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Related Experiment Video

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Isolation, Purification, and Differentiation of Osteoclast Precursors from Rat Bone Marrow

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Reduced bone formation and relatively increased bone resorption in absorptive hypercalciuria.

H J Heller¹, J E Zerwekh, F A Gottschalk

¹Department of Internal Medicine, UT Southwestern Medical Center at Dallas, Center for Mineral Metabolism and Clinical Research, Dallas, Texas, USA.

Kidney International

|February 22, 2007

Summary

Absorptive hypercalciuria type 1 (AH-1) involves high calcium absorption and excretion. Bone resorption may contribute to hypercalciuria in AH-1 patients, though intestinal absorption is the primary driver.

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Area of Science:

Nephrology
Endocrinology
Bone Metabolism

Background:

Absorptive hypercalciuria (AH) is a common condition leading to kidney stones, characterized by increased intestinal calcium absorption and hypercalciuria.
AH may be linked to bone loss, particularly in AH type 1 (AH-1) where hypercalciuria persists despite dietary calcium restriction.

Purpose of the Study:

To investigate the potential contribution of bone metabolism to hypercalciuria in patients with AH type 1 (AH-1).
To evaluate calcium homeostasis and the effect of inhibiting bone resorption in AH-1 patients.

Main Methods:

Histomorphometric analysis of iliac crest biopsies in nine AH-1 stone formers and nine controls.
Assessment of calcium homeostasis on a constant metabolic diet before and after short-term alendronate treatment to block bone resorption.

Main Results:

Stone formers with AH-1 exhibited lower bone formation indices and relatively higher bone resorption compared to controls.
Alendronate treatment corrected fasting urinary calcium and improved calcium balance, though increased intestinal calcium absorption and hypercalciuria persisted.

Conclusions:

The primary cause of hypercalciuria in AH-1 is increased intestinal calcium absorption.
Bone resorption in excess of bone formation appears to contribute to hypercalciuria in AH-1 patients.