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Evidence for Secondary Hyperparathyroidism in Idiopathic Hypercalciuria
Fredric L. Coe, Janet M. Canterbury, John J. Firpo, Eric Reiss
Fredric L. Coe, Janet M. Canterbury, John J. Firpo, Eric Reiss
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Research Article

Evidence for Secondary Hyperparathyroidism in Idiopathic Hypercalciuria

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Abstract

Circulating levels of immunoreactive parathyroid hormone (PTH) were measured in 40 patients with idiopathic hypercalciuria (IH) before and during reversal of hypercalciuria with thiazide, and in four normal subjects before and during induction of hypercalciuria with furosemide. 26 patients with IH had elevated serum PTH levels. The remaining patients had normal levels. Although the correlation was not complete, high PTH levels were generally found in patients who had more severe average urinary calcium losses. When initially elevated. PTH levels fell to normal or nearly normal values during periods of thiazide administration lasting up to 22 months. When initially normal, PTH levels were not altered by thiazide. Reversal of hyperparathyroidism by thiazide could not be ascribed to the induction of hypercalcemia, since serum calcium concentration failed to rise in a majority of patients. Renal hypercalciuria produced by furosemide administration elevated serum PTH to levels equivalent to those observed in patients with IH.

Authors

Fredric L. Coe, Janet M. Canterbury, John J. Firpo, Eric Reiss

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