Phosphorus Excretion in Tumoral Calcinosis: Response to Parathyroid Hormone and Acetazolamide*

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Abstract
The cause of hyperphosphatemia in patients with tumoral calcinosis has never been explained. We studied two related patients who had tumoral calcinosis and hyperphospha-temia and two normal controls to determine their renal tubular response to parathyroid hormone (PTH) and acetazolamide (ACZ). During baseline periods, the patients had abnormally low fractional excretion of phosphorus (FEp) despite their hy-perphosphatemia. Values for patients were 0.114 and 0.128; for controls, values were 0.193 and 0.165. PTH caused an increase in FEp and urinary cAMP in both patients and controls. ACZ also increased FEp in both groups, and the effects of PTH and ACZ were additive, suggesting that patients with tumoral calcinosis have normal sensitivities to PTH and normal responses to ACZ. Levels of vitamin D metabolites in thepatients were normal. We conclude that patients with tumoral calcinosis have a reduced ability to excrete phosphorus. This defect does nou seem to be due to impaired PTH secretion, an abnormal phosphaturic response to this hormone, or a disturbance of vitamin Dmetabolism.(J Clin Endocrinol Metab50: 648, 1980)