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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Urinary excretion of prostaglandin E2 is increased in patients with idiopathic hypercalciuria, but in order to conclude that hyperprostaglandinuria is a primary phenomenon, it must be demonstrated that high levels of urinary prostaglandin E2 can be dissociated from other factors, such as urine volume and natriuresis, and from the hypercalciuria itself. 2. We studied 10 patients with idiopathic hypercalciuria and 10 control subjects on high and low calcium diets providing daily calcium intakes of 30-35 mmol and 7.5-10 mmol, respectively, and similar sodium intakes. In addition, patients with idiopathic hypercalciuria and control subjects were studied during water restriction and water diuresis. 3. Urinary prostaglandin E2 excretion was more than twice as high in patients with idiopathic hypercalciuria than in control subjects on the low and high calcium diets as well as during water restriction and water diuresis (P less than 0.01). 4. Urinary prostaglandin E2 excretion was not affected by changes in urinary calcium excretion in patients with idiopathic hypercalciuria and in control subjects. Patients with idiopathic hypercalciuria on the low calcium diet and control subjects on the high calcium diet had similar levels of calciuria and natriuresis, yet urinary prostaglandin E2 excretion (mean +/- SEM) was 11.62 +/- 1.71 nmol/day in the patients with idiopathic hypercalciuria and 3.26 +/- 0.48 nmol/day in the control subjects (P = 0.0006). 5. These results indicate that increased urinary prostaglandin E2 excretion is a cardinal characteristic of patients with idiopathic hypercalciuria.
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PMID:Increased urinary excretion of prostaglandin E2 in patients with idiopathic hypercalciuria is a primary phenomenon. 132 25

Urinary excretion of sodium and calcium was examined in hypertensive (n = 8) and normotensive (n = 7) subjects following infusion of 2% saline at a rate of 11 mL/min for 90 min. The urinary sodium excretion was 204 +/- 38 (mean +/- SEM) muEq/min in normotensives and 233 +/- 28 muEq/min in hypertensives before infusion of saline and increased maximally to 499 +/- 114 muEq/min (P less than .05) and to 928 +/- 68 muEq/min (P less than .01), respectively, after saline infusion. In normotensives, urinary calcium excretion did not change significantly; however, in hypertensives excretion increased markedly (P less than .01) from 6.1 +/- 0.7 muEq/min to 12.3 +/- 1.6 muEq/min. Plasma atrial natriuretic peptide (ANP) levels increased significantly (P less than .05) in both groups. Serum ionized calcium and plasma parathyroid hormone (PTH) levels did not change significantly. The increments of urinary sodium and calcium and of plasma ANP, as well as the preinfusion plasma PTH level, were significantly (P less than .05) higher in hypertensives than in normotensives. The present study showed that exaggerated natriuresis was accompanied by hypercalcinuria and an enhanced rise in plasma ANP in hypertensives. Basal levels of plasma PTH were elevated in hypertensives. The calcium deficiency may be attributable to a close relationship between urinary sodium and calcium, and causally related to the disturbance of sodium and volume homeostasis in hypertension, which results in exaggerated natriuresis.
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PMID:Effect of saline infusion on urinary calcium excretion in essential hypertension. 182 96

To investigate our impression that hypercalciuria is relatively common in children with osteogenesis imperfecta, we performed a retrospective study of data accumulated from our pediatric population with this skeletal disorder. Children with osteogenesis imperfecta (17 girls, 30 boys; mean (+/- SD) age 7.8 +/- 4.6 years; range 0.7 to 16.8 years) had undergone detailed inpatient evaluation of mineral homeostasis during periods of clinical stability and controlled dietary calcium intake. Hypercalciuria was found in 36% of the patients and averaged (+/- SEM) 6.1 +/- 0.3 mg/kg per 24 hours (0.15 +/- 0.01 mmol/kg per 24 hours) or 392 +/- 28 mg/gm of creatinine (1.10 +/- 0.07 mmol calcium/mmol creatinine) in the group with hypercalciuria. There were no statistically significant differences in age, gender, or dietary calcium intake (per kilogram of body weight) between the normocalciuric and hypercalciuric children. However, the group with hypercalciuria was shorter than the normocalciuric group and had a greater lifelong fracture rate. When patient height z scores were regressed against urinary calcium levels, a significant negative correlation was found in the group with hypercalciuria (r = -0.76; p less than 0.001). Although serum alkaline phosphatase activity was lower in the group with hypercalciuria, no difference was found between groups with regard to serum levels of calcium, phosphate, magnesium, creatinine, immunoreactive parathyroid hormone, or osteocalcin. The groups were also similar with respect to both their total body mineral density, as determined by dual-photon absorptiometry (n = 17), and their static indexes of bone formation and resorption, as assessed histomorphometrically with iliac crest specimens (n = 19). We conclude that hypercalciuria occurs frequently in children with osteogenesis imperfecta, and that its magnitude appears to reflect the severity of the skeletal disease.
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PMID:Hypercalciuria in children severely affected with osteogenesis imperfecta. 206 61

1. To determine the relationships between parathyroid hormone activity and long-term sodium fluoride therapy in osteoporosis, cytochemical bioassays (for biologically active parathyroid hormone) were performed in 22 osteoporotic control patients and in 18 patients after 15 +/- 10 months of treatment (60 mg of sodium fluoride daily). Ten patients were studied longitudinally by repeated metabolic balances and were therefore common to both groups. All patients were receiving mineral supplements. 2. Cross-sectional data showed a fourfold mean increase in biologically active parathyroid hormone on fluoride treatment (P less than 0.005) together with a 51% increase in serum alkaline phosphatase (P less than 0.005). Longitudinal data showed, in addition, a significant increase in the calcium balance of 2.4 +/- 1.2 (SEM) mmol daily (P less than 0.05) and the development of a positive phosphorus balance (P less than 0.02). 3. Fluoride-treated patients were then analysed in two groups according to the level of biologically active parathyroid hormone. Thirty-two per cent of values were above the upper limit of normal (18 pg/ml). The mean serum alkaline phosphatase level in this group showed no elevation above that of the control patients, the overall rise being accounted for entirely by patients with normal levels of biologically active parathyroid hormone. High levels of biologically active parathyroid hormone were also associated with relative hypophosphataemia (P less than 0.01), relative hypercalciuria (P less than 0.05) and an increased urine/faecal calcium ratio (P less than 0.025). 4. Results show that long-term fluoride and calcium therapy increase biologically active parathyroid hormone in osteoporosis and that excessive parathyroid hormone activity may account for certain features of the refractory state.
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PMID:Fluoride therapy and parathyroid hormone activity in osteoporosis. 216 71

Idiopathic hypercalciuria is a common disorder whose inheritance suggests an enzyme abnormality in calcium transport. We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones. As compared with 41 healthy controls, the patients with hypercalciuria had increased erythrocyte-membrane calcium-magnesium-ATPase activity (64.2 +/- 2.19 vs. 51.6 +/- 1.91 nmol of ATP split per milligram per minute; P less than 0.01) and increased sodium-potassium pump activity (6866 +/- 233 vs. 6096 +/- 228 mumol of sodium per liter of red cells per hour; P less than 0.05). No significant difference between the two groups was found in erythrocyte sodium-potassium cotransport, sodium-lithium countertransport, or potassium content. In 66 patients with kidney stones (38 with hypercalciuria and 28 with normal calcium excretion), 24-hour urinary calcium excretion correlated with calcium-magnesium-ATPase activity (r = 0.46, P less than 0.001). Erythrocyte calcium-magnesium-ATPase activity remained unchanged in eight subjects studied after four months on a low-calcium diet. A study of 30 healthy families found significant correlations between mean values in parents and those in offspring for calcium-magnesium-ATPase (r = 0.68, P less than 0.001) and urinary calcium excretion (r = 0.45, P less than 0.02), with no significant correlations between parents with respect to these measures (r = 0.27 and r = 0.08, respectively). We conclude that abnormalities in erythrocyte calcium-magnesium-ATPase activity may represent an inherited defect in calcium transport related to the cause of idiopathic hypercalciuria.
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PMID:Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria. 297 Nov 39

The possibility that hypercalciuria could cause calcium stone formation through a mechanism other than by increasing urinary saturation of stone-forming calcium salts was explored. The effect of increasing calcium concentration on the inhibitor activity against the spontaneous precipitation of calcium oxalate was examined in whole urine (in the presence of naturally occurring inhibitors) and in synthetic media (with added inhibitors). In 11 patients with calcium nephrolithiasis, the induced hypercalciuria from calcium supplementation (600 mg/day) caused a significant fall in the urinary inhibitory activity against calcium oxalate precipitation, as shown by a decline in the formation product ratio from 12.6 +/- 1.1 SEM to 9.6 +/- 1.4 (P less than 0.005). In order to more fully explore this observation, the effect of increasing calcium concentration on the inhibitory activities of citrate (2 mM), chondroitin sulfate (0.05 mg/liter) and a heterogeneous group of naturally-occurring urinary inhibitors (1.0 mg/liter) against calcium oxalate precipitation was examined in vitro in synthetic solutions. The inhibitory actions of both citrate and chondroitin sulfate were significantly attenuated by increasing calcium concentration from 0.25 mM to 6.0 mM (P less than 0.01). However, raising the calcium concentration in synthetic media containing a mixture of partially purified urinary inhibitors produced a significant rise in the urinary inhibitory activity of this macromolecular mixture (P less than 0.01). We conclude that hypercalciuria can attenuate the inhibitory activities of citrate and chondroitin sulfate against calcium oxalate precipitation while at the same time accentuating the inhibitory activity of naturally-occurring urinary inhibitors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation by calcium of the inhibitor activity of naturally occurring urinary inhibitors. 313 70

Abnormalities in renal tubular function have been reported in adult patients with idiopathic renal hypercalciuria. To determine if such abnormalities are present early in the natural history of renal hypercalciuria, we evaluated renal tubular function in ten children with idiopathic renal hypercalciuria, aged 5-17 years. Seven of the children presented with urolithiasis and three with hematuria. Urinary calcium excretion ranged from 4 to 9 mg/kg per day, (5.2 +/- 0.5, mean +/- SEM) with a mean fasting urinary calcium to creatinine ration of 0.31 +/- 0.03. Studies described in this report were performed after 1 week of ingesting a diet containing 1,000 mg calcium, 3,000 mg sodium, and 100 mg purine. Clearance of creatinine ranged from 84 to 159 ml/min per 1.73 m2. Tm phosphate (mg/100 ml GFR) was normal in each child (mean 4.66 +/- 0.06 mg/100 ml GFR). Fractional excretion of uric acid, sodium and beta-2-microglobulin were also normal in each child. Serum bicarbonate concentrations ranged from 21.5 to 27 mEq/l with a mean of 24.4 +/- 0.5 mEq/l and all patients lowered urinary pH to less than 5.5. Hypotonic diuresis demonstrated normal free water clearance with a mean of 12.8 ml/min per 100 ml Cin. Distal sodium delivery and fractional distal sodium reabsorption were normal with a mean of 13.6 +/- 1.2% and 92.7 +/- 0.5%, respectively. Water deprivation studies demonstrated a range of maximum urinary osmolality from 711 to 1,020 mosmol/kg H2O with a mean of 864 +/- 34 mosmol/kg H2O. Seven healthy children, ingesting an identical study diet, concentrated their urine to a mean of 1,059 +/- 31 mosmol/kg h2O.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal function in children with idiopathic hypercalciuria. 315 15

Patients with acromegaly have alterations in mineral metabolism. To determine the effect of correction of excess GH secretion on calcium metabolism, we studied 12 acromegalic patients before and 3-4 weeks after pituitary adenomectomy. Treatment of acromegaly resulted in significant decreases in both serum calcium [from 9.3 +/- 0.2 to 8.7 +/- 0.1 mg/dl (mean +/- SEM); P less than 0.01] and urinary calcium excretion (from 200 +/- 24 to 88 +/- 12 mg/24 h; P less than 0.0002). Serum phosphate also decreased significantly (P less than 0.01) from 4.8 +/- 0.2 to 4.3 +/- 0.2 mg/dl. Both serum immunoreactive PTH and calcitonin levels were normal initially and did not change after surgery. The mean serum 25-hydroxyvitamin D (25OHD) level was significantly (P less than 0.01) lower and the 1,25-dihydroxyvitamin D [1,25-(OH)2D] level was significantly (P less than 0.0001) higher in acromegaly compared with measurements in 25 normal subjects. After surgery, the serum 25OHD level did not change; however, the serum 1,25-(OH)2D concentration fell significantly (P less than 0.0001) from 60 +/- 4 to 43 +/- 2 pg/ml. A positive correlation was found between the decrements in urinary calcium excretion and the serum 1,25-(OH)2D level when the comparison was made between the decrements as percentages of pretreatment values (r = 0.64; P less than 0.05). The accumulated data suggest that the hypercalciuria in acromegaly might be due to intestinal calcium hyperabsorption, which could be attributed to the elevated circulating 1,25-(OH)2D level. Excessive GH secretion might stimulate the production of 1,25-(OH)2D and might also directly stimulate calcium absorption.
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PMID:Changes in calcium homeostasis in acromegaly treated by pituitary adenomectomy. 383

Ionic calcium, calcium binding sites, and other urinary variables were measured in 58 patients with idiopathic calcium nephrolithiasis and 36 normal subjects. The patients showed higher urinary concentrations of calcium. The mean calcium excretion (mmole/24 hr) was 4.45 +/- 0.56 (+/- 1 SEM) in patients and 2.19 +/- 0.22 (+/- 1 SEM) in normal subjects. This difference was highly significant (P less than 0.001). The mean ionic calcium excretion (mmole/24 hr) was 1.90 +/- 0.21 (+/- 1 SEM) for patients and 0.97 +/- 0.12 (+/- 1 SEM) for control subjects. The normal subjects showed significantly higher (P less than 0.01) concentrations and total excretions of magnesium and citrate. Excretory patterns for sodium, potassium, phosphate, and oxalate were not significantly different. The normal subjects had higher mean urinary concentrations of binding sites for calcium ions (23.2 +/- 4.8 mM) than the patients (18.5 +/- 2.9 mM). However, as the patients had higher urinary volumes the difference in the 24-hr excretion of calcium binding sites was not significant statistically. Out of 58 patients 43 (74%) were hypercalciuric. Twenty patients (46%) were categorized as an absorptive group and one patient as a resorptive type, and for the rest of the patients (51%) the mechanism of hypercalciuria remained unidentified. Only two of the control subjects (5%) were found to be hypercalciuric under calcium restricted diet conditions. Though these "control" subjects excreted a high amount of calcium there was no associated increase in the fraction of the calcium in the ionic form (0.37). Patients, however, still had relatively high fractions of ionic calcium (0.48 +/- 0.03).
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PMID:Calcium dynamics in idiopathic calcium stone formers. 630 23

Earlier studies have shown that an oral sodium (Na) load may induce hypercalciuria in previously normocalciuric subjects and may also increase intestinal calcium (Ca) absorption. To probe the cause of the increased intestinal Ca absorption, we simultaneously measured parathyroid function, serum 1,25-dihydroxyvitamin D [1,25-(OH)2D], and fractional intestinal 47Ca absorption before and after a salt load. Eleven normal subjects and two patients with postsurgical hypoparathyroidism were placed on a 10 meq Na, 400 mg Ca per day diet for 10 days, followed by another 10-day period in which the same diet was supplemented by 240 meq Na daily. Measurements were performed on the final 3 days of each phase. In the normal subjects, urinary Na excretion increased from 7 +/- 2 to 226 +/- 8 meq/day (mean +/- SEM), urinary Ca rose from 110 +/- 14 to 167 +/- 16 mg/day, serum parathyroid hormone (PTH) increased from 20 +/- 1 to 22 +/- 1 muleq/ml, serum 1,25-(OH)2D rose from 38 +/- 4 to 51 +/- 7 pg/ml, and fractional intestinal 47Ca absorption increased from 0.39 +/- 0.03 to 0.49 +/- 0.03 (P less than 0.05 for all changes). Serum Ca corrected for total protein did not change (9.9 +/- 0.1 to 9.8 +/- 0.1 mg/dl). The patients with hypoparathyroidism who were maintained on vitamin D therapy also showed increases in urinary Na (20 +/- 12 to 245 +/- 11 meq/day) and urinary Ca (271 +/- 48 to 305 +/- 43; P less than 0.05). However, there were no increases in serum PTH (13 +/- 1 to 11 +/- 1 muleq/ml), serum 1,25-(OH)2D (44 +/- 1 to 40 +/- 6 pg/ml), or intestinal Ca absorption (0.41 +/- 0.03 to 0.42 +/- 0.05). Corrected serum Ca decreased from 9.4 +/- 0.2 to 8.6 +/- 0.2 mg/dl. We conclude that in normal subjects, Na-induced renal hypercalciuria is accompanied by increased 1,25-(OH)2D synthesis and enhanced intestinal Ca absorption. Since this adaptive mechanism did not occur in two patients with hypoparathyroidism, mediation by PTH is suggested.
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PMID:The role of dietary sodium on renal excretion and intestinal absorption of calcium and on vitamin D metabolism. 689 38


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