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Bone Loss Process Not Clear in Hypercalciuria, Kidney Stones

Last Updated: July 02, 2009.

Bone loss in patients with hypercalciuria and nephrolithiasis results from a poorly understood breakdown of the body's mineral metabolism involving the kidneys, the intestines and the bones themselves, according to a literature review reported in the July issue of Urology.

THURSDAY, July 2 (HealthDay News) -- Bone loss in patients with hypercalciuria and nephrolithiasis results from a poorly understood breakdown of the body's mineral metabolism involving the kidneys, the intestines and the bones themselves, according to a literature review reported in the July issue of Urology.

Andrea Tasca, M.D., of San Bortolo Hospital in Vicenza, Italy, and colleagues conducted a review of the literature published between 1985 and 2005 on bone loss in patients with primary hypercalciuria and nephrolithiasis. The disease complex results in bone fragility and vulnerability to fractures, particularly in trabecular bone, such as the vertebral bodies.

The reviewers discussed the disease mechanism and diagnosis of the metabolic disorder, but concluded that after 20 years of research, it is still unclear what happens in the intestines, kidneys and bones that results in the calcium and phosphate metabolism dysfunction.

"The pathogenesis of bone damage in patients with hypercalciuria stone formation still remains only partially understood. The organs and tissues normally involved in the control of calcium and phosphate metabolism appear to take an active part in the pathogenesis of the skeletal alterations in patients with primary hypercalciuria. The skeletal tissue, per se, the kidney, and the intestine are responsible for the appearance, persistence, and clinical course of bone loss in patients with hypercalciuric nephrolithiasis and operate together as a multitissue metabolic disorder," the authors write.

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