We present the case of a 64-year-old man with known HIV infection for 22 years, on treatment with didanosine, tenofovir and lopinavir/ritonavir. During the last two years, during outpatient examinations, he reported asthenia and diffuse bone pain. Several tests showed elevated total and bone alkaline phosphatase (ALP) and parathyroid hormone (PTH) levels. 25-hydroxyvitamin D (25-HCC), total and ionic calcium and other routine serum biochemical parameters, and urine elemental and sediment were normal. A plain spine X-ray showed degenerative signs, and a Tc99 scintigraphy was normal.

During the last month her condition worsened, with increased asthenia, decreased strength, difficulty walking and a 7 kg weight loss, and she was admitted to hospital. Physical examination was unremarkable, except for proximal muscle weakness. Laboratory findings included mild hyperglycaemia (154 mg/dl), marked glycosuria (4+), hypophosphataemia, inappropriately high phosphaturia, hypouricemia (2 mg/dl), mild metabolic acidosis (bicarbonate 19 mmol/l) and proteinuria (945 mg/24h). In addition, moderate aminoaciduria, with increased values of glycine (x2), valine (x2), serine (x4) and threonine (x4). Serum FGF23 was 6 pg/ml. Other parameters are shown in table 1.
From these results a diagnosis of incomplete Fanconi syndrome with severe hypophosphataemia and probable osteomalacia was established in association with TDF. TDF was withdrawn and treatment was started with raltegravir and ritonavir-boosted darunavir. In addition, phosphorus supplements, 25-HCC and 1,25-dihydroxyvitamin D (1,25 DHCC) were administered. As a result, his condition progressively improved. Six months after TDF withdrawal, bone pain and muscle weakness had disappeared, the patient had regained baseline weight and serum analytical abnormalities had normalised, although phosphate reabsorption remained slightly low.

