PAUL D. MITNICK, M.D.; STANLEY GOLDFARB, M.D.; EDUARDO SLATOPOLSKY, M.D.; JACOB LEMANN, M.D.; RICHARD W. GRAY, M.D.; ZALMAN S. AGUS, M.D.
Grant support: in part by NIH Research Grants from the National Heart, Lung, and Blood Institute (HL00340) and the National Institute of Arthritis, Metabolism, and Digestive Diseases (AM 19478 and AM 15089); NIH Clinical Research Center Grants 5-M01-RR0040 and RR00058; and NIH Training Grant T-32-AM07006. Dr. Agus is the recipient of Research Career Development Award K04-AM00258, and Dr. Goldfarb is the recipient of NIH Clinical Investigator Award 1-K08-AM00414.
▸Requests for reprints should be addressed to Stanley Goldfarb, M.D.; 860 Gates Pavilion, Hospital of the University of Pennsylvania, 3400 Spruce Street; Philadelphia, PA 19104.
MITNICK PD, GOLDFARB S, SLATOPOLSKY E, LEMANN J, GRAY RW, AGUS ZS. Calcium and Phosphate Metabolism in Tumoral Calcinosis. Ann Intern Med. 1980;92:482-487. doi: 10.7326/0003-4819-92-4-482
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Published: Ann Intern Med. 1980;92(4):482-487.
We have recently seen a patient with tumoral calcinosis, a syndrome comprising hyperphosphatemia, normocalcemia, normal glomerular filtration rate (GFR), and extensive periarticular calcific masses. Parathyroid hormone (PTH) deficiency or target organ resistance was ruled out by demonstration of normal serum PTH and urinary 3′5′ cyclic AMP excretion and normal response to exogenous PTH and to endogenous stimulation by ethylenediaminetetraacetate. An intrinsic proximal tubular defect allowing enhanced renal PO4 reabsorption was probably present because there was no phosphaturic response to acetazolamine and renal PO4 threshold remained abnormally elevated even after PTH infusion. We then studied the mechanism by which serum calcium level is maintained in the normal range despite hyperphosphatemia and absence of secondary hyperparathyroidism. Normal 1,25-(OH)2 vitamin D was found, suggesting normal gastrointestinal calcium absorption. This, combined with markedly reduced urinary calcium excretion, perhaps a direct effect of hyperphosphatemia, may maintain calcium balance and prevent secondary hyperparathyroidism. A rise in urinary cyclic AMP excretion after furosemide-induced calciuria supports this hypothesis.
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Endocrine and Metabolism, Nephrology, Parathyroid Disorders.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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