Inhibition of Renal Phosphate Transport by a Tumor Product in a Patient with Oncogenic Osteomalacia

Abstract

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 cellular concentrations of cyclic adenosine monophosphate (cAMP). The medium had parathyroid hormone (PTH)-like immunoreactivity but no PTH-related protein immunoreactivity, and its action was not blocked by a PTH antagonist.