Bone disease in idiopathic hypercalciuria

Heilberg, Ita Pfeferman; Weisinger, José R.

doi:10.1097/01.mnh.0000232880.58340.0c

Cited by 70 publications

(57 citation statements)

References 83 publications

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“…As expected and in agreement with previous reports, the three treatments induced a significant reduction in 24-hour urinary calcium excretion [Heilberg and Weisinger, 2006;Ceylan et al 2005;Weisinger et al 1997Weisinger et al , 1998]. Interestingly, the authors found that women in the combination therapy group (alendronate weekly plus indapamide daily) experienced the highest reduction in urinary calcium excretion, resulting in an additional effect of the two drugs.…”

supporting

confidence: 80%

“…Studies on humans, however, suggest that whereas some patients have a single specific defect resulting in hypercalciuria, most subjects do not have a specific site of mineral ion transport dysregulation. Therefore, IHC seems to be a systemic disorder of mineral ion homeostasis resulting from the interaction of different mechanisms [Heilberg and Weisinger, 2006].…”

Section: Methodsmentioning

confidence: 99%

“…In recent years, however, a number of studies have suggested that bone cells involved in bone formation and resorption could play a central role in the chain of events leading to hypercalciuria [Heilberg and Weisinger, 2006;Weisinger et al 1998;Pacifici, 1997;Pacifici et al 1990]. Several investigators, in the last 10 years, have reported increased bone turnover and reduced bone mineral density (BMD) in subjects with IHC [Heller et al 2007;Giannini et al 2003;Vezzoli et al 2003;Borghi et al 1991].…”

Section: Introductionmentioning

confidence: 99%

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Bisphosphonates in the management of idiopathic hypercalciuria associated with osteoporosis: a new trick from an old drug

Bianchi¹,

Giusti

Pioli³

et al. 2010

Therapeutic Advances in Musculoskeletal

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Idiopathic hypercalciuria (IHC) is defined as a 24-hour urinary calcium excretion that exceeds 4 mg/kg/day, regardless of gender and in absence of systemic diseases or pharmacological treatments that may cause normocalcemic hypercalciuria (eg sarcoidosis, normocalcemic primary hyperparathyroidism, vitamin D intoxication, hyperthyroidism). Patients with IHC and nephrolithiasis often present increased bone turnover, decreased bone mineral density (BMD) and increased susceptibility to fragility fractures. Although the pathogenesis of IHC seems complex and multifactorial, recent evidences suggest that cells involved in bone resorption may play a critical role in the chain of events leading to the excessive urinary calcium excretion. Therefore, it has been proposed that bisphosphonates, potent inhibitors of bone resorption, may have beneficial effects in hypercalciuric patients with low BMD. This manuscript reports recent findings regarding the role of bone tissue in the pathogenesis of IHC, and supports the use of bisphosphonates in such conditions. It also reviews the literature on the effects of bisphosphonates in subjects with osteoporosis-associated IHC.

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supporting

confidence: 80%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Bisphosphonates in the management of idiopathic hypercalciuria associated with osteoporosis: a new trick from an old drug

Bianchi¹,

Giusti

Pioli³

et al. 2010

Therapeutic Advances in Musculoskeletal

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“…Although hypercalciuria and bone-mass loss are classic features of primary hyperparathyroidism, there is also evidence that the prevalence of osteopenia is statistically increased in lithiasic patients with idiopathic hypercalciuria in comparison with normocalciuric patients (12,13).…”

Section: Discussionmentioning

confidence: 99%

Determinants of Osteopenia in Male Renal-Stone–Disease Patients with Idiopathic Hypercalciuria

Letavernier¹,

Traxer²,

Daudon³

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Bone demineralization is frequent in renal-stone formers with hypercalciuria. Although this pathologic link has been recognized for decades, the underlying mechanisms and risk factors associated with osteopenia/osteoporosis in this population remain partially understood.Design, setting, participants, & measurements This study retrospectively analyzed determinants of low bone mineral density (BMD) in 65 idiopathic hypercalciuric male renal-stone formers. Clinical and biologic evaluation included BMD measurement, bone-remodeling markers, analysis of calcium metabolism with oral calcium load test, and dietary inquiry.Results Patients with osteopenia (n ϭ 23, 35% of the population) presented significantly higher fasting calciuria as compared with normal bone density patients (n ϭ 42) (calcium/creatinine ratio was 0.32 versus 0.24 mmol/mmol; P ϭ 0.006). Analysis of the whole population revealed a negative association between fasting hypercalciuria and BMD (P ϭ 0.003), independent of confounding variables including body-mass index and tobacco consumption. The fasting calcium/creatinine ratio above 0.25 mmol/mmol was associated with a 3.8-fold increase in the risk of low BMD. ConclusionIn our study, fasting hypercalciuria after a 2-day calcium-restricted diet appears as the only biologic factor associated with low BMD, suggesting a bone-calcium efflux. Our results support the view of a parathyroid-independent pathologic process that remains to be identified. Hypercalciuric patients with low BMD do not excrete more calcium in 24-hour urine samples than patients without low BMD.

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“…Decreased bone mineral density (BMD) is commonly encountered in IH patients (23), and an increased prevalence of bone fractures has been reported for nephrolithiasis patients (24,25). GHS rats also exhibited reduced BMD and more brittle and fracture-prone bones (26) because of lower trabecular volume and mineralized volume and thickness.…”

Section: Discussionmentioning

confidence: 99%

Expression of Fibroblast Growth Factor 23, Vitamin D Receptor, and Sclerostin in Bone Tissue from Hypercalciuric Stone Formers

Menon

Moysés

Gomes

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives Increased bone resorption, low bone formation, and abnormal mineralization have been described in stone formers with idiopathic hypercalciuria. It has been previously shown that the receptor activator of NF-kB ligand mediates bone resorption in idiopathic hypercalciuria (IH). The present study aimed to determine the expression of fibroblast growth factor 23 (FGF-23), vitamin D receptor (VDR), and sclerostin in bone tissue from IH stone formers.Design, setting, participants, & measurements Immunohistochemical analysis was performed in undecalcified bone samples previously obtained for histomorphometry from 30 transiliac bone biopsies of idiopathic hypercalciuria stone-forming patients between 1992 and 2002 and 33 healthy individuals (controls). Serum parameters were obtained from their medical records.Results Histomorphometry disclosed 21 IH patients with high and 9 IH patients with normal bone resorption. Importantly, eroded surfaces (ES/BS) from IH patients but not controls were significantly correlated with VDR immunostaining in osteoblasts (r=0.51; P=0.004), sclerostin immunostaining in osteocytes (r=0.41; P=0.02), and serum 1,25-dihydroxyvitamin D (r=0.55; P,0.01). Of note, both VDR and sclerostin immunostaining were significantly correlated with serum 1,25-dihydroxyvitamin D in IH patients (r=0.52; P=0.01 and r=0.53; P=0.02, respectively), although VDR and sclerostin expression did not differ between IH and controls. IH patients with high bone resorption exhibited a significantly stronger sclerostin immunostaining than IH patients with normal bone resorption. FGF-23 expression in osteocytes from IH patients did not differ from controls and was not correlated with any histomorphometric parameter.Conclusions These findings suggest the contribution of VDR and sclerostin, as well as 1,25-dihydroxyvitamin D, to increase bone resorption in idiopathic hypercalciuria but do not implicate FGF-23 in the bone alterations seen in these patients.

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Bone disease in idiopathic hypercalciuria

Abstract: Whether 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.

Cited by 70 publications

References 83 publications

Bisphosphonates in the management of idiopathic hypercalciuria associated with osteoporosis: a new trick from an old drug

Bisphosphonates in the management of idiopathic hypercalciuria associated with osteoporosis: a new trick from an old drug

Determinants of Osteopenia in Male Renal-Stone–Disease Patients with Idiopathic Hypercalciuria

Expression of Fibroblast Growth Factor 23, Vitamin D Receptor, and Sclerostin in Bone Tissue from Hypercalciuric Stone Formers

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