Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In male healthy controls (n = 12), male renal calcium stone patients with either normocalciuria (NC; n = 12) or idiopathic hypercalciuria (I-HC; n = 12), all ideally matched for age and body weight, the response of variables of mineral metabolism to a calcium-rich oral test meal was evaluated. In all groups the postprandial urinary cyclic AMP is decreased as compared with fasting urine, indicating that the parathyroid glands are suppressible by oral calcium. However, in I-HC serum total calcium was significantly higher than in controls both basally and in the postprandial period; the associated mid-regional (bioinactive) serum parathyroid hormone was also elevated, but serum parathyroid hormone recognizing the amino terminal (bioactive) region of the molecule was significantly decreased. Also in I-HC, serum alkaline phosphatase is elevated, whereas urinary hydroxyproline in both fasting and postprandial urine is unchanged. The NC group holds an intermediate position between I-HC and controls. It can be concluded that I-HC subjects may suffer from a more basic disturbance of calcium metabolism which may help explain the nature of their hypercalciuria.
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PMID:Fasting and post-calcium load serum calcium, parathyroid hormone, calcitonin, in male idiopathic calcium urolithiasis--evidence for a basic disturbance in calcium metabolism. 366 61

1. Vitamin-D-deficient pigs were fed on a phytate-phosphorus diet and treated with vitamin D3 (+D) to examine the time-course of adaptative changes in plasma minerals, vitamin D metabolites, parathyroid hormone (PTH) and calcium balance and intestinal Ca-binding protein (CaBP). 2. The 5-week vitamin D repletion (25 micrograms cholecalciferol/kg diet) regimen restored plasma Ca, P and alkaline phosphatase (EC 3.1.3.1) to normal, decreased PTH and markedly and rapidly increased plasma 25-hydroxycholecalciferol (25-OHD, sevenfold after 4 d) and 1,25-dihydroxycholecalciferol (1, 25(OH)2D3, 1.8-fold after 4 d). 3. CaBP concentrations were markedly elevated all along the digestive tract, especially in the distal regions. 4. Ca absorption and retention were enhanced (fourfold and sixfold respectively) by the +D diet. 5. The improved Ca absorption, coupled with increased CaBP and 1,25(OH)2D3 levels, suggest that vitamin D metabolism in phytate-P-fed pigs is sensitive to the depressed Ca availability due to phytate feeding. It also indicates that CaBP may play an important role in the adaptation of Ca absorption. 6. Persistent hypercalciuria indicates that mineral metabolism was still affected by the phytate nature of the dietary P in spite of the vitamin D treatment.
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PMID:Effects of vitamin D on calcium regulation in vitamin-D-deficient pigs given a phytate-phosphorus diet. 367 38

The relation between signs and symptoms of Paget's disease of bone was studied in 180 patients consecutively submitted for treatment. In these patients 826 lesions were identified by scintigraphy. The intensity of scintigraphic uptake was correlated with long-term calcium uptake in bone. The frequency distribution of lesions over the patients was compatible with a 65 per cent chance of local disease once the patient had been exposed to an extraneous agent. The spatial distribution within a skeleton was related to the local density of the osteoclast population. The particular frequency distribution resulted in a log-normal distribution diagram for anatomical spread. Within lesions, increases in numbers of osteoclasts and osteoblasts were proportional and these too had a log-normal distribution. Increases of alkaline phosphatase levels and hydroxyproline excretion were closely related and reflected anatomical spread on the one hand and local activity on the other. They were also closely correlated with overall calcium fluxes. It was shown that alkaline phosphatase is the more sensitive and hydroxyproline the more accurate of the biochemical signs. Maximum values, corresponding to total skeletal disease, were approximately 25 times the upper limit of normal. Equilibrium between bone formation and resorption was not always maintained. There were, indeed, wide variations of urinary calcium, which were significantly related to the difference between bone formation and resorption, but the extracellular calcium homeostasis was generally maintained. This may explain the frequent occurrence of normocalcaemic and hypercalcaemic hyperparathyroidism. The hypercalciuria constitutes an additional risk for urolithiasis in men. The most frequent complaint was pain (86 per cent). Extent of lesions was important, but a major decisive factor was the specific nature of the bone affected. The findings allowed assessment of the relative importance of the various signs, symptoms and locations as criteria of disease severity and as indications for treatment.
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PMID:Relation between signs and symptoms in Paget's disease of bone. 371 67

A single case of hypophosphatemic rickets with hypercalciuria and an elevated level of serum 1,25 dihydroxyvitamin D is reported. The characteristic features (genu valgum, rickets, short stature, increased renal phosphate excretion, decreased serum phosphorus level, elevated serum alkaline phosphatase level, and normal serum calcium level) were comparable to those in hypophosphatemic vitamin D resistant rickets. Massive doses of 1 alpha-hydroxyvitamin D were not effective for the rickets and the biochemical defect in this patient. Long-term phosphate supplementation on its own resulted in the reversal of all clinical and biochemical abnormalities except for the decreased ratio between the maximum tubular reabsorption rate for phosphorus and the glomerular filtration rate. In this patient, the concentration of serum 1,25 dihydroxyvitamin D seemed to be controlled by the concentration of serum phosphorus rather than by the serum parathyroid hormone level. It is noted that this is the first case of a single hypophosphatemic rickets with hypercalciuria.
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PMID:A single case of hypophosphatemic rickets with hypercalciuria. 376 Nov 17

Fourteen very low birthweight infants (mean +/- SD 1,070 +/- 180 g and 29.3 +/- 1.9 weeks gestation) fed their own mother's milk were clinically followed until 3-4 months of age with frequent measurements of serum calcium, phosphorus, magnesium, 25-hydroxyvitamin D (25-OHD), parathyroid hormone, alkaline phosphatase, and albumin, and urine calcium, phosphorus, and magnesium. These infants were matched for birthweight and gestation with 14 infants (1,075 +/- 152 g and 29.0 +/- 1.7 weeks) who had been similarly followed during concomitant studies of infants fed standard formula (Similac 20 cal/oz). Urine phosphorus was markedly lower in the breast milk-fed group from initiation of feedings, and serum phosphorus became significantly lower at and after 6 weeks of age. The fall in serum phosphorus was accompanied by a marked calciuria. Parathyroid hormone was suppressed in the breast milk-fed group, although serum calcium was not elevated and did not differ from formula-fed infants. A high incidence of moderate-severe hypomineralization on radiographs was seen in both breast milk- and formula-fed groups. Six of 14 breast-fed infants required phosphorus supplementation at 8-10 weeks of age because of significant hypophosphatemia, hypercalciuria, and hypomineralization. These infants differed from those not requiring phosphorus supplements by being smaller at birth but not of lower gestation, and having persistently low serum 25-OHD at and after 6 weeks of age.
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PMID:Serial serum 25-hydroxyvitamin D and mineral homeostasis in very premature infants fed preterm human milk. 387 19

The stimulation of cyclic AMP production by human renal cortical membranes in the presence of the GTP analogue 5'-guanylimidodiphosphate and a calcium chelator represents a homologous assay system for the evaluation of biologically active parathyroid hormone (bioPTH) in human serum. Bioactive PTH was raised above normal (normal range: undetectable to 4.6 pmol human PTH(1-34) per 1) in 13/17 (76%) patients with primary hyperparathyroidism, in 5/6 (83%) patients with surgically proven hyperparathyroidism secondary to chronic renal failure, in 4/5 (80%) patients with hyperparathyroidism secondary to hypocalcaemia, in all three patients with pseudohypoparathyroidism, in 5/17 (29%) patients with osteoporosis and in 1/9 (11%) patients with renal stones and/or hypercalciuria. Bioactive PTH correlated positively with immunoreactive PTH (iPTH) measured with a radioimmunoassay predominantly recognizing the middle- and carboxyl-terminal region of the PTH molecule (r = 0.503, P less than 0.001). A positive correlation (r = 0.572, P less than 0.05) was found between values of serum calcium and bioPTH in the group with primary hyperparathyroidism. Immunoreactive PTH did not correlate significantly with calcium in this group. In the other patients except those who had chronic renal failure, a negative correlation between serum calcium and both bioPTH and iPTH was observed (P less than 0.01). When alkaline phosphatase was compared with bioPTH in all patients, the correlation was positive (r = 0.390, P less than 0.01); no significant correlation existed between iPTH and alkaline phosphatase in the patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal adenylate cyclase assay for biologically active parathyroid hormone: clinical utility and physiological significance. 394 39

Combined treatment with oral phosphate and 1 alpha (OH)D3 was carried out in nine children with familial hypophosphatemic rickets. All nine had positive responses over a four- to six-year period as judged by healing of rickets, change in growth rate, decrease in alkaline phosphatase activity, and symptomatic improvement. In two patients therapy was stopped for a short time because of hypercalcemia. In one patient in whom therapy was effective there was a significant reduction in creatinine clearance which necessitated cessation of treatment. The results of this study suggest that combined treatment with 1 alpha(OH)D3 and oral phosphate is an effective form of therapy for this condition, but that the balancing of these two modalities of therapy in each patient is essential if hypercalcemia and hypercalciuria, on the one hand, and secondary hyperparathyroidism, on the other, are to be avoided. A simple means of balancing these therapeutic modalities is suggested.
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PMID:Long-term treatment of familial hypophosphatemic rickets with oral phosphate and 1 alpha-hydroxyvitamin D3. 626 14

1. The effects of phosphorus deprivation on phytate digestibility, phosphorus utilization and intestinal phytase (EC 3.1.3.8) and alkaline phosphatase (EC 3.1.3.1) in rats were investigated. 2. P deprivation was achieved by giving rats a diet containing 3 g P/kg and resulted in hypophosphataemia, hypercalcaemia, hypercalciuria, and lower levels of P absorbed and retained, and calcium retained. 3. Rats adapted to P deprivation by increasing the digestion of total dietary-P and phytate-P. 4. Levels of intestinal alkaline phosphatase and alkaline phytase were not different between the two treatment groups. 5. P deprivation in the rats given the marginal-P diet may be a result of a lower absorption of total dietary-P or increased absorption of inositol phosphates formed during the enzymatic hydrolysis of phytate which are not readily utilized by the rat. 6. These results suggest that intestinal phytase and alkaline phosphatase do not play a role in the adaptive increase in phytate digestibility by rats given marginal-P diets. The adaptation may result from enhanced phytase or alkaline phosphatase synthesis by the gastrointestinal microflora stimulated by a lower level of P in the digesta.
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PMID:Adaptive increase in phytate digestibility by phosphorus-deprived rats and the relationship of intestinal phytase (EC 3.1.3.8) and alkaline phosphatase (EC 3.1.3.1) to phytate utilization. 629 37

Diabetes mellitus was induced in Lewis rats by streptozotocin, and these animals and control rats fed ad lib were studied after 7 weeks. At the time of sacrifice, nondecalcified histological sections of bone were prepared and subsequently quantitated by micromorphometric techniques. In addition, tibial alkaline phosphatase and mineral ash content were determined. The bones obtained from the diabetic animals are characterized by significant decrements in the quantities of osteoid and osteoclasts and by failure to acquire a tetracycline label. These histological features are attended by reduced quantities of urinary hydroxyproline and tibial alkaline phosphatase. As compared with control animals fed ad lib, diabetic rats are hyperphosphatemic and markedly hypercalciuric. Circulating alkaline phosphatase is also elevated and associated with a parallel increase in intestinal content of this enzyme. Although serum corticosterone levels are increased, diabetes is associated with decrements in both circulating immunoreactive parathyroid hormone and 1,25(OH)2D. We conclude that prolonged streptozotocin-induced diabetes mellitus in the rat results in reduced bone turnover. The relative roles that functional caloric deprivation, low circulating levels of 1,25(OH)2D, hypercalciuria, hypercortisolemia, and decreased blood parathyroid hormone levels play in the genesis of these skeletal abnormalities remain to be determined.
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PMID:The effect of streptozotocin-induced chronic diabetes mellitus on bone and mineral homeostasis in the rat. 645 Feb 54

Using an in vitro method, the uptake of radio-labelled Ca2+ by jejunal biopsy specimens from control subjects, patients with idiopathic hypercalciuria and patients with renal stones without hypercalciuria, were compared. Radio-labelled Ca2+ uptake was investigated over the concentration range 0.1-5.0 mmol/l. For all subjects there was a linear relationship between Ca2+ uptake and medium concentration suggesting that Ca2+ uptake was a passive process. There was no significant difference in Ca2+ uptake between control subjects and patients with renal stones without hypercalciuria. Patients with idiopathic hypercalciuria, both absorptive and renal subtypes, showed increased Ca2+ uptake at all incubation medium concentrations. Assays of various biochemical parameters including alkaline phosphatase, Ca2+-activated ATPase, cyclic AMP and Ca2+-binding protein, in jejunal biopsy specimens showed no significant differences between control subjects and patients with idiopathic hypercalciuria. The results suggest that the intestinal abnormality in idiopathic hypercalciuria is due to enhanced permeability of the brush border membrane to Ca2+, possibly mediated by alterations in membrane lipids.
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PMID:Studies on intestinal calcium absorption in patients with idiopathic hypercalciuria. 654 1


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