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Urolithiasis pp 841-845 | Cite as

Disturbed Terminal Mineralization of Bone in Idiopathic Hypercalciuria

  • H. H. Malluche
  • W. Tschope
  • W. Meyer
  • E. Ritz
  • S. G. Massry

Abstract

Hypercalciuric renal stone-formers are commonly divided into 3 different groups: Resorptive hypercalciuria, hyperabsorptive and renal hypercalciuria1–4. Patients with hyperabsorptive hypercalciuria have normal or low serum parathyroid hormone activities and normal to low urinary excretion of cAMP. In renal hypercalciuria elevated serum PTH levels and increased renal excretion of cAMP has been reported4–6. Bordier et al.6 published elevated immunoreactive parathyroid hormone levels and increased numbers of osteoclasts in bone biopsies obtained from patients with renal hypercalciuria. No information is available on bone histology in patients with hypercalciuria of the hyperabsorptive type. The present study evaluates quantitatively bone sections in 15 patients with hyperabsorptive hypercalciuria and recurrent stone-formation.

Keywords

Bone Biopsy Serum Phosphate Renal Tubular Acidosis Idiopathic Hypercalciuria Bone Histology 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    P. Adams, T. M. Chalmers, L. F. Hill, and B. Truscott, Br. Med. J. 4:582 (1970).PubMedCrossRefGoogle Scholar
  2. 2.
    M. Keynes, Lancet 1:1077 (1971).PubMedCrossRefGoogle Scholar
  3. 3.
    A. Hodgkinson and L. N. Pyrah, Br. J. Surg. 46:10 (1958).PubMedCrossRefGoogle Scholar
  4. 4.
    C. Y. C. Pak, M. Ghata, E. C. Lawrence, and W. Snyder, J. Clin. Invest. 54:387 (1974).PubMedCrossRefGoogle Scholar
  5. 5.
    B. E. C. Nordin, M. Peacock, and R. Wilkinson, in: “Clinics in Endocrinology and Metabolism,” J. Maclntyre, ed., Saunders, Philadelphia, (1972).Google Scholar
  6. 6.
    P. Bordier, A. Ryckewan, J. Gjuens, and H. Rasmussen, Am. J. Med. 63:398 (1977).PubMedCrossRefGoogle Scholar
  7. 7.
    H. Rasmussen and P. Bordier, in: “The Physiologican and Cellular Basis of Metabolic Bone Disease,” Williams and Wilkins, Baltimore, (1974).Google Scholar
  8. 8.
    F. Albright, P. Henneman, P. H. Benedict, and A. P. Forbes, Proc. R. Soc. Med. 46:1077 (1953).PubMedGoogle Scholar
  9. 9.
    F. H. Shen, D. J. Baylink, R. L. Nielson, D. J. Sherrard, J. L. Ivey, and M. R. Haussler, J. Lab. Clin. Med. 90:955 (1977).PubMedGoogle Scholar
  10. 10.
    H. H. Malluche, H. Henry, W. Meyer-Sabellek, D. Sherman, S. G. Massry, and A. W. Norman, in: “Vitamin D-Basic Research and its Clinical Application,” A. W. Norman, Schaefer, D. V. Herrath, H. G. Grigoleit, J. W. Coburn, H. F. DeLuca, E. B. Mawer, and T. Suda, eds., Walter de Gruyter, Berlin/New York, (1979).Google Scholar
  11. 11.
    A. Ornoy, D. Goodwin, D. Noff, and S. Edelstein, Nature 276:517, 1978.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1981

Authors and Affiliations

  • H. H. Malluche
    • 1
  • W. Tschope
    • 1
  • W. Meyer
    • 1
  • E. Ritz
    • 1
  • S. G. Massry
    • 1
  1. 1.Division of Nephrology and Department of MedicineUniversity of Southern California School of MedicineLos AngelesUSA

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