The use of antiretroviral medications in patients with human immunodeficiency virus (HIV) is highly effective in reducing HIV-related morbidity and mortality1,2. While HIV-positive patients continue to live longer with antiretroviral medications, adverse effects of long-term treatment include dyslipidemia, diabetes mellitus, and abnormalities of bone metabolism3,4. Metabolic bone disorders are common in patients with HIV infection, and many patients have premature osteoporosis and an increased risk of fracture5,6. While the mechanism of skeletal fragility in these patients remains inconclusive, antiretroviral medications have been described as a factor contributing to bone loss3,7. Tenofovir (Viread), a commonly prescribed antiretroviral drug, has recently been noted to cause Fanconi syndrome, a disorder characterized by renal tubular dysfunction, which leads to hypophosphatemia, hypokalemia, and metabolic acidosis as well as symptoms of polyuria and dehydration8. Patients with Fanconi syndrome can experience electrolyte disturbances due to impaired renal tubular reabsorption, which can ultimately lead to defects in bone mineralization8,9. In the following case report, we describe an HIV-infected patient who developed Fanconi syndrome as a result of tenofovir treatment and subsequently sustained bilateral hip fractures. Tenofovir-associated Fanconi syndrome places the patient at greater risk for developing abnormalities of bone metabolism, which, once detected, can be corrected by tenofovir cessation and electrolyte repletion. The objective of this case report is to raise orthopaedic surgeons’ awareness of the adverse drug complications that can occur in patients treated for HIV infection, which can lead to derangement of bone strength and thus result in fracture. The patient consented to the submission of the case data for publication. A fifty-four-year-old transgender woman with HIV infection presented with right hip pain after falling at her home. She had experienced increasing difficulty walking …