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

A total of 12 patients with absorptive hypercalciuria type II and 11 normal controls participated in a study to evaluate the effects of dietary protein levels on urinary calcium and oxalate excretion before and after a 1 gm. dose of oxalate. Two test periods were used during which calcium (less than 400 mg. per day) and oxalate were restricted. The first test was done under conditions of low dietary protein (12 per cent total caloric intake, 60 gm.) and the second test was done at a high protein level (25 per cent, 125 gm. protein). Twelve-hour urine specimens were obtained after dinner on day 3 of each diet (low and high protein) and again on day 4 when 1 gm. oxalate (spinach) was added to the dinner meal. The specimens were analyzed for calcium, oxalate and relative calcium oxalate saturation (concentration product ratio). There were no significant differences between the controls and subjects with absorptive hypercalciuria type II in oxalate excretion before the oxalate load on the low protein (controls 31.4 +/- 4.2 standard error, expressed as mmol. oxalate per mol. creatinine, and absorptive hypercalciuria type II 23.1 +/- 3.1) and high protein (controls 30.4 +/- 4.2 and absorptive hypercalciuria type II 28.8 +/- 5.9) diets. After the oxalate bolus the positive changes in oxalate excretion were 11.8 +/- 4.8 (low protein) and 17.8 +/- 4.7 (high protein) for controls, and 11.4 +/- 4.4 (low protein) and 31.8 +/- 5.2 (high protein) for patients with absorptive hypercalciuria type II. Thus, the increases in post-load urinary oxalate levels observed for controls and patients were greater on the high protein than on the low protein diets. After the oxalate load the increases in urinary oxalate and calcium oxalate supersaturation were significantly greater for patients with absorptive hypercalciuria type II than for control subjects for the high protein but not the low protein diets (p less than 0.05).
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PMID:Dietary protein levels affect the excretion of oxalate and calcium in patients with absorptive hypercalciuria type II. 356 Mar 23

As a practical contribution to an understanding of the usefulness of measuring some electrolytes in urine, the author first recalls that elements measured in a 24-h urine sample provide nutritional informations, whereas those assayed in fasting morning urine generate data on renal tubular function. To illustrate the first point the author describes assessment of the etiology of hypercalciuria based on a knowledge of concomitant 24-h excretions of sodium, phosphate, urate and creatinine. On the second point, the author suggests dissociating the parameters of which only the urinary concentration is of interest (pH, lysozyme, gamma-glutamyl-transferase) from the parameters of which the excretion--either fractional (Na, K, Cl, P, Mg) or absolute (Ca)--should be calculated. Finally, the reader is reminded how to use the nomogram of Peacock, Robertson and Nordin to evaluate fasting urinary excretion of calcium, and how to use the nomogram of Walton and Bijvoet to estimate the renal threshold phosphate concentration.
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PMID:[Usefulness of urinary electrolyte determination]. 356 52

Hematuria of unknown origin occurs in 30% of patients with diabetic nephropathy. In nondiabetic persons, hematuria may be caused by hypercalciuria with or without nephrolithiasis. Eight children with type I diabetes mellitus, hematuria, and hypercalciuria were observed in our clinic during a 1-year period. Two of these also had evidence of renal papillary necrosis. To assess the importance of hypercalciuria in the pathogenesis of hematuria in children with diabetes mellitus, we measured urinary calcium excretion in a large population of such patients. The calcium to creatinine ratio in the urine of diabetic children (0.21 +/- 0.01) was greater than that of nondiabetic children (0.12 +/- 0.01). A calcium to creatinine ratio of 0.28 was established as the upper limit of normal in our nondiabetic population, and 27% of the diabetic children were hypercalciuric on this basis. The diabetic children with hypercalciuria also had hyperphosphaturia and a urinary CaHPO4 X 2H2O molar ion product three times that found in the nondiabetic control population. These data suggest that many children with diabetes are at risk for renal damage due to hypercalciuria. Because hypercalciuria is more common in diabetic than nondiabetic children, it may play a previously unrecognized role in the renal disease associated with diabetes mellitus.
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PMID:Hematuria and hypercalciuria in children with diabetes mellitus. 357 34

Calcium and creatinine concentrations were analyzed in urine samples of 42 chronically institutionalized bedridden children, with neurologic disorders. Their ages ranged from 2 to 16 (mean 8.7) years. Hypercalciuria, defined as UCa/UCr ratio greater than 0.21, was recognized in 18 children (42.8%), the mean UCa/UCr ratio of this group was 0.40 +/- 0.18. Twenty-four children were normocalciuric, with a mean UCa/UCr ratio of 0.08 +/- 0.03. There were no significant differences between the two groups with regard to age, sex, length of institutionalization, the basic neurologic disorder, diet, anticonvulsive medications, exposure to sunlight and weekly hours of physiotherapy. Age- and sex-matched percentiles for fat and muscle areas were similar in both groups. Seven limb fractures had occurred in the hypercalciuric group during the last three years, but only in one of the normocalciuric patients (p less than 0.02). The hypercalciuric children were treated with a hydrochlorothiazide-amiloride preparation for three weeks, which resulted in reduction of their mean UCa/UCr ratio by 57.7%, to 0.17 +/- 0.13 (p less than 0.005); only four children remained hypercalciuric. We conclude that resorptive hypercalciuria is common among chronically immobilized bedridden children. Hypercalciuria in such children should be specifically looked for, because of its association with deranged bone metabolism and increased frequency of limb fractures. Treatment with thiazides was found to be efficient in reducing urinary calcium excretion in our hypercalciuric patients. This therapeutic modality for the reduction of morbidity in bedridden chronically immobilized children should be further explored.
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PMID:Hypercalciuria in chronically institutionalized bedridden children: frequency, predictive factors and response to treatment with thiazides. 358 54

Normocalcaemic male stone formers (n = 138), 31-51 years of age, were divided into a hypercalciuric group (n = 80), with calcium excretions exceeding 7.0 mmol/24 h, and a normocalciuric group (n = 58), with calcium excretions of 7.0 mmol/24 h or less. The hypercalciuric group of patients was further subdivided using two previously published methods for identifying hyperabsorbers--one based on fasting urinary calcium/creatinine ratios and renal threshold phosphate concentrations, Jongen and the other method based on an oral calcium load test, Pak et al. The first method identified 37 patients and the second method 12 patients as hyperabsorbers. However, of the latter 12 patients only 8 were identified as hyperabsorbers using the first method of classification. It is thus evident that the two methods used for subclassification may give surprisingly different results. In order to obtain better congruence, the consequences of changing the defining limits in the two different methods were investigated. On the basis of the results obtained a new model for identification of hyperabsorbers is presented and discussed. With these new selection criteria (TmPO4/GFR greater than or equal to 0.75, urinary fasting molar calcium/creatinine ratio less than 0.40, and an increase in urinary molar calcium/creatinine ratio after calcium load greater than or equal to 0.20), 27 of the hypercalciuric patients were identified as hyperabsorbers. This group included 23 of Jongen's 37 and all of Pak's 12 hyperabsorbers. No patient not identified as a hyperabsorber according to either Jongen's or Pak's method were found in this group. The suggested model for identifying hyperabsorbers seems to be practical at least in studies on the relation between hypercalciuria and metabolism of vitamin D3.
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PMID:Proposed criteria for identifying hyperabsorbers among normocalcaemic renal stone formers. 361

Hypercalciuria is a major cause of urolithiasis in adults and has reached increasing attendance in childhood. Traditionally urinary excretion of calcium is evaluated by 24-hour urine collection. Previous reports proposed the urinary calcium/urinary creatinine ratio (Ca/Cr-ratio) to diagnose hypercalciuric states. In 10 children with normocalciuria and 8 children with hypercalciuria the values of calcium excretion and Ca/Cr-ratio in a 24-hour urine collection were compared. 40 analyses showed a significant correlation (p = 0.001, r = 0.91) and hypercalciuria (urinary calcium greater than 4 mg/kg/day) is present if the Ca/Cr-ratio exceeds 0.23 (mg/mg). In 10 of the 18 patients the Ca/Cr-ratio of the 24-hour collection was compared with the Ca/Cr-ratio of a random urine sample collected 3 hours after breakfast. No significant difference was present. In 9 of 10 patients the correct diagnosis (normocalciuria or hypercalciuria) was possible by evaluation of this random urine sample. Our studies indicate that the evaluation of Ca/Cr-ratio in a random urine sample is a simple and reliable method to detect hypercalciuria and should be performed in all children with urolithiasis or unexplained hematuria. It is also a simple test for early detection of hypercalciuria in patients with long-term administration of vitamin D metabolites.
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PMID:[Use of the calcium-creatinine ratio in diagnosis and therapy]. 368 17

Seventeen patients who recurrently formed idiopathic calcium kidney stones (SF) and 25 age- and sex-matched healthy blood donors (H) were challenged by an oral calcium load (1 g) after an overnight fast. Their usual diet was not changed before the test. Urine samples were taken before, 2 1/2, and 4 h after the calcium load. A blood sample was drawn 3 3/4 h after calcium loading. Before and 2 1/2 h after calcium dosage urinary measurements of calcium, magnesium, phosphate, oxalate, uric acid, and creatinine did not reveal any differences between SF and H. According to the calciuria after 4 h SF were separated in normocalciurics (NCSF) and hypercalciurics (HCSF). Nine-tenths of the NCSF had higher serum ionic calcium levels than H after calcium load (P less than 0.001), whereas HCSF were not different from H. Serum phosphate in SF was lower than in H (P less than 0.001). Carboxy-terminal parathormone, measured in 3 NCSF and 2 HCSF, was normal. Depending on the calciuria or calcemia 4 h after an oral calcium load, 16 of 17 SF showed a metabolic abnormality (hypercalcemia or hypercalciuria). It is concluded that intestinal calcium absorption in SF might be increased to variable rates.
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PMID:[Peroral calcium administration test with free diet in idiopathic calcium nephrolithiasis--possibilities and limits]. 378 54

Among 59 closely related members of one Bedouin tribe, we identified 9 who had the characteristic features of hereditary hypophosphatemic rickets with hypercalciuria (HHRH). We found "idiopathic" hypercalciuria in 21 of the 50 asymptomatic members. The biochemical abnormalities observed in these 21 subjects were qualitatively similar to those in the 9 with HHRH, but were quantitatively milder. The urinary calcium concentration was 0.43 +/- 0.14 mg per milligram of creatinine (mean +/- SD) in the patients with HHRH, 0.34 +/- 0.07 in the subjects with idiopathic hypercalciuria, and 0.14 +/- 0.05 in normal subjects from the same tribe. Tubular reabsorption of phosphorus and serum phosphorus concentrations were 3.0 and 4.3 SD units below the age-related mean, respectively, in HHRH, and 1.1 SD units below the normal mean for both variables in idiopathic hypercalciuria. Mean serum levels of 1,25-dihydroxyvitamin D (1,25-(OH)2D) were 303 pg per milliliter in HHRH and 145 pg per milliliter in idiopathic hypercalciuria (upper normal limit, 110). We conclude that the subjects with hypercalciuria and the patients with HHRH shared a hereditary renal phosphate leak that led to hypophosphatemia, elevated serum concentrations of 1,25-(OH)2D, increased intestinal calcium absorption, and hypercalciuria. The magnitude of the hypophosphatemia, which regulates 1,25-(OH)2D levels, appears to determine which subjects will have hypercalciuria alone and which will also have bone disease.
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PMID:"Idiopathic" hypercalciuria and hereditary hypophosphatemic rickets. Two phenotypical expressions of a common genetic defect. 379 83

Inappropriately elevated concentrations of 1,25(OH)2 vitamin D in serum appear to be responsible for excessive gastrointestinal absorption of dietary calcium in patients with absorptive hypercalciuria. We have examined serum 1,25(OH)2 vitamin D concentrations in another group of children with hypercalciuria in whom urinary calcium excretion was excessive after an overnight fast. Eleven children with idiopathic fasting hypercalciuria (IH) (urinary calcium excretion greater than 4 mg/kg/24 hr and fasting urinary calcium/urinary creatinine ratio greater than 0.21) and seven healthy children were observed while they were eating a diet containing 1 gm calcium per day. Fasting serum 1,25(OH)2 vitamin D concentrations were elevated in children with IH compared with control values (35.3 +/- 3.2 vs 21 +/- 2 pg/ml, P = 0.003), whereas fasting serum parathyroid hormone, 25-OH vitamin D, phosphorus, and ionized calcium concentrations were similar in the two groups. These data suggest that disordered 1,25(OH)2 vitamin D metabolism occurs in children with fasting IH. Absorptive and fasting IH may represent a spectrum of a single disorder characterized by excessive urinary calcium excretion and inappropriately elevated serum concentrations of 1,25(OH)2 vitamin D.
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PMID:Increased serum concentrations of 1,25(OH)2 vitamin D in children with fasting hypercalciuria. 380 94

Sixteen children with idiopathic hypercalciuria and seven control children were observed. Patients were classified into two groups by means of an orally administered calcium loading test. Individuals with renal hypercalciuria (five children) had a high fasting urinary calcium/creatinine concentration ratio (0.27 +/- 0.05), a mild increase of this value after calcium administration (0.29 +/- 0.07, P less than 0.05), and elevated mean serum parathyroid hormone (PTH) concentrations (0.95 +/- 1.14 ng/ml). Patients with absorptive hypercalciuria (11 children) had fasting urinary calcium/creatinine concentration ratio of 0.11 +/- 0.04, a large increase of this index after calcium loading (0.25 +/- 0.06, P less than 0.0005), and normal levels of serum PTH (0.29 +/- 0.10 ng/ml). Next, we examined the effects of two different calcium intakes on urinary calcium excretion, serum calcium, PTH, and 1,25-dihydroxyvitamin D3 concentrations. In patients with absorptive hypercalciuria, the increased calcium intake resulted in significant increments of calciuria (P less than 0.0005), mild elevation of serum calcium concentration (P less than 0.05), and reduction of serum 1,25-dihydroxyvitamin D3 concentrations (P less than 0.005). By contrast, these values were not modified in children with renal hypercalciuria. Serum PTH did not change within each group. After dietary calcium supplementation, serum ratios of 1,25-dihydroxyvitamin D3 to calcium, phosphate, and PTH concentrations decreased significantly only in the group of children with absorptive hypercalciuria. Our data support the contention that 1,25-dihydroxyvitamin D3 metabolism is different in the two groups of patients with hypercalciuria.
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PMID:Idiopathic hypercalciuria in children: pathophysiologic considerations of renal and absorptive subtypes. 380 95


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