On the pathogenesis of so-called idiopathic hypercalciuria

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      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 D3 (25(OH)D3). 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)D3 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.
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        • Albright F
        • Henneman P
        • Benedict PH
        • et al.
        Idiopathic hypercalciuria.
        in: 4th ed. Proc R Soc Med. 46. 1953: 1077
        • Adams P
        • Chalmers TM
        • Hill LF
        • et al.
        Idiopathic hypercalciuria and hyperparathyroidism.
        Br Med J. 1970; 4: 582
        • Anderson J
        • Lee HA
        • Tominson RWS
        Some metabolic aspects of idiopathic hypercalciuria.
        Nephron. 1967; 4: 129
        • Bernstein DS
        • Newton R
        The effect of oral sodium phosphate on the formation of renal calculi and on idiopathic hypercalciuria.
        Lancet. 1966; 2: 1105
        • Brickman AS
        • Massry SG
        • Coburn JW
        Changes in serum and urinary calcium during treatment with hydrochlorothiazide: Studies on mechanisms.
        J Clin Invest. 1972; 51: 945
        • Davies DR
        • Dent CE
        • Watson L
        Idiopathic hypercalciuria and hyperparathyroidism.
        Br Med J. 1971; 1: 108
        • Edwards NA
        • Russell RGC
        • Hodgkinson A
        The effect of oral phosphate in patients with recurrent renal calculi.
        Br J Urol. 1965; 37: 390
        • Henneman PH
        • Benedict PH
        • Forbes AP
        Idiopathic hypercalciuria.
        N Engl J Med. 1958; 259: 802
        • Hodgkinson A
        • Pyrrah LN
        The urinary excretion of calcium and phosphate in 344 patients with calcium stone of renal origin.
        Br J Surg. 1958; 46: 10
        • Nordin BEC
        Metabolic Bone and Stone.
        (chap 3)in: Disease. The Williams & Wilkins Co, Baltimore1973
        • Nordin BE
        • Peacock M
        • Wilkinson R
        Hypercalciuria and calcium stone disease.
        in: 4th ed. Clinics in Endocrinology and Metabolism. vol 1. W.B. Saunders Co, Philadelphia1972: 169
        • Pak CYC
        • East DA
        • Sanzenbacher LJ
        • et al.
        Gastrointestinal calcium absorption in nephrolithiasis.
        J Clin Endocrinol Metab. 1972; 35: 261
        • Pak CYC
        • Ohata M
        • Lawrence EC
        • et al.
        The hypercalciurices: cause, parathyroid function and diagnostic criteria.
        J Clin Invest. 1974; 54: 387
        • Parfitt AM
        • Higgins BA
        • Nassim JR
        • et al.
        Metabolic studies in patients with hypercalciuria.
        Clin Sci. 1964; 27: 463
        • Schrott HG
        • Jubiz W
        • Frailey J
        • et al.
        Calcium infusion and phosphate deprivation tests in patients with primary hyperparathyroidism and with normocalcemic and nephrolithiasis.
        Metabolism. 1972; 21: 205
        • Yendt ER
        • Gagne RJA
        • Cohanim M
        The effects of thiazides in idiopathic hypercalciuria.
        Am J Med Sci. 1966; 251: 107
        • Coe FL
        • Canterbury JM
        • Firpo JJ
        • et al.
        Evidence for secondary hyperparathyroidism in idiopathic hypercalciuria.
        J Clin Invest. 1973; 52: 134
        • Keynes M
        Normocalcemic primary hyperparathyroidism.
        Lancet. 1971; 1: 1077
        • Willis MR
        • Pak CYC
        • Hammond WG
        • et al.
        Normocalcemic primary hyperparathyroidism.
        Am J Med. 1969; 47: 384
        • Yendt ER
        • Gagne RJA
        Detection of primary hyperparathyroidism with special reference to its occurrence in hypercalciuria females with “normal” or borderline serum calcium.
        Can Med Assoc J. 1968; 98: 331
        • Bijvoet OLM
        Relation of plasma phosphate concentration to renal tubular reabsorption of phosphate.
        Clin Sci. 1969; 37: 23
        • Bordier Ph
        • Séze S de
        • Miravet L
        • et al.
        Physiopathologie de l'ostéoporose de l'adulte jeune.
        Sem Hôp Paris. 1974; 50: 197
        • Arnaud CD
        • Goldsmith RS
        • Bordier Ph
        • et al.
        Influence of immunoheterogeneity of circulating parathyroid hormone on results of radioimmunoassays of serum in man.
        Am J Med. 1974; 56: 785
        • Bordier Ph
        • Tun-chot S
        Quantitative histology of metabolic bone diseases.
        J Clin Endocrinol Metab. 1972; 1: 197
        • Rasmussen H
        • Bordier Ph
        The Physiological and Cellular Basis of Metabolic Bone Disease.
        The Williams & Wilkins Co, Baltimore1974
        • Agus ZS
        • Gardner LB
        • Beck LH
        • et al.
        Effect of PTH on renal tubular reabsorption of calcium, sodium and phosphorus.
        Am J Physiol. 1973; 224: 1143
        • Baylink D
        • Wergedal J
        • Stauffer M
        Formation: mineralization and resorption of bone in hypophosphatemic rats.
        J Clin Invest. 1971; 50: 2519
        • Benswanger U
        • Feist E
        • Rich C
        Bone resorption without parathyroid hormone: Influence of a low phosphorus diet.
        Z Gesamte Exp Med. 1971; 156: 61
        • Coburn JW
        • Massry SG
        Changes in serum and urinary calcium during phosphate depletion Studies on mechanisms.
        J Clin Invest. 1970; 49: 1073
        • DeLuca HF
        Vitamin D: The vitamin and the hormone.
        in: 4th ed. Fed Proc. 33. 1974: 2211
        • Haussler MR
        • Baylink DJ
        • Hughes MR
        • et al.
        The assay of 1α,25-dihydroxyvitamin D3. Physiologic and pathologic modulation of circulating hormone levels.
        Clin Endocrinol. 1976; 5: 151s
        • Hughes MR
        • Brumbaugh PF
        • Haussler MF
        • et al.
        Regulation of serum 1,25-dihydroxyvitamin D3 by calcium and phosphate in the rat.
        Science. 1975; 190: 578
        • Lotz M
        • Zesman E
        • Bartter FC
        Evidence for a phosphorusdepletion syndrome in man.
        N Engl J Med. 1968; 278: 409
        • Tanaka Y
        • DeLuca HF
        The control of 25-hydroxyvitamin D metabolism by inorganic phosphorus.
        Arch Biochem Biophys. 1973; 154: 566
        • Widrow SH
        • Levensky NG
        The effects of PTH on renal tubular calcium reabsorption in the dog.
        J Clin Invest. 1962; 41: 2151
        • Albright F
        • Ellsworth R
        Studies on the physiology of the parathyroid glands. I. Calcium and phosphorus studies on a case of idiopathic hypoparathyroidism.
        J Clin Invest. 1929; 7: 183
        • Albright F
        • EC Jr, Reifenstein
        The Parathyroid Glands and Metabolic Bone Disease.
        The Williams & Wilkins Co, Baltimore1948
        • Thompson ER
        • Baylink DJ
        • Wergedal E
        Increases in number and size of osteoclasts in response to calcium and phosphorus deficiency in the rat.
        Endocrinology. 1975; 97: 283
        • Dent CE
        Some problems of hyperparathyroidism.
        Br Med J. 1962; 2: 1419
        • Bordier Ph
        • Miravet L
        • Hioco D
        Young adult osteoporosis.
        in: 4th ed. Clinics In Endocrinology and Metabolism. vol 2. W. B. Saunders Co, Philadelphia1973: 277
        • Hioco D
        • Ryckewaert A
        • Bordier Ph
        • et al.
        Le metabolisme calcique et phosphase au cours des osteomalacies vitamina-resistentes du syndrome de Fariconi et des syndromes apparentes.
        in: Hioco DJ L'Osteomalacia. Maison & Cie, Paris1967: 299
        • Scriver CR
        Rickets and the pathogenesis of impaired tubular transport of phosphate and other solutes.
        Am J Med. 1974; 57: 43