cholecalciferol and Urinary-Calculi

The Women's Health Initiative (WHI) double-blind, placebo-controlled clinical trial randomly assigned 36,282 postmenopausal women in the U.S. to 1,000 mg elemental calcium carbonate plus 400 IU of vitamin D(3) daily or placebo, with average intervention period of 7.0 years. The trial was designed to test whether calcium plus vitamin D supplementation in a population in which the use of these supplements was widespread would reduce hip fracture, and secondarily, total fracture and colorectal cancer.. This study further examines the health benefits and risks of calcium and vitamin D supplementation using WHI data, with emphasis on fractures, cardiovascular disease, cancer, and total mortality.. WHI calcium and vitamin D randomized clinical trial (CT) data through the end of the intervention period were further analyzed with emphasis on treatment effects in relation to duration of supplementation, and these data were contrasted and combined with corresponding data from the WHI prospective observational study (OS).. Among women not taking personal calcium or vitamin D supplements at baseline, the hazard ratio [HR] for hip fracture occurrence in the CT following 5 or more years of calcium and vitamin D supplementation versus placebo was 0.62 (95 % confidence interval (CI), 0.38-1.00). In combined analyses of CT and OS data, the corresponding HR was 0.65 (95 % CI, 0.44-0.98). Supplementation effects were not apparent on the risks of myocardial infarction, coronary heart disease, total heart disease, stroke, overall cardiovascular disease, colorectal cancer, or total mortality, while evidence for a reduction in breast cancer risk and total invasive cancer risk among calcium plus vitamin D users was only suggestive.. Though based primarily on a subset analysis, long-term use of calcium and vitamin D appears to confer a reduction that may be substantial in the risk of hip fracture among postmenopausal women. Other health benefits and risks of supplementation at doses considered, including an elevation in urinary tract stone formation, appear to be modest and approximately balanced.

Topics: Aged; Bone Density Conservation Agents; Calcium Carbonate; Cardiovascular Diseases; Cholecalciferol; Dietary Supplements; Double-Blind Method; Drug Administration Schedule; Drug Therapy, Combination; Female; Hip Fractures; Humans; Middle Aged; Neoplasms; Osteoporosis, Postmenopausal; Osteoporotic Fractures; Risk Assessment; United States; Urinary Calculi

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.

Topics: Adult; Aged; Bone and Bones; Calcium; Chlorothiazide; Cholecalciferol; Clinical Trials as Topic; Dihydrotachysterol; Drug Interactions; Ergocalciferols; Female; Humans; Hypoparathyroidism; Kidney Tubules; Magnesium; Male; Methyclothiazide; Middle Aged; Natriuresis; Parathyroid Hormone; Phosphates; Potassium; Urinary Calculi; Vitamin D

Previous studies have described the inhibitory effects of citrate on calcium oxalate crystallization in place of crystal growth, but the effects of citrate on matrix proteins of stones has not been studied in vivo. To examine the effect of citrate on the matrix, we investigated the effect of citrate on osteopontin (OPN) expression, which we had previously identified as an important stone matrix protein. Control rats were treated with saline while rats of the stone group were treated with ethylene glycol (EG) and vitamin D3, and the citrate groups (low-dose and high-dose groups) were treated with a citrate reagent compound of sodium citrate and potassium citrate, in addition to EG and vitamin D3. The rate of renal stone formation was lower in the citrate groups than in the stone group. This was associated with a low expression of OPN mRNA in citrate-treated rats relative to that in the stone group. Citrate was effective in preventing calcium oxalate stone formation and reduced OPN expression in rats. Our results suggest that citrate prevents renal stone formation by acting against not only the crystal aggregation and growth of calcium oxalate but also OPN expression.

Topics: Animals; Blotting, Northern; Chelating Agents; Cholecalciferol; Citric Acid; Disease Models, Animal; Ethylene Glycol; Gene Expression; Immunohistochemistry; In Situ Hybridization; Male; Osteopontin; Oxalates; Rats; Rats, Wistar; RNA, Messenger; Sialoglycoproteins; Urinary Calculi

Urinary calcium stones are a pathological substance, and they show similarities to physiological mineralization and other pathological mineralizations. The expression of messenger (m) RNAs of osteopontin (OPN), matrix Gla protein (MGP), osteonectin (ON) and osteocalcin (OC) in bones and teeth has been described. We previously identified OPN as an important stone matrix protein. In addition, the spontaneous calcification of arteries and cartilage in mice lacking MGP was recently reported, a finding which indicates that MGP has a function as an inhibitor of mineralization. Here, we examined the mRNA expressions of OPN, MGP, ON, and OC in the kidneys of stone-forming model rats administered an oxalate precursor, ethylene glycol (EG) for up to 28 days. The Northern blotting showed that the mRNA expressions of OPN and MGP were markedly increased with the administration of EG, but their expression patterns differed. The OPN mRNA expression reached the maximal level at day 7 after the initiation of the EG treatment and showed no significant difference after 14 and 28 days, whereas the MGP mRNA expression rose gradually to day 28. The in situ hybridization demonstrated that the cell type expressing OPN mRNA was different from that expressing MGP. We suggest that OPN acts on calcification and MGP acts on suppression.

Topics: Animals; Blood Urea Nitrogen; Blotting, Northern; Calcium Oxalate; Calcium-Binding Proteins; Cholecalciferol; Disease Models, Animal; Ethylene Glycol; Extracellular Matrix Proteins; In Situ Hybridization; Kidney; Male; Matrix Gla Protein; Osteocalcin; Osteonectin; Osteopontin; Oxalic Acid; Rats; Rats, Wistar; RNA, Messenger; Sialoglycoproteins; Time Factors; Urinary Calculi

Topics: Animals; Calcium; Calcium, Dietary; Cholecalciferol; Magnesium; Rabbits; Urinary Calculi

After feeding various diets we studied the effects of dietary calcium, magnesium and phosphorus on the formation of struvite stones in rats with urinary tract infections, and also studied the effects of the administration of vitamin D3 and aluminium gel on stone formation. A low-magnesium diet decreased urinary magnesium and prevented stone formation, but a medium-calcium diet did not significantly decrease stone weight. A high-calcium diet decreased urinary phosphorus and inhibited stone formation. A high-calcium and high-phosphorus diet decreased urinary excretion of magnesium and inhibited stone formation. Although the administration of vitamin D3 did not inhibit stone formation, aluminium gel decreased the urinary level of phosphorus and prevented stone formation. A marked decrease in urinary magnesium and/or phosphorus may prevent struvite stone formation in rats with urinary tract infections.

Topics: Aluminum; Animals; Calcium, Dietary; Cholecalciferol; Magnesium; Magnesium Compounds; Male; Phosphates; Phosphorus, Dietary; Proteus Infections; Proteus mirabilis; Rats; Rats, Inbred Strains; Struvite; Urinary Calculi; Urinary Tract Infections

Topics: Adolescent; Age Factors; Calcium Metabolism Disorders; Child; Child, Preschool; Cholecalciferol; Female; Humans; Infant; Male; Sex Factors; Urinary Calculi; Urinary Tract Infections

Hypophosphateamia in patients with Ca lithiasis leads to the activation of the vitamin D endocrine system: the plasma 1.25(OH)2-D3 concentration is raised. The raised 1,25(OH)2-D3 biosynthesis causes an increase in intestinal Ca absorption, which in its turn explains the hypercalciuria. The syndrome originally presented by Albright and his pupils as "idiopathic hypercalciuria" in fact corresponds to a secondary, reactive D hypervitaminosis. According to the present findings the often wrongly used term "so-called idiopathic calciuria" should be replaced by the pathogenetically correcter term "hypophosphataemic calciuria". Efficient treatment of this syndrome consists in sufficient oral orthophosphate substitution. In the interests of a better understanding as a requirement for suitable treatment of this metabolic disorder, the vitamin D metabolites and their renal key enzymes, 25-OH-Vitamin-D3-1-Hydroxylase and 25-OH-Vitamin -D3-24-Hydroxylase, are described. The hormonal control add the activation and inactivation of the vitamin D endocrine system are explained independently of the individual Ca and phosphate requirement of the organism. The dependence of renal Ca excretion on the rate of glomerular filtration is pointed out once again. The clinical-diagnostic term hypercalciuria must not be applied globally but individually. Indications, counter-indications, dosage, duration and side-effects of the orthophosphate therapy are discussed.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Calcium; Cholecalciferol; Cytochrome P-450 Enzyme System; Female; Humans; Hypophosphatasia; Male; Phosphates; Rats; Steroid Hydroxylases; Urinary Calculi; Vitamin D; Vitamin D3 24-Hydroxylase

Patients with urolithiasis were divided into two groups, one (n = 38) with a urinary excretion of calcium exceeding 6.0 mmol/24 h and one (n = 32) with a calcium excretion lower than 6.1 mmol/24 h. The group of patients with a high urinary excretion of calcium had a significantly higher level of 25-hydroxy vitamin D3 (26.2 +/- 1.6 ng/ml) than had the group of patients with a normal urinary excretion of calcium (17.6 +/- 0.9 ng/ml) (p less than 0.001). A highly specific and accurate method, based on isotope dilution--mass spectrometry was used in the assay of 25-hydroxy vitamin D3. There was no over-all correlation between level of 25-hydroxy vitamin D3 and serum level of calcium (r = 0.1). The results are in accordance with the contention that the vitamin D3-status might be of some importance for the development of hypercalciuria in these patients.

Topics: Adolescent; Adult; Aged; Calcifediol; Calcium; Cholecalciferol; Female; Humans; Male; Mass Spectrometry; Middle Aged; Phosphates; Seasons; Urinary Calculi

Topics: Animals; Calcium; Cholecalciferol; Gastrointestinal Hormones; Hormones; Humans; Insulin; Intestinal Absorption; Somatostatin; Urinary Calculi

Urinary calculi composed of calcium oxalate were produced in male hooded Wistar rats fed a vitamin B6 deficient diet over 16 weeks. This basic diet was modified by doubling the phosphate content or loading with vitamin C or D3 in three treatment groups. The number of rats developing oxalate stones was not altered by the addition of vitamin D3 or phosphate, but there was a significant increase in total weight of stone formed and histological evidence of extensive renal damage in rats on the high vitamin D3 diet. The addition of vitamin C to the vitamin B6 deficient rats resulted in a reduction in the number of rats with uroliths and a fall in urinary oxalate excretion, while similarly loaded vitamin B6 supplemented controls were free of oxalate calculi. It is concluded that the oxalate urolithiasis induced by vitamin B6 deficiency was exacerbated by added vitamin D3 and reduced by vitamin C.

Topics: Animals; Ascorbic Acid; Body Weight; Calcium Oxalate; Cholecalciferol; Diet; Kidney; Male; Phosphates; Pyridoxine; Rats; Urinary Calculi; Vitamin B 6 Deficiency

Topics: Adolescent; Adult; Aged; Calcitonin; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Hypocalcemia; Intestinal Absorption; Kidney Tubules; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Urinary Calculi