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)

The cuase for the intestinal hyperabsorptionof calcium (Ca) in various forms of hypercalciurias was explored by a careful measurement of plasma 1 alpha, 25-dihydroxycholecalciferol [1 alpha, 25-(OH)I D] and by an assessment of intestinal Ca absorption and of parathyroid function. In 18 cases of primary hyperparathyroidism (PHPT), the mean plasma concentration of 1 alpha, 25-(OH)2D was significantly increased (4.9 +/- 2.2 SD ng/dl vs. 3.4 +/- 0.9 ng/dl for the control group), and was significantly correlated with fractional Ca absorption (alpha) (r = 0.80, P less than 0.001). Plasma 1 alpha, 25-(OH)2D was also correlated with urinary Ca (P less than 0.05), but not with serum Ca or phosphorus (P), P clearance, urinary cyclic AMP, or serum immunoreactive parathyroid hormone. In 21 cases of absorptive hypercalciuria (AH), plasma 1 alpha, 25-(OH)2D was elevated in one-third of cases, and the mean value of 4.5 +/- 1.1 ng/dl was significantly higher than that of the control group (P less than 0.01). Since relative hypoparathyroidism may be present, the normal absolute value of plasma 1 alpha, 25-(OH)2D, found in two-thirds of cases of AH, may be considered to be inappropriately high. Moreover, in the majority of cases of AH, the data points relating plasma 1 alpha, 25-(OH)2D and alpha fell within 95% confidence limits of values found in non-AH groups (including PHPT). The results suggest that the intestinal hyperabsorption of Ca in PHPT aw AH may be vitamin D dependent. However, the disturbance in vitamin D metabolism may not be the sole cause for the high Ca absorption in AH, since in some patients with AH, the intestinal Ca absorption appears to be inapp
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PMID:The role of 1 alpha, 25-dihydroxyvitamin D in the mediation of intestinal hyperabsorption of calcium in primary hyperparathyroidism and absorptive hypercalciuria. 19 63

We have investigated an 18-yr-old hypercalciuric female with features of both renal hypercalciuria and pseudohypoparathyroidism. She had increased circulating parathyroid hormone levels, which are common to both diseases. She also had a modest hypocalcemia and low normal basal cAMP excretion, both of which are more likely to occur in pseudohypoparathyroidism. She also had Albright's osteodystrophy, which is frequent in patients with pseudohypoparathyroidism and has never been reported in patients with renal hypercalciuria. In contrast to patients with pseudohypoparathyroidism, her serum 1,25-dihydroxycholecalciferol level was increased and her renal responses to parathyroid hormone infusion, including renal calcium reabsorption, were normal. This patient, therefore, raises the possibility that some patients with renal hyperalciuria may have a forme fruste of pseudohypoparathyroidism.
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PMID:Albright's osteodystrophy in a patient with renal hypercalciuria. 22 62

Vitamin D-dependent CaBP isolated from Rat renal cortex (rCaBP) was measured in phosphorus-depleted (OP) and control (C) Rats, either vitamin D-deficient (OD) or vitamin D-supplemented (1 or 10 i. u.). A low molecular weight fraction was isolated from renal cortex by "Sephadex G-100" chromatography and rCaBP activity quantitated by saturation analysis using a 45 Ca chelex assay. The results indicated that phosphorus deprivation resulted in the increase in the vitamin D-dependent rCaBP as well as in the intestinal CaBP. As a marked hypercalciuria was noted in all OP Rats and as the rCaBP activity was high in vitamin D-supplemented Rats and hardly detectable in vitamin D-deficient Rats, the implication of the rCaBP in the large hypercalciuria can be definitely ruled out. Furthermore when vitamin D-supplementation ranged from 1 to 10 i. u. vitamin D, while the serum calcium level was increasing a decrease could be noticed in the large hypercalciuria. This deserves to be related to the increase in rCaBP activity. The high CaBP activity probably resulting from the renal synthesis of 1,25-dihydroxycholecalciferol stimulated by phosphorus-deprivation could represent the molecular basis of the calcium tubular reabsorption increased by vitamin D. Thus a vitamin D-dependent protein implicated in an ion-selective transport could be involved in the tubular calcium reabsorption as well as in the intestinal calcium absorption.
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PMID:[Increase in the renal calcium-binding protein (CaBPr) in the presence of vitamin D in growing, phosphate deficient rats. Possible role in tubular calcium reabsorption]. 82 36

The rate of reversal of hypercalcaemia or hypercalciuria induced by calciferol, dihydrotachysterol, 1-alpha-hydroxycholecalciferol (1-alpha-OHD3), or 1-alpha, 25-dihydroxycholecalciferol (1-alpha, 25-(OH)2D3) was measured in three normal subjects, two patients with osteoporosis, and 14 patients with disorders resistant to vitamin D. The half time for reversal after stopping 1-alpha, 25 (OH)2D3 was less than that after stopping 1-alpha-OHD3, calciferol, or dihydrotachysterol. The differences observed were independent of the dose given or length of treatment. When 1-alpha-OHD3 or 1-alpha-25-(OH)2D3 was stopped patients with vitamin D resistant states (hypoparathyroidism, renal tubular hypophosphataemia, or chronic renal failure) showed less rapid reversal of hypercalcaemia and hypercalciuria than did normal subjects. These studies show one potential advantage of 1-alpha-25-(OH)2D3 over vitamin D, and possibly over 1-alpha-OHD3, in the management of vitamin D resistant states.
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PMID:Rate of reversal of hypercalcaemia and hypercalciuria induced by vitamin D and its 1alpha-hydroxylated derivatives. 83 19

Magnesium absorption was studied in the normal human jejunum and ileum by in vivo intestinal perfusion, using test solutions containing from 0 to 20 mM Mg (as MgCl2). As luminal Mg concentration was increased, the rate of absorption in the jejunum rose progressively with a tendency towards saturation at the higher concentrations. The kinetics and rates of Mg absorption in the ileum were comparable to those in the jejunum, with the exception that at higher luminal concentrations the ileal absorptive process was fully saturated. Using test solutions containing various combinations of Ca and Mg, we found that Ca had little or no influence on Mg absorption, even through Mg depressed Ca absorption to a modest extent. Patients with end-stage renal disease, who had a reduced rate of Ca absorption (presumably due to deficiency of 1,25-dihydroxycholecalciferol) were found to have a severe depression of Mg absorption. On the other hand, patients with absorptive hypercalciuria and nephrolithiasis, who had an increased rate of Ca absorption, were found to absorb Mg normally. These results suggest that Mg absorption in the human is mediated by a transport process different from that which facilitates Ca absorption, and that normal Mg absorption may be dependent on vitamin D. Our results do not establish whether or not the normal intestine can absorb Mg against an electrochemical gradient.
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PMID:Magnesium absorption in the human small intestine. Results in normal subjects, patients with chronic renal disease, and patients with absorptive hypercalciuria. 93 89

Treatment with 1,25-(OH)2D3 (calcitriol) was compared with placebo in a double-blind, randomized, parallel clinical trial of 24 months' duration. Subjects were white women with postmenopausal osteoporosis. The study was completed by 15 patients who received placebo and 12 patients who received calcitriol. Positive slopes were observed in the active treatment group for total body calcium, bone mineral content of the radius, bone mineral density of the lumbar spine, and radiographic absorptiometry of the middle phalanges. In contrast, negative slopes were observed for the bone mineral measurements in the placebo group. Measurement of urinary hydroxyproline and of serum alkaline phosphatase and osteocalcin suggested that the mechanism of action of 1,25-(OH)2D3 involved reduction of bone resorption. Hypercalciuria occurred regularly and preceded hypercalcemia by about 2 weeks. A decline in creatinine clearance was observed in two patients, one of whom had nephrolithiasis on sonography. Calcitriol is effective in preventing bone loss, but must be used with caution.
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PMID:Role of calcitriol in the treatment of postmenopausal osteoporosis. 218 76

Concentrations of total calcium and albumin were measured in serum specimens from 41 women at intervals before, during, and after 42 pregnancies. The albumin concentration decreased but the calcium decreased more slowly, so that the albumin-adjusted calcium concentration increased from conception to term. These findings, taken in conjunction with published observations of hypercalciuria, increased concentrations of 1,25-dihydroxycholecalciferol and calcitonin in serum, and decreased concentrations of intact parathyrin in serum, strongly suggest that maternal ionized calcium increases throughout normal pregnancy.
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PMID:Albumin-adjusted calcium concentration in serum increases during normal pregnancy. 229 7

In order to assess the long-term effects of calcitriol treatment in postmenopausal osteoporotic patients, 1.0 micrograms/d of calcitriol was administered in two divided doses for 1 to 8 years to 270 women with symptomatic, histologically proven postmenopausal osteoporosis. No calcium supplementation was given. Clinically, the treatment resulted in substantial relief from pain, with improvement of ambulancy. Intestinal calcium absorption, which was lower than normal at baseline, increased significantly and remained higher than the baseline value as long as calcitriol was administered. Urinary calcium absorption also increased, but hypercalcemia occurred, exceptionally and transiently, in only a few patients. Urinary hydroxyproline excretion did not increase, indicating that hypercalciuria was not of resorptive origin. Total-body density, determined by dual-photon total-body absorptiometry in 56 patients, showed an increase after 18 to 24 months of therapy in most cases. The occurrence of nontraumatic, clinically relevant fractures decreased noticeably as compared with the period preceding calcitriol treatment. No change occurred in renal function, and no renal stones developed. Calcitriol was an effective and safe treatment of postmenopausal osteoporosis.
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PMID:Long-term treatment with calcitriol in postmenopausal osteoporosis. 232 71

Idiopathic hypercalciuria (IH) is a heterogeneous disorder frequently observed in patients with nephrolithiasis. At one extreme of its clinical spectrum is fasting hypercalciuria (FH), a condition characterized by increased bone resorption and turnover. In previous studies we have shown that monocytes from patients with high turnover osteoporosis and from women in early postmenopause elaborate increased amounts of interleukin-1 (IL-1), a cytokine that stimulates bone resorption in vitro and in vivo. Since IL-1 could also mediate the resorptive mechanism of FH and cause a clinically significant bone loss, we have studied the relationship of IH, vertebral mineral density, bone turnover, and monocyte IL-1 activity in 47 patients with absorptive hypercalciuria (AH), 23 with FH, and 38 nonhypercalciuric subjects with recurrent nephrolithiasis (controls). Vertebral mineral density, as measured by quantitative computer tomography, was decreased in each of the three patient groups, but was significantly lower in FH patients than in AH patients or control subjects. Twenty-four-hour total urinary hydroxyproline excretion was increased in FH patients compared to that in AH patients or controls, but blood levels of osteocalcin were not. Monocytes from FH subjects yielded significantly more IL-1 (alpha + beta) activity than those from AH patients or controls; levels of IL-1 activity in monocytes of AH and control patients were similar. In IH subjects, significant correlations were found between IL-1 and hydroxyproline (r = 0.70; P less than 0.0001), IL-1 and quantitative computer tomography values (r = -0.49; P less than 0.005), and IL-1 and urinary calcium (r = -0.36; P less than 0.05). Serum PTH levels were within normal limits in all subjects and were similar in the three study groups, 1,25-Dihydroxyvitamin D3 levels, although higher in IH patients than in controls, were not significantly different in FH and AH subjects. Increased IL-1 activity and decreased vertebral mineral density are features of a subset of patients with IH. Although a cause-effect relationship remains to be established, increased monocytic IL-1 activity, rather than elevated PTH or 1,25-dihydroxyvitamin D3 levels, could underlie the resorptive component of FH.
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PMID:Increased monocyte interleukin-1 activity and decreased vertebral bone density in patients with fasting idiopathic hypercalciuria. 237 Feb 92

Adult cats with normal renal function were fed a nutritionally balanced, vitamin A-replete, experimental dry diet with or without ammonium chloride (NH4Cl) for 6 mo to study the effects of chronic dietary acidification on acid-base parameters and the metabolism of selected minerals. Dietary balance studies were performed monthly. Blood and urine samples were collected monthly to evaluate acid-base parameters, plasma parathyroid hormone (PTH) and 1.25-dihydroxycholecalciferol levels. Ammonium chloride-treated cats had significantly lower blood and urinary pH, and lower blood bicarbonate concentrations. Treated cats also had higher blood ionized calcium concentrations, hypercalciuria and lower intestinal calcium absorption relative to baseline (prior to feeding the experimental diet) and to control cats. This resulted in the development of lower calcium balance in the first several months. PTH levels were unaffected by dietary acidification; however, 1.25-dihydroxycholecalciferol levels were significantly decreased in treated cats. Treated cats had negative potassium balance during 5 mo of dietary acidification. Magnesium, sodium, and phosphorus balances were lower, but positive, in treated cats compared to control cats. Cats consuming the NH4Cl-supplemented diet had increased chloride balance. Thus, chronic dietary acidification with 1.5% NH4Cl produced chronic metabolic acidosis and lower or negative, calcium and potassium balance.
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PMID:The effect of chronic dietary acidification using ammonium chloride on acid-base and mineral metabolism in the adult cat. 274 72


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