On the pathogenesis of so-called idiopathic hypercalciuria

Abstract

Forty-seven patients were identified as having persistent hypercalciuria during a period of low calcium intake (< 400 mg/24 hours). They were divided into two types on the basis of their serum immunoreactive parathyroid hormone (PTH) values: type 2 patients had increased, and type 3 patients had normal or low values. It was concluded that in type 3 patients hypercalciuria developed as a result of a primary renal phosphate leak. Type 2 patients were divided into two subtypes on the basis of their response to the administration of methylchlorothiazide and 25-hydroxyvitamin D 3 (25(OH)D 3). Type 2a patients responded to either treatment with little change in serum calcium, an increase in serum phosphate and a decrease in serum immunoreactive PTH concentration. They were classified as having suppressible hyperparathyroidism secondary to a primary renal calcium leak. Type 2b patients responded to both thiazide and 25(OH)D 3 therapy with an increase in serum calcium concentration and no decrease in immunoreactive PTH. They were classified as having nonsuppressible normocalcemic hyperparathyroidism and underwent successful parathyroid surgery. However, they had persistent postoperative hypercalciuria, and several had suppressible hyperparathyroidism several years after their successful parathyroid surgery. On the basis of these facts, type 2b patients were also considered to have a long-standing primary renal calcium leak that led initially to secondary hyperparathyroidism but eventually to tertiary or nonsuppressible hyperparathyroidism.