A severe case of tenofovir-associated acute kidney injury requiring hemodialysis in a patient with chronic hepatitis B

as a first-line monotherapy for chronic hepatitis B (CHB) [1]. Although there are cases of acute kidney injury (AKI) caused by TDF [2,3], there has been no report of a case in a patient who underwent renal replacement therapy in Korea. Here, we describe a severe case of TDF-associated AKI that required hemodialysis in a patient with CHB. A 55-year-old Korean male with CHB visited the emergency department in our center for evaluation of general weakness and lower extremity edema. He was hepatitis B e-antigen-negative, and a physician at a local clinic had prescribed TDF 300 mg daily over the previous 18 months. Before starting TDF, the patient’s estimated glomerular filtration rate (eGFR) was 58 mL/min/1.73 m, whereas the eGFR decreased to 32 mL/min/1.73 m 3 months prior to admission. His other medications included losartan 50 mg daily for 1 year for hypertension. On admission, the patient’s pulse measured 76 beats per minute, and his blood pressure was 110/80 mmHg. His lower extremities demonstrated grade 2 pretibial pitting edema. Ultrasonography showed normal dimensions of both kidneys (right kidney, 11.0 cm × 5.8 cm; left kidney, 11.5 cm × 5.2 cm). Blood urea nitrogen and serum creatinine concentrations were 92 mg/dL and 15.7 mg/dL, respectively. Initial arterial blood gas analysis revealed severe metabolic acidosis (pH = 7.190, pCO2 = 25.0 mmHg, and HCO3 = 9.5 mmol/L) with a high anion gap of 27.5, but the lactate concentration was normal. Other laboratory evaluation revealed the following: serum sodium, 134 mEq/L; urine sodium, 54 mEq/L; urine creatinine, 56.1 mg/dL (fractional excretion of sodium, 11.3%); serum calcium, 8.6 mg/dL; phosphorus, 7.3 mg/ dL; potassium, 5.3 mg/dL; serum uric acid, 8.7 mg/dL; urine uric acid, 24.8 mg/dL (fractional excretion of uric acid, 79.8%); urinary β2-microglobulin, > 20,000 μg/L, (reference range: 0 to 300 μg/L); and urinary anion gap, 33.3 mEq/L. The patient also had proteinuria (urinary protein-to-creatinine ratio, 2.3), hematuria, and glycosuria. Electrophoresis of the serum and urine was negative for monoclonal gammopathy, and his serum alanine aminotransferase was 319 IU/L. Serum albumin was 2.7 g/dL, and prothrombin time was 1.03 international normalized ratio. Hepatitis B virus DNA was undetectable on admission. His initial urine output was 25 mL/hour over a period of 6 hours. Under the clinical impression of oliguric AKI with metabolic acidosis, we initiated hemodialysis and did not perform a biopsy due to the patient’s generalized edema on admission. On hospital day 38, percutaneous A severe case of tenofovir-associated acute kidney injury requiring hemodialysis in a patient with chronic hepatitis B A Young Cho , Ju Hwan Oh , Hee-Chan Moon , Gum Mo Jung , Young Suk Lee , Yeong Jin Choi , In O Sun , Kwang Young Lee Division of Nephrology, Department of Internal Medicine, Presbyterian Medical Center, Jeonju, Republic of Korea Division of Gastroenterology, Department of Internal Medicine, Presbyterian Medical Center, Jeonju, Republic of Korea Department of Hospital Pathology, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea Correspondence