Tenofovir alafenamide
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Acute lactic acidosis: case report A 76-year-old woman developed acute lactic acidosis during treatment with tenofovir alafenamide for HIV. The woman, whose medical history was notable for type 2 diabetes, congestive heart failure, and HIV for which she had been receiving tenofovir alafenamide [route and dosage not stated], bictegravir and emtricitabine, presented to hospital with tachycardia and increasing confusion. On presentation, she was afebrile and her BP was normal; however, she exhibited a mild tachycardia (HR 105 bpm). Initial laboratory analyses revealed the following: creatinine 1.6 mg/dL, bicarbonate 22 meq/L, anion gap 22, AST 142 IU/L, ALT 110 IU/L and total bilirubin 2.4 mg/dL. Chest X-ray revealed a small right lower-lobe consolidation and mild pulmonary oedema, which raised concerns for pneumonia and exacerbation of congestive heart failure. She was admitted and received unspecified antibiotics and diuretics. However, about 12 hours post admission, she became increasingly confused. Repeat laboratory analyses at this time revealed the following: creatinine 2.0 mg/dL, bicarbonate 9 meq/L, anion gap 35, further elevation of liver transaminases, venous pH 7.16 and serum lactate 14 mmol/L. Therefore, she was shifted to the ICU, where she developed worsening oliguria and haemodynamic compromise. Since she was afebrile, her WBC count, abdominal examination and imaging were normal, and her blood and urine cultures were negative, the diagnosis of tenofovir alafenamide-induced lactic acidosis was considered [duration of treatment to reaction onset not stated]. Nephrology consultation was performed for the management of her acute lactic acidosis. In the background of woman’s oligoanuric acute kidney injury (AKI), pulmonary oedema and the development of hypotension, dialysis was thought to be the safer method of bicarbonate supplementation. A replacement fluid rate of 4 L/h was selected, with a dialysate rate of 2 L/h, to provide 138 meq/h of bicarbonate, with plans to titrate the continuous renal replacement therapy (CRRT) volumes down as her bicarbonate levels normalised. After about 10 hours, her serum bicarbonate levels were noted at 22 meq/L, and her CRRT volumes were decreased accordingly. Within 48 hours, her lactate levels began to fall, and CRRT was discontinued. Her liver enzymes gradually improved, and creatinine levels returned to a near baseline of 1.2 mg/dL. She was eventually discharged. Morales A, et al. Management consideration in drug-induced lactic acidosis. Clinical Journal of The American Society of Nephrology: CJASN 15: 1511-1512, No. 10, Oct 803517403 2020. Available from: URL: http://doi.org/10.2215/CJN.14781219
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Reactions 28 Nov 2020 No. 1832
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