Endocrine Abstracts (2013) 32 P306 | DOI: 10.1530/endoabs.32.P306

Adefovir diproxivil-induced acquired Fanconi's syndrome presenting as hypokalemia

Shang Ming Samuel Lee, Cherng Jye Seow & Melvin Khee-Shing Leow


1Tan Tock Seng Hospital, Singapore, Singapore; 2Ministry of Health Holdings, Singapore, Singapore.


Introduction: Adefovir, commonly used for the treatment of hepatitis B, has dose-related nephrotoxicity, especially at doses of 60 mg daily and above. We describe a patient with Fanconi’s syndrome after being on low dose adefovir for more than 5 years.

Case report: A 62-year-old Chinese man, a chronic carrier of Hepatitis B on adefovir 10 mg daily for over 5 years, presented with the incidental finding of profound yet asymptomatic hypokalemia (K 1.9 mmol/l, RI: 3.5–5.0 mmol/l). There were no previous plasma electrolyte screens. He had weight loss, fatigue and bone pain for months. A high trans-tubular potassium gradient suggested renal potassium wasting. In addition, there was an associated non-anion gap metabolic acidosis, hypophosphatemia of 0.4 mmol/l (RI: 0.8–1.6 mmol/l) and hypouricemia of 154 μmol/l (RI: 250–550 μmol/l). The fractional excretion of phosphate was raised (59%, RI: 5–20%). The 24 h urine uric acid was 2778 μmol/day (RI: 500–5800 μmol/day) which was inappropriately normal. Urine protein excretion (24 h urinary total protein 0.880 g/day) and urinary amino acids were also raised, and glucose urinary dipstick was positive (2+). Dual energy X-ray absorptiometry showed osteoporosis. A diagnosis of acquired Fanconi’s syndrome secondary to adefovir was made. Upon substitution with entecavir, we expect resolution of the electrolyte abnormalities to occur over the next few months.

Conclusion: It has been shown that adefovir depletes mitochondrial DNA which contributes mechanistically to proximal tubular dysfunction and hence acquired Fanconi’s syndrome. Patients on adefovir therapy should therefore be screened periodically for electrolyte abnormalities, even when used at low doses.

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