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

Under controlled dietary conditions the level of dietary protein has a profound and sustained effect on urinary calcium and calcium retention of man. Young adults achieve calcium balance at low intakes of 500 mg calcium and 700 to 1,000 mg phosphorus when protein intake is 50 g. Large calcium losses occur at the same calcium and phosphorus intakes when the protein intake is increased approximately threefold. The protein-induced hypercalciuria is due mainly to a decrease in fractional renal tubular reabsorption of calcium, although an increase in glomerular filtration rate is also involved. The changes in kidney function appear to result from the catabolism of excess dietary sulfur amino acids to sulfate and the subsequent excretion of sulfate in the urine. An increase in both protein and phosphorus intakes has a much less dramatic effect on urinary calcium and calcium retention than an increase in protein intake alone. An increase in dietary phosphorus greatly reduces urinary calcium by increasing the fractional renal tubular reabsorption of calcium. It appears therefore that high protein intakes may increase the requirements for both calcium and phosphorus.
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PMID:Protein-induced hypercalciuria. 725 Mar 87

Diets containing different sources of protein were evaluated for their effect or urinary calcium (Ca) excretion in adult male rats. High protein diets were prepared by adding 24 g N/kg as lactalbumin (Hi-Lact), egg white (Hi-EW), casein (Hi-Cas) or gelatin (Hi-Gel) to a control diet containing 24 g N/kg ascasein (Cas). There were significant differences in the degree of hypercalciuria produced by different dietary protein mixtures. A peak in Ca excretion occurred at about 2 days, when the relative values were as follows (Cas = 100): Hi-Lact, 489; Hi-EW, 429; Hi-Cas, 340, and Hi-Gel, 263. Subsequently urinary Ca declined, but a moderate hypercalciuria persisted to the end of the 8-weekexperiment, when the corresponding values (% Cas) were 200, 183,160 and 136, respectively. The degree of hypercalciuria was proportional to the sulfur content of the diets, i.e., Hi-Lact greater than Hi-EW greater than Hi-Cas greater than Hi-Gel greater than Cas. Supplementing the Cas diet with sulfur amino acids to the level present in the Hi-Lact diet resulted in a comparable increase in Ca excretion. Supplementing the Cas diet with 1.42% sulfate produced a 570% increase in urinary Ca on day 2 and a 306% increase at 5 weeks. There was a linear relationship between Ca excretion and sulfate excretion. It is proposed that a major factor in the hypercalciuria of high protein feeding is the production and excretion of sulfate. Variability in the calciuric effect of different proteins appears to be related mainly to differences in their sulfur amino acid content.
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PMID:The role of sulfate in the calciuria of high protein diets in adult rats. 735 92

A human metabolic study was conducted to observe the effect of level of protein intake on urinary calcium, calcium absorption and calcium balance in older adults and to further study the mechanisms of protein-induced hypercalciuria. An increase in protein intake from about 47 to 112 g while maintaining calcium, magnesium and phosphorus intakes constant caused an increase in urinary calcium and a decrease in calcium retention. Glomerular filtration rate was increased and fractional renal tubular reabsorption was decreased by the increase in protein intake; total renal acid, ammonium and sulfate excretions more than doubled, whereas urinary sodium decreased by 38%. The changes in urinary calcium were positively correlated with the increase in total renal acid and sulfate excretion as well as with the decrease in fractional renal tubular reabsorption of calcium. Thus, the data indicate that protein-induced hypercalciuria is due to an increase in glomerular filtration rate and a decrease in fractional renal tubular reabsorption of calcium, the latter of which may be caused by the increased acid load on the renal tubular cells.
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PMID:Studies on the mechanism of protein-induced hypercalciuria in older men and women. 735 1

Quantitative methods are described for the analysis of pH, sodium, ammonium, potassium, calcium, magnesium, chloride, phosphate, and sulfate, as well as terephthalic acid and dimethyl terephthalate, in a single urine sample as small as 20 microliter. The procedure utilizes ion chromatography and atomic absorption for electrolyte analysis, a microelectrode for pH measurement, and high-performance liquid chromatography for analysis of the organic compounds. The techniques are applied to urine samples freshly collected from rats ingesting dietary dimethyl terephthalate. Specific changes in urinary ions, including hypercalciuria and urinary acidosis, are shown to develop as a consequence of dimethyl terephthalate ingestion. The results indicate that metabolism of dimethyl terephthalate to terephthalic acid occurs extensively in Fischer-344 rats, and accounts for the ion changes that are observed.
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PMID:Microanalysis of urinary electrolytes and metabolites in rats ingesting dimethyl terephthalate. 744 34

Prolonged infusion of magnesium sulfate has been used for the treatment of refractory preterm labor. Long-term magnesium sulfate tocolytic therapy either alone or in combination with other tocolytic agents has been reported to be safe and effective with minimal maternal side effects. There has been only one previous report of a disturbance in maternal calcium homeostasis, which included decreased distal radius bone density and hypercalciuria as a result of prolonged magnesium sulfate infusion. This article reports the first case of bilateral fracture of the calcanei in the postpartum period secondary to osteoporosis associated with prolonged magnesium sulfate tocolysis and bed rest. A 35-year-old white female with a triplet pregnancy of 25 weeks' gestation was admitted in preterm labor. Bed rest, intravenous magnesium sulfate tocolysis, and intermittent subcutaneous terbutaline were necessary to maintain uterine quiescence for 65 days. The patient received weekly betamethasone for 6 weeks for the acceleration of fetal lung maturation. Daily prenatal multivitamins and low-dose subcutaneous heparin for thromboprophylaxis were given. Efforts at tocolysis were ultimately not successful and the patient underwent a cesarean section delivery at 34 2/7 weeks' gestation. The patient's postoperative course was complicated by osteoporosis and bilateral stress fractures of the calcanei. This case report demonstrates that stress fractures secondary to osteoporosis may be associated with prolonged magnesium sulfate therapy and bed rest in higher order multiple pregnancy. Other possible contributing factors to osteoporosis include heparin thromboprophylaxis and suboptimal calcium supplementation. Therefore, in circumstances of prolonged bed rest and magnesium sulfate tocolysis, additional daily calcium supplementation would be well advised.
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PMID:Long-term magnesium sulfate tocolysis and maternal osteoporosis in a triplet pregnancy: a case report. 947 87

The relationships between dietary protein and sulfur amino acid (methionine and cystine or taurine) intakes and urinary calcium excretion were examined both in animals and in young men. Thirty-two adult Wistar rats were divided into 4 groups, i.e., basal diet (group I), supplemented with albumin (II), methionine and cystine (III), or taurine (IV). During the 5-week feeding period, food consumption was recorded and 48 h urine samples were collected 4 times for each rat. Urinary calcium, creatinine and sulfate were measured. The results showed that the calcium and sulfate excretion in rats in group II and III were significantly higher than rats in the basal diet group. In contrast, supplementing a basal diet with taurine did not increase sulfate excretion and failed to induce hypercalciuria. The same result was also observed in the study carried out in Chinese young men. An increase in protein intake from 67 g to 107 g caused an increase in urinary calcium and sulfate. Supplementation with methionine and cystine in an amount to simulate those in the high protein diet had a similar effect. Adding taurine to the diet had no effect on urinary calcium and sulfate excretion. About 60 percent of the supplemented taurine in the diet was detected in the urine.
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PMID:The effect of dietary sulfur-containing amino acids on calcium excretion. 963 66

Distal renal tubular acidosis (dRTA) is generally associated with hypercalciuria, hypocitraturia, and nephrolithiasis. Our intention was to study glycosaminoglycans (GAGS) and nephrocalcin (NC), two well-known crystal growth inhibitors, in a population with endemic dRTA and nephrolithiasis in northeast (NE) Thailand. We studied 13 patients, six with dRTA and seven with nephrolithiasis with normal or undefined acidification function. Six healthy adults living in the same area as the patients and another six from the Bangkok (BKK) area were used as controls. We measured urinary pH, ammonia, calcium, citrate, magnesium, oxalate, potassium, sodium and uric acid. GAGS were determined by an Alcian blue precipitation method and were qualitated by agarose gel electrophoresis after being isolated using 5% cetyltrimethylammonium bromide at pH 6.0. NC isoforms were isolated as previously described by Nakagawa et al. Citrate was higher in BKK controls ( p<0.04). There was a striking difference among GAGS from BKK when compared with other groups (103.85+/-10.70 vs. 23.52+/-8.11 for dRTA, 22.36+/-14.98 for kidney stone patients and 14.73+/-2.87 mg/ml in controls from the NE region, ( p<0.0001). dRTA and stone-forming patients excrete proportionally more (C+D) than (A+B) NC isoforms ( p<0.05). Also, their NC showed a 100-fold weaker binding capacity of calcium oxalate monohydrate crystals. The ratio of chondroitin sulfate/heparin sulfate in GAGS was approximately 9/1. In addition to the traditional risk factors for nephrolithiasis in dRTA, GAGS and NC might play an important role in the pathogenesis of stone formation in this population.
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PMID:Kidney stone inhibitors in patients with renal stones and endemic renal tubular acidosis in northeast Thailand. 1475 48

Urinary calcium excretion increases by 1-2-fold during gestation in normal, uncomplicated pregnant women. Hypercalciuria occurs in all trimesters and elevates urine supersaturation with regards to calcium oxalate. However, crystalluria has not been a frequent clinical finding and stone formation is not a common complication of pregnancy. To elucidate this discrepancy we measured various chemical entities (i.e. calcium, oxalate, uric acid, phosphorous, magnesium, citrate, sulfate and thiosulfate) in urine at the end of each trimester of 25 pregnant women. Twenty-five healthy women served as controls. Our observations show that endogenous thiosulfate, a natural component of urine, increased considerably during pregnancy to approximately 36, 38 and 40 microM/24 hour at the end of each three trimesters. One month after delivery, endogenous thiosulfaturia and hypercalciuria, in parallel, returned to initial normal values. Consequently, it seems that gestational hyperthiosulfaturia protects hypercalciuric normal pregnant women from the risk of nephrolithiasis.
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PMID:Gestational urinary hyperthiosulfaturia protects hypercalciuric normal pregnant women from nephrolithiasis. 1578 22

Although idiopathic hypercalciuria (IH) is associated with reduced bone mineral density (BMD), no studies to date have identified predictors of BMD change over an extended period of observation. We have studied change in femoral neck and spine BMD z-scores in men and women with IH and stone disease (IHSF) and their first-degree relatives in order to determine the predictive value of commonly made clinical measurements. Urine calcium excretion was inversely correlated with change in femoral neck z-score over 3 years, and marginally correlated with fall in spine z-score. Markers of bone turnover, serum calcitriol, and urine measurements of acid-base balance such as ammonium and sulfate had no predictive value, nor did calcium intake assessed using a well-established questionnaire. It would appear that IHSF with the highest 24-h urine calcium excretion rates are at highest risk for loss of femoral neck bone mineral over a 3-year period.
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PMID:Urine calcium excretion predicts bone loss in idiopathic hypercalciuria. 1694 Oct 29

The Westernized diet is acidogenic due to the high content of sulfur-containing amino acids and relative deficiency of potassium organic anions. Chronic acid loads result in hypercalciuria and negative calcium balance often associated with loss of bone mineral. Alkali therapy tends to reverse the hypercalciuria but little is known regarding its effect on bone as assessed by bone histomorphometry. The present study utilized dynamic bone histomorphometry to evaluate the effects of alkali therapy on acid-induced changes in bone turnover. Serum and urine analyses and bone histomorphometry were assessed in adult rats after 2 months of either a low casein (LC) or high casein (HC) diet supplemented with either potassium chloride (KCl) or potassium citrate (KCit). Compared to animals on LC-KCl diet, HC-KCl diet delivered a substantial acid load as shown by significant increases in urinary sulfate, ammonium, and net acid excretion, and a lower urinary pH and citrate excretion without detectable changes in serum parameters. The acid load also resulted in hypercalciuria. Dynamic and static bone histomorphometry disclosed a significant reduction in cancellous bone volume and trabecular number associated with a 2.5-fold increase in eroded and a 3.5-fold increase in osteoclastic surfaces. There was also a near 2-fold increase in bone formation rate in rats on the HC-KCl diet. When animals on the HC diet were given KCit instead of KCl, all of the aforementioned changes in urine biochemistry and bone turnover were significantly attenuated or entirely prevented. These findings underscore the deleterious effects of high animal protein intake in promoting hypercalciuria and increasing bone turnover. Co-administration of potassium alkali attenuates or prevents these changes. In this animal model of high dietary animal protein intake, the major skeletal effect of alkali therapy is to reduce bone resorption, with little or no effect on bone formation.
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PMID:Biochemical and histological assessment of alkali therapy during high animal protein intake in the rat. 1965 Dec 55


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