Severe hypophosphatemic osteomalacia secondary to fanconi syndrome due to adefovir: A case report

Andrea Palermo, Rocky Strollo, Rocco Papalia, Luca D'Onofrio, Ernesto Maddaloni, Silvia Irina Briganti, Nicola Napoli, Umberto Vespasiani, Sebastiano Costantino, Paolo Pozzilli, Vincenzo Denaro, Silvia Manfrini

Research output: Contribution to journalArticlepeer-review


Generalized proximal, type 2, renal tubular acidosis, also known as Fanconi syndrome, is a generalized dysfunction of the proximal renal tubule characterized by impaired reabsorption and increased urinary loss of phosphate and other solutes, such as uric acid, glucose, amino acids, and bicarbonate. Chronic hypophosphatemia is the second most common cause of osteomalacia after vitamin D deficiency in adult patients and can have a heterogeneous presentation, ranging from mild symptoms such as muscle weakness and skeletal pain to more severe presentation, such as disabling myopathy, severe bone and joint pain, difficulty walking, and even bone fractures.Methods: This report describes a case of severe hypophosphatemic osteomalacia with multiple fragility fractures induced by adefovir, which was worsened and confounded by a previous treatment with zoledronic acid and required prolonged intravenous potassium phosphate administration.Results: We highlight the limited diagnostic value of dual X-ray absorptiometry and bone scintigraphy in this challenging diagnosis. Bone metabolism should always be assessed in patients treated with adefovir for early detection of osteomalacia due to Fanconi syndrome.Conclusion: Although rare, this condition may be life-threatening and mimic other bone metabolic disorders that are treated with drugs that may further impair phosphate balance.

Original languageEnglish
Pages (from-to)e246-e249
JournalEndocrine Practice
Issue number12
Publication statusPublished - Dec 1 2014

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism


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