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

Inadequate low intake of phosphorus can induce a hypophosphatemic depletion syndrome resulting in hypercalcemia, hypercalciuria, hypophosphatemia, and rickets. Tubular reabsorption for phosphate per liter glomerular filtration rate (TP/GFR) has been proposed as a reliable index of renal phosphate handling for all age groups. In the present study, carried out in 12 healthy premature babies fed unmodified pooled human milk and then a preterm formula for two periods of 10 days, we demonstrated clearly that TP/GFR as well as calciuria can reflect the poor phosphorus intake and that the kidney of preterm babies is able to rapidly adapt itself to an increase in phosphorus diet content.
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PMID:Phosphorus intake in preterm babies and variation of tubular reabsorption for phosphate per liter glomerular filtrate. 152 68

A decrease in bone density of the spine has been reported in individuals with hypercalciuria and the finding of the latter in osteoporosis patients is not uncommon. We studied 21 men and 8 women (mean age 47 +/- 13) with idiopathic hypercalciuria (IHCU) defined by an urinary calcium of more than 7.5 mmol/24 h in men and 6.25 mmol/24 h in women. The duration of IHCU was 10 (+/-) 8 years. Among the 29 patients, 24 had one or more renal calculi. Twenty one had been treated, by low calcium diet only (and diuresis), combined with a thiazide diuretic, or sodium phytate, or phosphorus. Bone mineral content (BMC) was measured in the lumbar spine and the upper end of the femur using an ORIS ODC 200 densitometer and compared with 29 control subjects paired for age and sex. No difference was found between the two groups concerning BMC values in either the spine or the 3 femoral sites (neck, Ward, trochanter). BMC was not correlated with urinary calcium. Thus individuals with IHCU showed no decrease in their bone mass, among this group seen in a department of nephrology. The influence of the treatment of IHCU remains to be defined.
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PMID:[Idiopathic hypercalciuria and bone density]. 157 44

We report on a 7-week-old infant with idiopathic hypercalcemia, hypercalciuria and nephrocalcinosis. At the time of admission, serum concentrations of parathyroid hormone and 1,25(OH)2D3 were found to be inadequately high, and those of calcitonin and 24,25(OH)2D3 too low, relative to the hypercalcemia. Treatment with calcitonin normalized serum calcium concentrations within 4 days, and a 3-week course of thiazides combined with a decreased dietary calcium:phosphorus ratio corrected the hypercalciuria. A repeat profile of the calcium-regulating hormones done at the age of 5.5 months was normal. Based on the clinical course and the hormonal profiles, we hypothesize that the idiopathic infantile hypercalcemia in this patient could have resulted from a generalized maturational delay of calcium homeostasis. Treatment with calcitonin, therefore, seems to be the most appropriate way to control the hypercalcemia.
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PMID:Idiopathic infantile hypercalcemia: rapid response to treatment with calcitonin. 160 83

Some cereal by-products, such as bran, exhibit a high phytase activity that may enhance phytate P digestibility. This was studied in growing pigs fed a phytase-rich (1,200 IU/kg) diet containing 20% rye bran. The trial involved 12 animals; six were fed a control diet and six were fed a diet containing rye bran for 2 mo. Both diets contained the same levels of energy, protein, Ca (.7%) and total P (.4%). No inorganic P was added; thus, the dietary P was mainly phytic. Pigs fed the control diet, in contrast to those fed the diet containing rye bran, developed a P deficiency, as indicated by hypophosphatemia, hypophosphaturia, hyperhydroxyprolinuria, hypercalcemia, and hypercalciuria. Phosphorus from the rye bran diet was more completely absorbed (55 vs 36%) and retained (50 vs 36%) than that from the control diet. Calcium absorption was equal for the two diets, but Ca retention was higher in pigs fed rye bran than in controls. Pigs fed the rye bran diet showed greater bone density, ash content, and bending moments than controls. In conclusion, high dietary phytase levels or phytase-rich by-products increased phytate P availability and consequently improved bone scores.
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PMID:Enhancement of phosphorus utilization in growing pigs fed phytate-rich diets by using rye bran. 164 62

1. Acromegaly is associated with metabolic disturbances of calcium and phosphorus which can also contribute to renal lithogenesis. 2. In order to characterize these disturbances more precisely, an oral calcium load test was performed on 14 active acromegalic patients. Serum and urinary levels of calcium, phosphorus, uric acid, creatinine and urinary cyclic AMP were determined. 3. Of the 14 patients, 5 (36%) presented hypercalciuria, 5 (36%) presented intestinal calcium hyperabsorption, and 6 (43%) had uric acid hyperexcretion. Two patients (14%) presented nephrolithiasis. 4. The medical records of 32 additional acromegalic patients with or without active disease were reviewed for a history of previous stones, which was observed in three cases (9.5%). 5. The present data suggest that nephrolithiasis occurs more frequently among acromegalic patients because of the underlying metabolic disturbances of calcium presented by this population.
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PMID:Metabolic factors for urolithiasis in acromegalic patients. 166 2

The addition of sucrose to drinking water of rats at the rate of 2.5 or 5 grams per 100 ml, for one month, induced hypercalciuria which appeared to be dependent on the degree of supplementation. In spite of these disorders, calcium deposits were not observed in treated animals. This protection against renal calculi was probably due to high urinary excretions of magnesium, phosphorus, zinc and copper. These lithogenesis inhibitors varied, like oxaluria and calciuria, in parallel with dietary sucrose intake.
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PMID:[Is sucrose a risk factor in calculus formation?]. 174 29

Hypercalciuria and bone disease are frequently associated with total parenteral nutrition (TPN) in children and adults. The aim of this study was to assess the influence of calcium, phosphorus, and vitamin D intakes on hypercalciuria. We observed seven children aged 4-13 years receiving home cyclic TPN for 4 consecutive years. Calcium and phosphorus intakes, constant during the 1st year, were reduced during the last 3 years to 50 and 30% of the initial intakes, and vitamin D was stopped during the 3rd and the 4th years. All children had hypercalciuria and one of them had acute painful osteopenia and nephrocalcinosis at the beginning of the study. Hypercalciuria was corrected and painful bone disease did not occur during the three following years, with TPN daily intakes of calcium, 0.35 mmol/kg, and phosphorus, 0.70 mmol/kg. Cessation of vitamin D administration during 48 months led to no further decrease in calciuria nor to the occurrence of clinical or biological signs of vitamin D deficiency. However, we hypothesize that excessive vitamin D intake may have facilitated the occurrence of the TPN-related bone disease in one patient and should be avoided. The possible role of parenteral aluminum loading is also discussed.
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PMID:Calcium metabolism in children during long-term total parenteral nutrition: the influence of calcium, phosphorus, and vitamin D intakes. 177 10

We have previously shown the synergistic interaction between fructose and magnesium (Mg) deficiency on renal calcification of female rats. The purpose of the present study was to determine whether the calcification formed in the kidneys of female rats fed an Mg-deficient fructose diet is due to phosphate or oxalate precipitates of calcium. The rats were divided into two dietary groups: fructose without Mg and starch with Mg. Rats were fed their respective diets for 9 weeks, and 24 h urine was collected for measuring urinary output, pH, Mg and calcium (Ca). The rats were then fasted overnight and after decapitation, blood was immediately collected for measuring plasma Ca and Mg, and the kidneys were removed. Left kidneys were used to determine their Mg and Ca contents, and right kidneys were dissected and fixed in neutral buffered formalin. Formalin-fixed specimens for microscopy were processed in paraffin using conventional procedures. Histochemical analysis was conducted by staining serial paraffin sections with haematoxylin, eosin, PAS-Schiff, alcian blue and trichrome. The sections were stained by the von Kossa method for calcium phosphate and by the silver hydroperoxide method for calcium oxalate. Only calcium phosphate was detected in the corticomedullary junction of the kidneys of female rats fed Mg-deficient fructose. The hypercalcaemia, hypercalciuria, and hypomagnesuria observed in the fructose group may cause calcium phosphate crystallization. A possible mechanism for the interaction between magnesium deficiency, fructose and oestrogen may be through parathyroid hormone which increases tubular fluid Ca and phosphorus (TF[Ca]x[P]). Further studies are required to prove the mechanism proposed here.
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PMID:Fructose precipitates calcium phosphate in the kidneys of female rats fed magnesium-deficient diets. 179 51

We have studied urinary sodium and magnesium excretion in 30 normal subjects (15 women and 15 men, mean age 43 +/- 14 years, mean weight 74 +/- 18 Kg) and in 60 hypercalciuric stone-forming patients, 30 with renal hypercalciuria (HR) (15 women and 15 men, mean age 39 +/- 10 years, mean weight 71 +/- 16 Kg) and 30 with absorptive hypercalciuria (HA), (15 women and 15 men, mean age 41 +/- 13 years, mean weight 69 +/- 12 Kg). The diagnosis of hypercalciuria and the classification in HA and HR was made with our ambulatory study protocol. Hypercalciuria was defined by a daily calcium excretion above 300 mg (men) or 220 mg (women), and patients with fasting calcium to creatinine ratio, and calcium per 100 ml of glomerular filtrate average value above 0.11 were considered to have HR. Control subjects and hypercalciuric patients were maintained on a diet containing 1200 mg Ca, 800 mg P, 200 mg Mg and 100 mmol Na per day for a 7-day period. Two 24-hour urine samples were collected on days 6 and 7 of this diet. On the morning of day 8, following a 12-hour fast, 300 ml of distilled water was drunk and a 2-hour urine sample was collected. A blood sample was taken halfway this time. In all blood and urine samples, calcium, magnesium, sodium, phosphorus and creatinine were quantified. Creatinine clearance and calcium, sodium and magnesium per 100 ml of glomerular filtrate were calculated from these determinations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Urinary excretion of sodium and magnesium in idiopathic hypercalciuria]. 182 17

Hypercalciuria is one of the main causes of recurrent generation of urinary calcium-containing calculi. 107 patients with recurrent calcium nephrolithiasis were examined and results presented. Concentrations of potassium, sodium, chlorides, calcium, phosphorus, uric acid and creatinine were investigated in serum and urine, as well as indices of acid-base balance in arterial blood. pH-metry, "preliminary" and oral calcium tolerance test were also carried out. The microcomputer data analysis established that the diagnosis of primary hyperparathyroidism may be identified in case of increased serum calcium level before and after calcium load test, the same of parathyroid, and increased urinary cAMP excretion. Renal hypercalciuria is characterized by low blood calcium level in both periods of the oral test, high basal calciuria, increased urinary cAMP excretion and its slight decrease after the oral calcium load test, by a tendency to lower serum magnesium levels in high magnesuria. The patients with absorptive hypercalciuria had an upper normal or increased blood calcium level, a significant calcemic and calciuric "response" to the calcium load, reduction in urinary cAMP elimination and more severe decrease (close to 0) of these indices after oral calcium load and normal magnesium levels in blood and urine. On a base of the "preliminary" test data the patients with relapsing calcium nephrolithiasis and metabolic disorders may be differed from those without calcium and phosphorus metabolic deteriorations. The "preliminary" test defines indications for the oral calcium tolerance test, automatic diagnosis and computer data storage facilitate physician to work and to solve problems of the patients' survey.
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PMID:[The comprehensive examination of patients with recurrent calcium nephrolithiasis]. 185 97


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