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)

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 established prophylaxis for vitamin D-deficient rickets today is 400 IU vitamin D3 given daily during the first year of life. With this regimen, vitamin D intoxication is a rare event. Nevertheless, we have recently seen 4 infants with vitamin D intoxication after a so called "stoss" prophylaxis, i.e. twice 300,000 units (7.5 mg) vitamin D3 orally within 4 weeks. One patient presented with failure to thrive due to marked hypercalcemia (3.9 mmol/l) and nephrocalcinosis, 2 patients showed medullary nephrocalcinosis on ultrasonography and one patient had gross hematuria and spontaneous passage of a calculus. Three patients had massive hypercalciuria (calcium/creatinine ratio 1.8-4.8 mol/mol, normal less than 1). The 25 (OH) vitamin D3 plasma levels, measured only in 2 patients, were strikingly increased (270 and 158 nmol/l, respectively, normal 25-80). Urinary calcium excretion slowly decreased to normal values on a low calcium diet and high fluid intake. Nephrocalcinosis, however, persisted in 2 patients and showed a slight progression ultrasonographically in one patient. The short time interval between vitamin D administration and onset of symptoms and the subsequent clinical course provide strong evidence that hypercalciuria and nephrocalcinosis were due to vitamin D "stoss" prophylaxis in all four cases. In conclusion, there is no indication for vitamin D "stoss" prophylaxis for vitamin D-deficient rickets in infants. Vitamin D intoxication still has to be considered as a possible cause of hypercalciuria.
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PMID:[Vitamin D poisoning in infants: a preventable cause of hypercalciuria and nephrocalcinosis]. 131 65

Vitamin D has complex effects in bone: it stimulates matrix formation and bone maturation but also enhances osteoclastic activity and may influence differentiation of bone cell precursors. Calcitonin inhibits the function of osteoclasts, reducing bone resorption, thus, the combination of vitamin D and calcitonin could result in a positive bone balance. We tested the hypothesis that chronic treatment with high doses of vitamin D (150,000 U/week), moderate doses of salmon calcitonin (120 MRC U/week), and adequate Ca supplementation (1 g/day) could be beneficial in osteoporosis. Thirteen women with postmenopausal osteoporosis received this treatment for 2-6 years (mean 3.5 years). No side effects, hypercalcemia, or hypercalciuria occurred. There was marked reduction in bone pain. The fracture rate in 11 patients with vertebral compression fracture was 240/1,000 patient years, threefold lower than the reported 834 fractures for untreated patients of similar age. Single photon bone densitometry of the radius did not change. Iliac crest bone biopsies obtained at the initiation and conclusion of the study showed a 43% increment in trabecular bone volume (P = 0.0003), without changes of the normal osteoid thickness, surface, and volume. Because single photon densitometry reflects mostly cortical bone, the data suggest that the combination of vitamin D and calcitonin increases trabecular bone mass and prevents the fall of cortical bone mass in osteoporosis. Previous reports suggest that calcitonin alone or with small doses of vitamin D increased bone mass for about 2 years. The present study suggests a prolonged beneficial effect of the combination of high doses of vitamin D with rather moderate (less than 150 MRC U/week) doses of calcitonin in postmenopausal osteoporosis.
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PMID:Effect of calcitonin and vitamin D in osteoporosis. 250 3

In order to clarify the mechanisms of thiazide diuretic-induced hypocalciuria, the effect of a thiazide was studied for 7 days in seven patients with hypoparathyroidism on Vitamin D and one on calcium infusion, and seven euparathyroid patients with hypercalciuria. In the control group, calcium excretion (mg/24 hr) fell by 44% from 415 to 232 within 4 days and remained at this level. Plasma total calcium corrected for total protein did not change. In the hypoparathyroid group, calcium excretion fell by 11% from 351 to 311 and then returned to the base line level. Plasma total calcium (mg/100 ml) increased from 10.09 to 10.88, 11.29 and 10.77 at the end of the 2nd, 4th, and 7th day of thiazide administration. In the patient having i.v. calcium and no Vitamin D, neither plasma nor urinary calcium changed significantly. In both groups sodium excretion increased on the first 2 days and fell to or below base line level thereafter. Urinary phosphate, magnesium, and potassium increased, plasma phosphate rose, and magnesium and potassium fell. It is concluded that: (a) The hypocalciuric effect of thiazides requires the presence of parathyroid hormone and is not solely a result of sodium depletion. (b) The hypercalcemic effect of thiazides in hypoparathyroidism is due to increased release of calcium from bone and requires the presence of a pharmacologic dose of Vitamin D. (c) Thiazides enhane the action of parathyroid hormone on bone and kidney; Vitamin D can replace parathyroid hormone in this interaction in bone but not in kidney.
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PMID:The interactions of thiazide diuretics with parathyroid hormone and vitamin D. Studies in patients with hypoparathyroidism. 433 23

The state of vitamin D nutrition depends on synthesis in the skin under the influence of sunlight as well as on dietary intake. In European countries that do not fortify milk with vitamin D, reduced sun exposure is the major factor leading to a fall in body stores of vitamin D with age and to a high frequency of hypovitaminosis D in the elderly sick. In the US, because vitamin D is added to milk and the use of vitamin D supplements is more common, the dietary intake of vitamin D is relatively more important than in Europe, and the total vitamin D intake and body stores of vitamin D are generally higher. Nevertheless, body stores of vitamin D probably fall with age in the US as they do in Europe, and it is likely that some sick elderly persons in the US, especially among those confined to institutions, become vitamin D deficient. For several reasons, the vitamin D requirement increases with age, and a total supply of 15 to 20 micrograms/day (600 to 800 IU) from all sources is recommended. Special attention should be paid to persons most likely to need supplementation, such as the housebound, persons with malabsorption, and persons with interruption of the enterohepatic circulation. Osteomalacia, the bone disease produced by severe vitamin D deficiency, is less common in the US than in Europe, but subclinical vitamin D deficiency may contribute to the pathogenesis of hip fractures, both through increased liability to fall and through PTH-mediated bone loss. The extent to which vitamin D deficiency contributes to hip fractures in the US is unknown, and is an important area for future research. Excess intake of vitamin D or of its metabolites may result in hypercalcemia and extra-osseous calcification, particularly in arterial walls and in the kidney, leading to chronic renal failure. The dose of vitamin D that causes significant hypercalcemia is highly variable between individuals but is rarely less than 1000 micrograms/day. Smaller doses can cause hypercalciuria and nephrolithiasis and possibly impaired renal function. Vitamin D administration may raise plasma cholesterol but there is no convincing evidence that the risk of myocardial infarction is increased. The recommended total supply for the elderly of 20 micrograms/day is most unlikely to be harmful, except in patients with sarcoidosis or renal calculi.
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PMID:Vitamin D and bone health in the elderly. 676 68

Vitamin D and its metabolites are well-established regulators of bone mineral homeostasis. Their clearest role is in the prevention and treatment of rickets and osteomalacia, bone diseases characterized by inadequate bone formation, and mineralization. Much of the effectiveness of vitamin D and its active metabolite 1,25(OH)2D in treating such disorders rests with their ability to increase serum levels of calcium and phosphate principally by stimulating intestinal calcium and phosphate absorption. Osteoporosis is not a disease resulting from obvious deficiencies in vitamin D, calcium, and phosphate. More subtle deficiencies, however, may be found, especially among the elderly with decreased intake of dairy products, reduced sunlight exposure, and less efficient intestinal absorption of bone minerals. Such subtle deficiencies may account for the ability of vitamin D and calcium supplementation to have a beneficial effect on bone mineral density in this population. Estrogen administration to postmenopausal females raises 1,25(OH)2D levels, presumably through increased renal production, and this increase is associated with increased intestinal calcium transport. Serum measurements of the vitamin D metabolites in general, however, and 1,25(OH)2D in particular do not consistently show evidence of a decrease at the time of menopause. Although most studies show a fall in intestinal calcium transport with age, which can be reversed with 1,25(OH)2D or estrogen, even these observations have not been found consistently. Thus, some investigators have addressed the issue of tissue resistance to 1,25(OH)2D and have noted decreased VDR in the intestine and reduced 1,25(OH)2D accumulation by bone with age. Despite no obvious deficiency of vitamin D in most patients with osteoporosis, clinical trials with vitamin D or 1,25(OH)2D show promise. Vitamin D treatment will probably prove most efficacious in populations with marginal vitamin D intake and/or limited sunlight exposure; high doses would not be required, and the treatment would be safe. This would be a physiologic and not a pharmacologic use of vitamin D. The use of 1,25(OH)2D for treatment of osteoporosis in individuals with adequate nutrition and sunlight exposure may require somewhat higher than physiologic doses to be effective. Perhaps such doses are necessary to stimulate osteoblast activity and/or differentiation; by raising the serum calcium level, such doses of 1,25(OH)2D might block its otherwise stimulatory effect on osteoclast number and activity. Such doses run the risk of hypercalcemia and hypercalciuria, leading to nephrolithiasis and/or nephrocalcinosis. These undesirable side effects appear to be less common with the use of 1 alpha OHD compared with 1,25(OH)2D, but this may be because of the lower levels of calcium consumption in Japan where 1 alpha OHD is widely prescribed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of vitamin D, its metabolites, and analogs in the management of osteoporosis. 798 88

Vitamin D intoxication is a rare cause of hypercalcemia, which is associated with severe and prolonged morbidity. Hypercalcemia and/or hypercalciuria are the consequence of increases in both intestinal absorption and bone resorption. We report on 7 cases of vitamin D overdose (25-hydroxyvitamin D: 710 +/- 179 nmol/l; normal range: 20-90). The indications for vitamin therapy were osteoporosis (5), hypoparathyroidism (1), and osteomalacia (1). Enhanced bone resorption was demonstrated by increased fasting urinary calcium excretion (0.192 +/- 0.067 mmol/l GFR, normal < 0.045). Sequential biochemical measurements in the hypoparathyroid patient showed the persistence of abnormally elevated fasting urinary calcium and of serum 25-hydroxyvitamin D concentrations, even after normalization of plasma calcium, emphasizing that enhanced bone resorption is a prominent feature of vitamin D action. The intravenous administration of a single infusion of the bisphosphonate clodronate to 3 patients led to a correction of hypercalcemia/hypercalciuria, whereas prednisone therapy given to 2 other cases barely affected the abnormal biochemical values. These results indicate that enhanced bone resorption encountered in vitamin D intoxication could be favorably influenced by bisphosphonate treatment.
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PMID:Hypercalcemia and hyperosteolysis in vitamin D intoxication: effects of clodronate therapy. 808 37

Vitamin D topical analogues are now considered an excellent adjunct to the therapy of psoriasis. Systemic vitamin D3 treatment has been used occasionally, especially in case of associated hypocalcemia. We report five patients (aged 6, 16, 36, 58 and 79 years) successfully treated with vitamin D3 per os. Four had erythrodermic and/or pustulous psoriasis, and two of these had concomitant hypocalcemia. The fifth patient was a girl with pseudohypoparathyroidism and psoriasis vulgaris. The association of hypocalcemia and severe psoriasis is classical and was an incentive to try vitamin D treatment. A review of the literature showed that vitamin D can also be reported as a treatment of psoriasis vulgaris. Hypercalciuria and hypercalcemia are limiting risks. However calcium toxicity seems to be minor when vitamin D is given once a day at bedtime in doses lower than 2 micrograms/24 h. Double blind studies should be performed to determine the real efficacy of this treatment.
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PMID:[Treatment of psoriasis by oral calcitriol. A study of 5 cases and review of the literature]. 783 59

1. Vitamin D seems to play an essential role in the pathogenesis of idiopathic hypercalciuria at least in part via intestinal hyperabsorption of calcium. Hyperabsorption of calcium, in turn, might enhance the intestinal uptake of free oxalate, thus leading to hyperoxaluria. To verify this hypothesis we studied 75 calcium-stone-formers subdivided as follows: group 1 (15 patients) with isolated hyperoxaluria; group 2 (25 patients) with hyperoxaluria and hypercalciuria; group 3 (22 patients) with isolated hypercalciuria; group 4 (12 patients) with no metabolic abnormalities. 2. As expected, urinary calcium excretion differed in the various groups (P < 0.001), being highest in groups 2 and 3; urinary oxalate excretion, by definition highest in groups 1 and 2, was even more pronounced in group 2 than in group 1 (P < 0.05). Although in the normal range, the serum 1,25-dihydroxyvitamin D concentration was higher (P < 0.001) in the two hypercalciuric groups (2 and 3), showing peak levels in group 2. 3. When the data from the 75 stone-formers were pooled, there was a positive correlation between the serum concentration of 1,25-dihydroxyvitamin D and urinary calcium excretion (P < 0.001) and urinary oxalate excretion (P < 0.003), the latter relationship also being present when only the two hypercalciuric groups (groups 2 and 3) were considered together (P < 0.05). 4. Our data seem to confirm a relevant role for the vitamin D system in the pathogenesis of calcium nephrolithiasis due to increased intestinal calcium absorption, but also because this in turn induces a greater intestinal absorption of oxalate, thus leading to the occurrence or exacerbation of hyperoxaluria.
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PMID:Possible link between vitamin D and hyperoxaluria in patients with renal stone disease. 838 34

Vitamin D dependency is classified into two clinical disorders which are caused by genetic defect of vitamin D metabolism. Vitamin D dependent rickets type I and type II are the deficiency of 25-hydroxyvitamin D-1 alpha-hydroxylase and the defect of receptor for 1 alpha,25-dihydroxyvitamin D, respectively. In contrast, vitamin D resistance shows hypophosphatemia derived from disorder(s) of phosphate transport system in renal brush border membrane. There are three clinical entities such as hereditary hypophosphatemic rickets with hypercalciuria, familial hypophosphatemic rickets and oncogenic hypophosphatemic osteomalacia. However, the real pathogenesis of these disorders have not well been understood at present.
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PMID:[Vitamin D dependency and vitamin D resistance]. 838 22


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