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Hyperphosphatemia and Tumoral Calcinosis
- JOHN F. WILBER, M.D.; and
- EDUARDO SLATOPOLSKY, M.D.
- Requests for reprints should be addressed to John F. Wilber, M.D., Metabolic Division, Barnes Hospital, St. Louis, Mo. 63110.
SUMMARY
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.
Article and Author Information
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From the Department of Medicine, Washington University School of Medicine, St. Louis, Mo.
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This study was supported in part by Clinical Research Center grant FR-36, U. S. Public Health Service, Washington, D. C.
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Dr. Wilber was supported in this study by training grant AMO 5027, U. S. Public Health Service.
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- Received November 17, 1967.
- Accepted January 24, 1968.
