Evidence for Secondary Hyperparathyroidism

This work was presented in part at the Annual Meeting of the Association of American Physicians, Atlantic City, N. J., May 1971. The present address of Dr. Canterbury and Dr. Reiss is Department of Medicine, University of Miami School of Medicine, Miami, Fla. Received for publication 1 August 1972 and in revised formn 19 September 1972. of hypercalciuria. Primary renal loss of calcium could explain the variable occurrence of reversible hyperparathyroidism in IH, since renal hypercalciuria from furosemide elevates serum PTH in normal subjects. Consequently, a reasonable working hypothesis is that IH is often due to a primary renal defect of calcium handling that leads, by unknown pathways, to secondary hyperparathyroidism. INTRODUCTION Idiopathic hypercalciuria (JH) ' is a syndrome characterized by normocalcemia and hypercalciuria that is unexplained by an established cause such as sarcoidosis, renal tubular acidosis, excessive intake of vitamin D or calcium, malignancy, immobilization, or rapidly progressive osteoporosis (1). Kidney stones are very common, and there is a tendency towards hypophosphatemia. The syndrome occurs in approximately 3% of normal persons and in 30-40% of patients with nephrolithiasis (2-4). The mechanism of hypercalciuria has not been established. At present, three theories deserve special consideration. (a) Gastrointestinal calcium absorption is generally elevated in IH (5, 6), and in certain patients hyperabsorption appears to be the predominent mechanism of hypercalciuria (7). (b) Idiopathic hypercalciuria resembles primary hyperparathyroidism except that, by definition, hypercalcemia is absent. Because of this resemblance and the known variability of serum calcium levels in hyperparathyroidism, it has long been suspected that many patients who appear to have IH have instead a normocalcemic variety of primary hyperparathyroidism (8, 9). (c) Excessive renal calcium loss 1Abbreviations used in this paper: IH, idiopathic hypercalciuria; PTH, parathyroid hormone. 134 The Journal of Clinical Investigation Volume 52 January 1973 Downloaded from http://www.jci.org on April 18, 2017. https://doi.org/10.1172/JCI107156