We report the case of a 64-year-old male with HIV infection known for 22 years, treated with didanosine, tenofovir and lopinavir/ritonavir.
During the last two years, in outpatient visits, the patient reported asthenia and diffuse bone pain.
In several determinations, an elevation of total alkaline phosphatase (ALP) and bone parathyroid hormone (PTH) was observed.
25-hydroxyvitamin D (25-HCC), total and ionized calcium and other routine biochemical parameters in serum, and elemental and sediment urine were normal.
A simple radiography of the spine showed degenerative signs, and a Tc99 scintigraphy was normal.
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During the last month his condition worsened, with greater asthenia, decreased strength, difficulty sleeping and loss of 7 kg of weight, so he was admitted to the hospital.
Physical examination was normal except for proximal muscle weakness.
Analytical data included mild hyperglycaemia (154 mg/dl), marked glycosuria (4+/24 mg), hypophosphatemia and proteinuria (biuria in mmol/high), mild metabolic acidosis (945 mg/dl).
Additionally, amino aciduria was moderate, 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.
Based on these results, the diagnosis of incomplete Fanconi syndrome with severe hypophosphatemia and probable osteomalacia was established in relation to TDF.
This drug was withdrawn and treatment with raltegravir and darunavir boosted with ritonavir was started.
In addition, phosphorus supplements, 25-HCC and 1,25-dihydroxyvitamin D (1.25 DHCC) were administered.
With this his condition gradually improved.
Six months after the removal of the DFD, the patient had recovered bone pain and muscle weakness. The patient had regained baseline weight and normalized serum laboratory abnormalities, although mild phosphate reabsorption remained.
