 mmol/L, phosphorus 2 mg/dL, and magnesium 1.88 mg/dL; urine sediment was unremarkable; 24 h urine potassium was 49 mEq/day, sodium 86 mEq/day, and calcium 89 mg/day. A renal ultrasound showed a normal-size kidney, without hydronephrosis. Kidney biopsy was performed.

Two fragments of kidney tissue were obtained (Fig. 1), By stereoscopic evaluation 11 glomeruli were identified. By light microscopy 9 glomeruli were observed; three were globally sclerosed and the remaining glomeruli were normal. Tubular atrophy was seen in 15–20% of the tubules; the remaining tubules showed vacuolated, granular cytoplasm, focal sloughing of the epithelium, and regenerative changes of the brush edge of tubular cells and hyaline casts (Fig. 1a). By Masson’s trichrome stain (Fig. 1b and c), the interstitium exhibited 0–15% fibrosis, with inflammatory infiltrate by lymphocytes, plasma cells, and few eosinophils, that penetrated the tubular epithelium. Arterioles and medium-caliber arteries were permeable without vasculitis or thrombi. By Jones (Fig. 1d) tubule-interstitial nephritis infiltrated with abundant inflammatory cells were observed. Immunofluorescence (Fig. 1e) was negative for IgM, IgG, IgA, C3c, C1q, kappa, lambda, fibrinogen, and albumin. Histological findings were consistent with acute tubular necrosis and acute tubulointerstitial nephritis.

Due to persistent hypokalemia oral and intravenous potassium replacement was started with good tolerability and no adverse events, symptoms improved; the patient was discharged 4 days later with a serum potassium of 3.1 mEq/L; oral replacement of potassium was continued until serum potassium levels were > 3.5 meq/L, after few days later she restart her normal life.

Hypokalemia and acute kidney injury due to oral acyclovir.