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

We studied a new hereditary syndrome of hypophosphatemic rickets and hypercalciuria in six affected members of one kindred. In all patients, the manifestations of disease began in early childhood. The characteristic features are rickets, short stature, increased renal phosphate clearance (the ratio between the maximal tubular reabsorption rate for phosphorus and the glomerular filtration rate [TmP/GFR] is 2 to 4 S.D. below the age-related mean), hypercalciuria (8.6 mg of urinary calcium per kilogram of body weight per 24 hours vs. the upper normal value of 4.0), normal serum calcium levels, increased gastrointestinal absorption of calcium and phosphorus, an elevated serum concentration of 1,25-dihydroxyvitamin D (390 +/- 99 pg per milliliter vs. the upper normal value of 110), and suppressed parathyroid function (an immunoreactive parathyroid hormone level of 0.33 +/- 0.1 ng per milliliter and a cyclic AMP level of 1.39 +/- 0.12 nmol per deciliter of glomerular filtrate vs. the lower normal values of 0.3 and 1.5, respectively). Long-term phosphate supplementation as the sole therapy resulted in reversal of all clinical and biochemical abnormalities except the decreased TmP/GFR. We propose that the pivotal defect in this syndrome is a renal phosphate leak resulting in hypophosphatemia with an appropriate elevation of 1,25-dihydroxyvitamin D levels, which causes increased calcium absorption, parathyroid suppression, and hypercalciuria. This syndrome may represent one end of a spectrum of hereditary absorptive hypercalciuria. Our observations support the importance of phosphate as a mediator in controlling 1,25-dihydroxyvitamin D production in human beings.
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PMID:Hereditary hypophosphatemic rickets with hypercalciuria. 298 3

Extensive metabolic studies were performed in a 14-year-old boy suffering from the rare clinical entity known as childhood idiopathic hypercalciuria associated with dwarfism, renal tubular abnormalities and bone lesions. The salient features were: hyperphosphaturia with hypophosphatemia, hypercalciuria with normocalcemia, elevated serum 1,25-dihydroxycholecalciferol[1,25(OH)2D3] levels, marked intestinal hyperabsorption of calcium and phosphorus, with low serum parathyroid hormone (PTH) and urinary adenosine 3':5'-cyclic monophosphate (c-AMP). Bone biopsy confirmed the clinical and radiological diagnosis of rickets. It appears that the following pathophysiological sequence is operating: primary renal phosphate leak with hypophosphatemia, increased 1,25(OH)2D3 synthesis, enhanced intestinal calcium absorption which in turn inhibits release of PTH and c-AMP. Hypercalciuria is seen to be secondary to both avid intestinal calcium absorption and depressed PTH activity, and rickets the result of phosphate depletion. Treatment with oral phosphorus only resulted in an acceleration of growth rate, cure of rickets, and return of urinary calcium excretion to normal values.
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PMID:Hypercalciuric rickets: metabolic studies and pathophysiological considerations. 298 52

Phosphorus intake was evaluated in 27 appropriate weight for gestational age, critically ill neonates who required total parenteral nutrition for 2 weeks. All received approximately 30 mg/kg/d elemental calcium. The low P intake group (1.01 mmol/kg/d, 30 mg/kg/d) showed signs of phosphate depletion: hypercalciuria, hypophosphatemia, and absence of phosphaturia. The high P intake group (1.67 mmol/kg/d, 50 mg/kg/d) did not have signs of P depletion; however, they had high urinary cyclic adenosine monophosphate excretion and marked phosphaturia, suggesting secondary hyperparathyroidism. The moderate P intake group (1.34 mmol/kg/d, 40 mg/kg/d) had evidence of neither phosphate depletion nor secondary hyperparathyroidism. This phosphorus dose appears to be appropriate for the very sick, poorly growing infant receiving total parenteral nutrition.
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PMID:Effect of phosphorus intake in total parenteral nutrition infusates in premature neonates. 303 Dec 60

In contrast to corn, wheat and triticale exhibit high phytase activities. This enzyme enhances phytic phosphorus availability, as demonstrated in pigs given wheat diets. To study the utilization of triticale phosphorus in pigs, the importance of dietary phytase content and the mineral and bone disorders related to high phytate feeding, a nutritional experiment was carried out in 12 growing pigs fed either a corn- or a triticale-based diet for 6 wk. The diets were almost identical except for the cereal component; their phosphorus contents were low (0.4%) and mainly phytic. The following parameters were measured: calcium and phosphorus balances, bone and plasma contents of calcium and phosphorus, plasma vitamin D metabolites and parathyroid hormone (PTH), bone bending moments and intestinal phosphatase activities. Both diets provoked a phosphorus deficiency, but hypophosphatemia occurred less rapidly, hypercalciuria and hypophosphaturia were less marked and phosphorus availability was greater when the triticale diet was fed. This was attributed to the high phytase content of triticale because intestinal phytase and alkaline phosphatase activities were similar in pigs fed either diet. Calcium absorption was not modified by calcium retention was greater for pigs fed triticale and led to higher bone scores. In conclusion, the higher the phytase activity of the diet, the greater the phytate P availability and the lower the bone-mineral disorders.
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PMID:Importance of cereal phytase activity for phytate phosphorus utilization by growing pigs fed diets containing triticale or corn. 303 49

1,25-Dihydroxyvitamin D (1,25-(OH)2D) plays a crucial role in the maintenance of blood calcium and phosphorus levels and in normal skeletal mineralization. The concentration of this metabolite in the blood is, by necessity, tightly regulated. The most important stimuli for renal 1,25-(OH)2D synthesis include parathyroid hormone (PTH), its second messenger cyclic adenosine monophosphate (cAMP) and phosphate deprivation. Hypocalcemia and calcitonin, initially thought to act via stimulation of PTH release, have now been shown to directly stimulate 1-hydroxylation. Estrogens also increase 1,25-(OH)2D production, probably by upregulating renal PTH receptors. Inhibitors of the renal 25-(OH)D 1 alpha-hydroxylase include 1,25-(OH)2D itself, hypercalcemia, and phosphate loading. The PTH-vitamin D axis as modulated by the serum ionized calcium level controls adaptation to alterations in dietary calcium and sodium intake and to changes in skeletal turnover based on the level of physical activity. Although normally the renal production of 1,25-(OH)2D is tightly regulated and changes little in response to vitamin D challenge, there are certain conditions in which 1,25-(OH)2D appears to be substrate-dependent. These include hypoparathyroidism, hyperparathyroidism, vitamin D deficiency, sarcoidosis and the anephric state, conditions in which PTH is not well-modulated by alterations in serum ionized calcium or in which extrarenal synthesis of 1,25-(OH)2D occurs. In several disorders, including absorptive hypercalciuria, pseudohypoparathyroidism, hypophosphatemic rickets, and tumoral calcinosis, the regulation of the renal 1 alpha-hydroxylase appears to be altered.
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PMID:Normal and abnormal regulation of 1,25-(OH)2D synthesis. 306 16

Hypercalciuria and negative calcium balance are potential complications of total parenteral nutrition (TPN). Dietary phosphorus has been observed to have an hypocalciuretic effect. The present study evaluates the effects of administration of increasing intravenous phosphorus (P) loads on urinary calcium excretion in TPN patients. Urinary calcium exceeded daily calcium intake by 50 mg/d when 700 mg/d P was administered, was equal to intake at 1000 mg/d P, and was 30 mg/d less than calcium intake when 1300 mg/d P was given. These findings suggest that TPN-induced hypercalciuria can be attenuated in the short-term by intravenous phosphate. Reevaluation of the phosphorus requirement in patients receiving long-term TPN should be considered.
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PMID:Reduction of total parenteral nutrition-induced urinary calcium loss by increasing the phosphorus in the total parenteral nutrition prescription. 308 31

This study was performed to evaluate the antihypercalciuric effect of calcitonin (CT), a potent inhibitor of bone osteoclastic activity, on idiopathic hypercalciuria (IH). Forty-two stone formers were studied: 18 suffered from fasting hypercalciuria (FH), 12 from nonfasting hypercalciuria (NFH) and 12 were normocalciuric stone formers (NSF). All patients received CT, 25 U/day sc for a period of 15 days. CT caused a statistically significant drop in urine calcium, phosphorus and hydroxyproline (OH-proline) excretion in FH patients and a concomitant increase in serum PTH levels. In this group the percentage variation (D%) of urine calcium decrease was linearly correlated with D% decrease in urine OH-proline. These results support the hypothesis that pathological bone reabsorption might be involved in the genesis of FH.
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PMID:The effects of calcitonin on idiopathic nephrolithiasis. Evidence of bone involvement in fasting hypercalciuria. 317 Nov 10

The linkage between immune cells and the osteoclast has become partially understood in the laboratory, but the full spectrum of clinical disorders of this relationship remain to be elucidated. We report a 29-month-old girl with recurrent infections and multiple fractures. Immune evaluation showed normal quantitative serum immunoglobulins but absent antibodies to the respiratory viruses and tetanus toxoid and decreased in vitro polyclonal-induced immunoglobulin production. Further analysis in vitro with separated lymphocyte populations showed normal B cell function but markedly increased suppressor T cell activity. The bone evaluation showed diffuse osteopenia on x-ray. Serum calcium, phosphorus, PTH, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D were normal for age. Urinary calcium excretion (24 h) was, however, two times normal. An iliac crest biopsy confirmed the presence of extreme osteopenia with normal mineralization and numerous small atypical osteoclasts resorbing the bone. No circulating plasma resorptive activity was demonstrated. Calcitonin therapy markedly diminished the patient's hypercalciuria. We speculate that this patient's increased bone resorption, decreased bone formation, and suppressor activity may be linked by a common pathway involving the abnormal function of immune cells. Since no similar constellation of findings has been previously reported, this case may represent a new congenital disorder: severe osteopenia associated with increased osteoclast activity in association with a defect in T cell immunoregulation.
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PMID:Malignant osteoporosis and defective immunoregulation. 319 63

The influence of continuous imbalanced high protein intake on the metabolism of minerals (calcium, magnesium, phosphorus) and renal function was the subject of a long-term experiment with rats. In the first part of the study particular attention was directed to the contribution of protein-induced endogenous acid production and renal excretion of hydrogen ions and sulphate to the development of hypercalciuria. For 61 weeks 200 male Wistar rats in eight groups were fed isocaloric diets, whose protein contents were increased from 13 to 26 and 40 J% at the expense of carbohydrate intake. The fat content of the diets was 40 J%. In two groups with 13 and 26 J% protein the effect of different kinds of animal protein was also studied, replacing casein by beef. Mineral contents were kept constant in these diets. To examine the excretion mechanisms of calcium and phosphorus especially under conditions of excessive protein intake, the ratio of calcium to phosphorus was varied in three diets with 40 J% protein by increasing both minerals alternatively or together from 0.6 to 1.2%. An increase in dietary protein content from 13 to 26 or 40 J% produced a sustained hypercalciuria and also hypermagnesiuria over a period of more than 400 days (after 58 weeks: 3.3, 5.9, and 6.8 mg calcium/day; 2.2, 3.3, and 3.4 mg magnesium/day; p less than or equal to 0.05). No adaptation to high protein intake occurred. Hypermagnesiuria, which equally hasn't been described before as a result of high protein intake, was accompanied by a reduced fecal excretion of magnesium. With increased protein intake (casein and beef) hypercalciuria and also hypermagnesiuria were positively correlated with an increased formation and renal excretion of hydrogen ions and sulphate, which resulted from protein catabolism. The dietary protein source influenced the extent of hypercalciuria, irrespective of a constant phosphorus intake. Although leading to equal increases in renal total acid and sulphate excretion, beef as the main protein source caused a lower calciuria than casein. High phosphorus intake caused the highest total acid excretion of all groups, but resulted in a reduced hypercalciuria and hypermagnesiuria and counteracted the influence of an increased protein intake.
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PMID:[The effect of long-term increased protein administration on mineral metabolism and kidney function in the rat. I. Renal and enteral excretion of calcium, magnesium, phosphorus, sulfate and acid]. 323 5

In the Federal Republic of Germany the average daily protein intake exceeds the Recommended Dietary Allowances for adults (0.8 g protein/kg body weight) by about 100%. On the other hand calcium intake is below the recommendations for certain age groups. Protein-induced hypercalciuria involves the risk of depletion of skeletal calcium stores, especially for older people who have a decreased absorption capacity for calcium. As a result of our study we postulate, that an altered renal function probably is one inducing factor of hypercalciuria. While urea excretion and serum urea concentration increased with an elevated dietary protein content from 13 to 26 or 40 J%, glomerular filtration rate remained unchanged. Fractional tubular reabsorption of calcium was significantly reduced by about 3% with increased endogenous acid production and renal excretion of hydrogen ions (first part of the study), which were accompanying a higher protein intake of 40 J% compared to 13 J% protein in the control group. Increasing the phosphorus content of the diet improved the reabsorption of calcium and magnesium. The kidneys of rats fed diets high in protein and phosphorus were hypertrophied. Histology of the kidneys showed signs of glomerulonephrosis. While the calcium content of the femora was slightly reduced with a higher protein intake of 40 compared to 13 J%, the magnesium content was increased (after 61 weeks: calcium from 261.4 to 257.1 mg/g dry fat-free wt [p less than or equal to 0.05]; magnesium from 3.2 to 3.5 mg/g dry fat-free wt [p less than or equal to 0.001]). Calcium and magnesium metabolism depends not only on the level of protein intake, but also on its interrelation with the dietary phosphorus content. With continuous high protein intake higher intakes for calcium, phosphorus and magnesium should be recommended, especially for older people.
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PMID:[The effect of long-term increased protein administration on mineral metabolism and kidney function in the rat. II. Kidney function and bone mineralization]. 323 6


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