Two teenage negro brothers with chronic hyperphosphatemia, one of whom exhibited heterotopic calcifications around large joints, underwent studies of phosphate metabolism. Both patients demonstrated normal inulin clearance and increased phosphate clearance in response to exogenous parathyroid hormone. Increased phosphaturia after ethylene-diaminetetraacetic acid infusion suggested normal endogenous parathormone (PTH) secretory reserve. Immunoassays of serum PTH concentration revealed values within the normal range. Serum growth hormone after arginine infusion rose appropriately in one patient studied. Karyotype analyses of leukocyte cultures yielded 46 XY patterns. It is postulated that hyperphosphatemia was due to inherited reduction in renal tubular responsiveness to the phosphaturic action of PTH, and that chronic high serum phosphate was a contributing factor to the development of extraskeletal calcifications.
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John F. Wilber (1968) studied this question.
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