Bone disease in idiopathic hypercalciuria

Bone disease in idiopathic hypercalciuria

Author Heilberg, Ita P. Google Scholar
Weisinger, Jose R. Google Scholar
Institution Cent Univ Venezuela
Universidade Federal de São Paulo (UNIFESP)
Abstract Purpose of reviewDecreased bone mineral density and increased prevalence of bone fractures have been found in patients with idiopathic hypercalciuria. the purpose of this review is to summarize the recent published evidence that supports a potential role of the bone, and its link to the kidney and intestine, in the pathogenesis of idiopathic hypercalciuria. the effects of hypercalciuria on bone and the implications for treatment are also reviewed.Recent findingsEvidence suggests that the incidence of a first fracture in kidney stone patients is fourfold higher than the control population. Support for the role of bone in the pathophysiology of hypercalciuria has been corroborated. New studies have detailed the effects of several cytokines increased number and sensitivity of vitamin D receptors, and increased acid production - upon the bone acting cells. Similarly, recent clinical and experimental studies have suggested that genetic factors confer a predisposition to the formation of renal calcium stones and bone demineralization.SummaryWhether hypercalciuria is the result of a primary bone disorder, a consequence of a persisting negative calcium balance or a combination of both still remains to be determined. Nevertheless, bone status must be evaluated and followed up in patients with idiopathic hypercalciuria.
Keywords bisphosphonates
bone
bone fractures
bone mineral density
hypercalciuria
idiopathic hypercalciuria
kidney stones
lithiasis
osteoporosis
thiazides
urine calcium
Language English
Date 2006-07-01
Published in Current Opinion in Nephrology and Hypertension. Philadelphia: Lippincott Williams & Wilkins, v. 15, n. 4, p. 394-402, 2006.
ISSN 1062-4821 (Sherpa/Romeo, impact factor)
Publisher Lippincott Williams & Wilkins
Extent 394-402
Origin http://dx.doi.org/10.1097/01.mnh.0000232880.58340.0c
Access rights Closed access
Type Review
Web of Science ID WOS:000239103000007
URI http://repositorio.unifesp.br/handle/11600/29034

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