New Insights Into the Pathogenesis of Idiopathic Hypercalciuria

Worcester, Elaine M.; Coe, Fredric L.

doi:10.1016/j.semnephrol.2008.01.005

Cited by 141 publications

(128 citation statements)

References 56 publications

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“…Osmotic actions of glycosuria and hyperglycaemia may work together in causing hypomagnesaemia and hyperglycaemia per se alone, which are known to depress the net tubular reabsorption of magnesium in normal humans [22,24,25,27].…”

Section: Discussionmentioning

confidence: 99%

Trace Elements in Diabetes Mellitus

Praveeena¹,

Pasula²,

K³

2013

JCDR

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Introduction: Diabetes Mellitus is the commonest major metabolic disease and most prevalent diseases worldwide. Its related morbidity is due to its micro and macro angiopathic complications. Aim:The aim of this study was to measure and compare the serum levels of zinc and magnesium in normal individuals and in diabetic patients.Method: Analysis of minerals was done in plasma by using a Varian Spectra AA 220 model atomic absorption spectrophotometer. Result:Our observations showed a definite lowering of serum magnesium (p<0.001) and serum zinc levels (p<0.001) were significant in diabetic group. Conclusion:The cause of diabetic hypomagnesaemia is multifactorial. An altered metabolism, a poor glycaemic control and osmotic diuresis may be contributory factors. Decreased serum zinc levels in diabetes may be caused by an increase in urinary loss. These decreased levels of trace elements cause disturbances in glucose transport across cell membrane lead to insufficient formation and secretion of insulin by pancreas which compromise in the antioxidant defense mechanisms.

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Section: Discussionmentioning

confidence: 99%

Trace Elements in Diabetes Mellitus

Praveeena¹,

Pasula²,

K³

2013

JCDR

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“…An absorptive hypercalciuria not accompanied by other disruptions in normal calcium metabolism would not be expected to lead to osteoporosis. Furthermore, many patients with hypercalciuria that partially remits on a low calcium diet continue to have negative calcium balance, suggesting that they are mobilizing bone calcium, which implies more than a disorder in intestinal absorption (16).…”

Section: Hypercalciuriamentioning

confidence: 99%

A Woman with Recurrent Calcium Phosphate Kidney Stones

Goldfarb

2012

Clinical Journal of the American Society of Nephrology

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SummaryKidney stones composed predominantly (50% or more) of calcium phosphate constitute up to 10% of all stones and 15%-20% of calcium stones, 80% of which are composed of calcium oxalate. Calcium phosphate is a minor component of up to 30% of calcium oxalate stones as well. The cause of calcium phosphate stones is often obscure but most often related to a high urine pH. Some patients with calcium phosphate stones may have incomplete renal tubular acidosis. Others have distal renal tubular acidosis characterized by hyperchloremic acidosis, hypocitraturia, and high urine pH. The use of carbonic anhydrase inhibitors such as acetazolamide, topiramate, and zonisamide leads to a similar picture. Treatment options to specifically prevent calcium phosphate stone recurrence have not been tested in clinical trials. Increases in urine volume and restriction of sodium intake to limit calcium excretion are important. Citrate supplementation is probably effective, although the concomitant increase in urine pH may increase calcium phosphate supersaturation and partially offset the inhibition of crystallization resulting from the increased urine citrate excretion and the alkali-associated reduction in urine calcium excretion. Thiazides lower urine calcium excretion and may help ensure the safety of citrate supplementation.

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“…Idiopathic hypercalciuria (IH) represents a generalized dysregulation of calcium homeostasis, which includes increased gut calcium absorption, decreased renal calcium reabsorption, and a tendency to lose calcium from the bone (1,2).…”

Section: Introductionmentioning

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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New Insights Into the Pathogenesis of Idiopathic Hypercalciuria

Cited by 141 publications

References 56 publications

Trace Elements in Diabetes Mellitus

Trace Elements in Diabetes Mellitus

A Woman with Recurrent Calcium Phosphate Kidney Stones

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

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