Hypercalciuria is a common and important finding in postmenopausal women with osteoporosis
Sandro GianniniM. NobileLuca Dalle CarbonareM. G. LodettiS. SellaGabriele VittadelloNadia MinicuciG Crepaldi
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Abstract:
The prevalence and the effects of hypercalciuria on bone in patients with primary osteoporosis are poorly defined. We therefore retrospectively analyzed the data of 241 otherwise healthy women. They were 45-88 years of age and had been referred for their first visit to our Unit for Metabolic Bone Diseases over a 2-year period because of primary osteoporosis (bone density T-score < -2.5).The main parameters of calcium and skeletal metabolism had been analyzed in all subjects. This population was then divided into two groups, according to the presence (HC+) or absence (HC-) of hypercalciuria.Elevated urinary calcium was present in 19% of the subjects. Due to the selection criteria, spinal and femoral bone loss was similar in the two groups. Urinary calcium, phosphate and fractional calcium excretion were higher in hypercalciuric patients. In a logistic regression model, the higher the Tm of phosphate, the lower the risk of hypercalciuria (odds ratio 0.33, confidence interval 0.18-0.62). On the contrary, hypercalciuria was the most important predictor of low bone mass in HC+ (accounting for more than 50% of the variance in spinal bone density).Hypercalciuria is a common feature in postmenopausal bone loss. Since increased urinary calcium excretion and low bone mass appear to be linked, hypercalciuria seems to be an important determinant of reduced bone density in this setting as well.Keywords:
Urinary calcium
Bone remodeling
To reduce urinary calcium excretion, 50 mg of hydrochlorothiazide per day was given to 35 patients with hypercalciuria. Urinary calcium decreased significantly after 4 weeks of drug administration, but urinary magnesium did not change. Magnesium calcium ratio increased significantly. Although serious side effects were not seen, serum potassium decreased and serum uric acid increased significantly. From these results thiazide seems to be a useful and safe medicine to reduce urinary calcium excretion. The dose and method of administration require further examination because the patients have to take the drug for a long time.
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Aim: Hypercalciuria is an important cause of urinary tract symptoms, and also frequently results in urolithiasis.Urinary calcium excretion varies for geographic areas.We aimed to assess percentiles of urinary calcium excretion and prevalence of hypercalciuria for school-aged children in Tokat (city located in inner northern region of Turkey).Material and Methods: One thousand three hundred seventy-five children aged 6 to 18 years were enrolled in the study.Urine samples were obtained randomly.The children's variables as sex, age, length, and weight were recorded.Urinary calcium and creatinine determined from the urine samples and urinary calcium/creatinine ratios (mg/mg) were calculated.Percentiles of urinary calcium/creatinine ratios were also assessed for each age of the children.Results: Six hundred eighty-three of the 1 375 children were girls and 692 were boys.The mean age of the children was 11.68±3.43years.Some 23.9% of the children were living in rural regions and 76.1% were were living in urban regions.The mean urinary calcium/creatinine ratio was 0.080±0.24and the 95th percentile value of the urinary calcium/creatinine ratio was 0.278.The hypercalciuria prevalence for school-aged children was 4.7% when the urinary calcium/creatinine ratio value for hypercalciuria was accepted as ≥0.21.The prevalence of hypercalciuria in rural and urban regions was 7.60% and 3.82%, respectively (p<0.05).Hypercalciuria was present in 7 of 141 patients who were obese (4.96%) and 58 of 1 234 patients who were not obese (4.70%) (p>0.05). Conclusion:The prevalence of hypercalciuria and urinary calcium excretion vary for different geographic areas, not only for countries.The percentiles of urinary calcium excretion should be assesed for every geographic region and the prevalance of hypercalciuria should be determined with these values.There is controversy as to whether obesity is a risk factor for hypercalciuria.
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Hypercalciuria in children is diagnosed when the urinary calcium excretion is greater than 4.0 mg/kg in 24 hours, the ratio of urinary concentration of calcium to creatinine (UCa/UCr) is greater than 0.20, and there is normal serum calcium. Hypercalciuria may be the result of increased intestinal absorption of calcium (absorptive hypercalciuria) or an impaired proximal tubular defect in calcium reabsorption (renal hypercalciuria). Oral calcium load tests will differentiate the two types of hypercalciuria. Elevated fasting UCa/UCr with normal levels of parathormone (PTH) or urinary cyclic-AMP indicates renal hypercalciuria. After an oral calcium load, the UCa/UCr ratio will be greater than normal in absorptive hypercalciuria. However, Hymes and Warshaw suggest that both subtypes may coexist in some patients.
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Reference values for the urinary calcium/creatinine ratio (Ca/Cr ratio) in the first morning urine were established in 361 healthy children aged 5 to 15 years, on unrestricted diets. The urinary Ca/Cr ratio in the urine upon arising was independent of sex but dependent upon age. The measurement of the urinary Ca/Cr ratio in the urine upon arising while on unrestricted diets may be a reasonable screening test for elevated calcium excretion. On the basis of the urinary Ca/Cr ratios in the urine upon arising during unrestricted diets and the calciuric response to calcium restricted diets and the oral calcium loading test, idiopathic hypercalciuria (IH) was subclassified into three groups: (1) absorptive hypercalciuria; (2) renal hypercalciuria; (3) dietary hypercalciuria. The pathogenesis of IH is controversial. Our data suggest that disordered 1,25 (OH) 2 vitamin D metabolism with excessive urinary phosphate excretion occurs in absorptive hypercalciuria.
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Prior cross-sectional studies have demonstrated an association between hypercalciuria and low bone mineral density (BMD) in children and adults. However, the natural history of BMD in children with hypercalciuria and its response to therapy has not been evaluated. The objective of this retrospective study was to determine the change over time in lumbar (L1 - L4) BMD Z-score measured on sequential DXA scans in 19 children with hypercalciuria treated with dietary recommendations without (n = 12, Group A) and with citrate (n = 7, Group B). The mean lumbar bone density Z-score/year decreased in Group A (-0.11 ±/0.41) indicating that children with hypercalciuria lose L1 - L4 BMD over time. In contrast, the L1 - L4 BMD Zscore/ year increased in Group B (0.19 ± 0.38) suggesting that pharmacologic therapy may reverse this trend. Similarly 75% of patients in Group A, but only 29% patients in Group B had a decrease in L1 - L4 BMD. There was a definite, although not significant, trend towards improved mean bone mineral density Z-score per year and a lower percentage of patients with a decreased Z-score in hypercalciuric children treated with potassium citrate. Our findings suggest the possibility that dietary recommendations alone is not adequate as the bone mineral density of children with hypercalciuria will decrease over time, potentially increasing the risk for osteoporosis as an adult.
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A test was developed to diagnose various forms of hypercalciuria. A two-hour urine sample after an overnight fast and a four-hour urine sample after 1 g of calcium by mouth were tested for calcium, cyclic AMP and creatinine. The 24 patients with absorptive hypercalciuria had normocalcemia and normal fasting urinary calcium (< 0.11 mg per milligram of urinary creatinine). Urinary calcium was high (≥ 0.2 mg per milligram of creatinine) after a calcium load. Of the 28 patients with primary hyperparathyroidism (resorptive hypercalciuria), 25 had hypercalcemia and 21 had high fasting urinary calcium. Urinary cyclic AMP, elevated in 30 per cent of fasting patients, was high (> 4.60 μ moles per gram of creatinine) in 82 per cent of cases after calcium load. Six patients with renal hypercalciuria had normocalcemia, high fasting urinary calcium, and high (> 6.86 μ moles per gram of creatinine) or high-normal fasting urinary cyclic AMP. After a calcium load, urinary cyclic AMP was normal. This simple test should facilitate the differentiation of various causes of hypercalciuria. (N Engl J Med 292:497–500, 1975)
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Local reference values are important for ihe correct approach lo the diagnosis and management of idiopathichypercalciuria. Ninety seven healthy children were evaluated lo determine daily normal urine calcium excretion. A meanvalue of 0.1 3 (M « 0.08), was obtained for the calcium/aeatinine urinary index. We also studied ihe relationshipbetween urinary calcium and sodium excretion (n = 47). A positive, stalislically significant relation could be stablished |p< 0.01 ]. To examine the relationship between calcium-creatinine urinary index and calcium excretion in a 24 hour urinesample, 44 children whilh hypercalciuria were evaluated. A strong correlation (r = 0.89} was obtained showing theclose association among results from both methods, p < 0.001. Two lest were evaluated In seventy eighl patients withhypercalciuria in ofder to identify renal and absortive hypercalciuria subtypes. A one week calcium restriction testshowed less non diagnosis results (0/45 cases) than the classic calcium loadig tesl (6/33 cases), leading to belterclassification of these patients.[Key words: calcium metabolism disorders, idiopathic hypercalcluria, urine calcium/creatinine index.)
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