Elsevier

Seminars in Nephrology

Volume 28, Issue 2, March 2008, Pages 133-142
Seminars in Nephrology

Bone Disease and Idiopathic Hypercalciuria

https://doi.org/10.1016/j.semnephrol.2008.01.006Get rights and content

Summary

Observational and epidemiologic studies alike have shown that idiopathic hypercalciuric (IH) stone-forming patients typically show bone mineral density scores that are significantly lower than those observed for age- and sex-matched normal subjects or those for nonhypercalciuric stone-forming patients. Most of these studies have relied on changes in bone mineral density and have not explored the mechanism(s) involved. There have been a small number of studies that have relied on dynamic bone histomorphometry to ascertain the nature of the bone defect in IH patients. When performed, these studies clearly have shown increased bone resorption and high bone turnover in patients with fasting hypercalciuria whereas suppressed bone formation indices are the most consistent finding in patients with the absorptive variant of IH. The causes of this apparent difference in bone remodeling between the 2 variants of IH still is uncertain. Available evidence suggests that potential mechanisms may be dependent in large part to genetic, metabolic, and nutritional causes of hypercalciuria and bone loss in patients with IH.

Section snippets

Clinical Studies

Several of the earliest studies that assessed BMD in patients with idiopathic hypercalciuria (IH) suggested that bone mass or bone mineral content (BMC) was lower than that observed for age- and sex-matched normal subjects. However, most of these studies did not clearly define the underlying mechanism for the hypercalciuria or consistently present urinary calcium data. For example, Alhava et al1 used single-photon absorptiometry (SPA) to quantitate the BMC of the radius in an unselected

What is the Nature of the Defect in Bone Remodeling in Idiopathic Hypercalciuric Patients?

There have been relatively few studies directed at examining bone remodeling dynamics in IH patients. This is probably the result of the need for controlled diets before evaluation, the invasive nature of some procedures such as bone biopsy, and lack of willing patients because of relatively mild asymptomatic bone disease. Two studies have used only biochemical markers of bone turnover. In the study by Jaeger et al,9 urinary hydroxyproline as well as the collagen cross-links, pyridinoline and

What Mechanisms are Responsible for Bone Loss in IH?

From the foregoing discussion, it is apparent that 2 general types of bone remodeling defects are present in patients with IH and are dependent on the nature of the hypercalciuria. For those with a clear picture of renal hypercalciuria resulting from either renal calcium leak or from increased filter load of calcium, the remodeling defect is consistent with one of increased bone turnover, whereas in those with the absorptive form of hypercalciuria the defect appears to be more consistent with

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    Supported in part by National Institutes of Health grant P01-DK20543.

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