A case of renal hypophosphatemic ostemalacia (RHO) that was unmasked by hyperthyrodism is presented. The patient presented at age 64 with pathologic leg fractures. There was no family history of ostemalacia or rickets. Initial evaluation reveled hyperthyroidism, which was treated with radioactive iodine. Despite control of thyroid function, the patient had recurrent pathologic fractures. Further evalulation reveled hisologically proven osteomalacia and the biochemical findings of RHO: elevated serum alkaline phosphaings of RHO: elevated serum alkaline phosphatase, decreased serum phosphate and tubular resorption of phosphate, and normal serum calcium parathyroid hormone, and vitamin D levels. Other cause of osteemalacia were extriol reversed the ostemalacia. This case demonstrates thathyperthyrodism, and possibly other illnesses that affect vitamin D or bone metabolism, may unmask metabolic bone diseaease and that physicians should be alert for the subtle clinical and biochemical indicators of unrecognized metabolic bone disease in adults.