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Analysis of Minerals Produced by hFOB 1.19 and Saos-2 Cells Using Transmission Electron Microscopy with Energy Dispersive X-ray Microanalysis
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The relation between bone and stone formation.

Nancy S Krieger1, David A Bushinsky

  • 1Division of Nephrology, Department of Medicine, University of Rochester School of Medicine, 601 Elmwood Ave., Box 675, Rochester, NY, 14642, USA, nancy_krieger@urmc.rochester.edu.

Calcified Tissue International
|December 19, 2012
PubMed
Summary
This summary is machine-generated.

Hypercalciuria, a common cause of kidney stones, leads to bone loss and fractures. Genetic hypercalciuric stone-forming rats show intrinsic bone defects, offering insights into human bone health.

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Comprehensive Characterization of Tissue Mineralization in an Ex Vivo Model
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Published on: September 27, 2024

Area of Science:

  • Nephrology
  • Endocrinology
  • Bone Biology

Background:

  • Hypercalciuria is linked to kidney stones and decreased bone mineral density (BMD).
  • Patients with hypercalciuria experience net calcium loss, likely from skeletal demineralization.
  • The exact cause of reduced BMD in hypercalciuric individuals remains unclear.

Purpose of the Study:

  • To investigate the impact of hypercalciuria on bone health using a genetic hypercalciuric stone-forming (GHS) rat model.
  • To understand the systemic dysregulation of calcium homeostasis in GHS rats.
  • To elucidate the pathogenesis of bone disease in hypercalciuric stone formers.

Main Methods:

  • Utilized genetically engineered hypercalciuric stone-forming (GHS) rats.
  • Compared GHS rats with control rats under identical dietary conditions.
  • Assessed urinary calcium excretion, BMD, bone turnover markers, and fracture incidence.

Main Results:

  • GHS rats exhibit significantly higher urinary calcium excretion and form kidney stones.
  • GHS rats demonstrate reduced BMD and increased fracture susceptibility, even on a high-calcium diet.
  • Hypercalciuria in GHS rats is associated with increased intestinal calcium absorption, bone resorption, and decreased renal calcium reabsorption, linked to vitamin D receptor changes.

Conclusions:

  • Hypercalciuria is associated with an intrinsic bone disorder, not solely diet-related.
  • GHS rats serve as a valuable model for studying the bone complications of hypercalciuria and kidney stones.
  • Findings suggest a systemic dysregulation of calcium homeostasis contributing to both kidney stone formation and bone fragility.