In tumor-induced osteomalacia, a rare syndrome characterized by hypophosphatemia, hyperphosphaturia, low plasma 1,25-dihydroxyvitamin D concentrations, and osteomalacia,1–5 all biochemical and pathological abnormalities disappear when the tumor is removed. Tumors associated with this syndrome are thought to secrete a substance that inhibits the renal tubular reabsorption of phosphate,1–5 but whether this factor interacts directly with renal tubular cells is not known. We investigated the ability of medium in which sclerosing hemangioma cells from a patient with oncogenic osteomalacia were cultured to alter sodium-dependent phosphate transport in opossum-kidney epithelial cells. We found that the medium inhibited phosphate transport, without increasing.
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