Adefovir-induced Fanconi syndrome: diagnostic pearls and perils of late or missed diagnosis

Abstract

Low-dose adefovir therapy has been increasingly recognised as a cause of Fanconi syndrome. Being relatively novel, early diagnosis is both fraught with difficulty and yet of paramount importance given its far-reaching consequences, many of which are amenable to treatment. We discuss a patient who presented with hypokalemia and other electrolyte abnormalities suggestive of Fanconi syndrome whilst on adefovir for hepatitis B. A trans-tubular potassium gradient (TTKG = 9.4) and urinary fractional phosphate excretion (39.4 %) consistent with renal potassium and phosphate wasting together with euglycemic glycosuria, aminoaciduria and hypophosphatemic osteomalacia supported the diagnosis of adefovir-induced Fanconi syndrome. With the cessation of the culprit drug, the patient has achieved partial recovery after 9 months. A high index of suspicion coupled with regular symptom surveillance and electrolyte monitoring is recommended in the course of adefovir therapy.

Keywords: Adefovir; Fanconi syndrome; Hypokalemia; Hypophosphatemia; Osteomalacia.

Fig. 1

Nomogram for derivation of renal threshold phosphate concentration (reproduced with permission from Elsevier)

Fig. 2

Bone scan showing multiple insufficiency fractures. A bone mineral densitometry scan showed osteoporosis, and a bone scan showed multiple fragility fractures