THE EFFECTS OF ORAL ADMINISTRATION OF MAGNESIUM OXIDE ON RENAL CALCIUM EXCRETION IN CREW MEMBERS DURING A SUBMARINE PATROL

1969 ◽  
Author(s):  
Clayton T. Drake
Keyword(s):  
Oral Administration ◽  
Magnesium Oxide ◽  
Calcium Excretion ◽  
Renal Calcium Excretion

scholarly journals Effects of Pioglitazone on Renal Calcium Excretion

2011 ◽  
Vol 96 (9) ◽  
pp. E1482-E1485 ◽  
Author(s):  
Anne Zanchi ◽  
Antoinette Pechère-Bertschi ◽  
Michel Burnier ◽  
Olivier Bonny
Keyword(s):  
Calcium Excretion ◽  
Renal Calcium Excretion

Idiopathic infantile hypercalcemia: case report and review of the literature

2016 ◽  
Vol 29 (2) ◽  
Author(s):  
Brynn E. Marks ◽  
Daniel A. Doyle
Keyword(s):  
Vitamin D ◽  
Enzyme Activity ◽  
Calcium Absorption ◽  
Calcium Excretion ◽  
Review Of The Literature ◽  
Active Vitamin ◽  
Supplemental Vitamin ◽  
Idiopathic Infantile Hypercalcemia ◽  
Therapeutic Doses ◽  
Renal Calcium Excretion

AbstractThe widespread use of supplemental vitamin D has dramatically reduced the incidence of rickets. While generally considered a safe practice, there is potential for toxicity in patients with idiopathic infantile hypercalcemia (IIH). Inadequate 24-hydroxylase-enzyme activity renders these individuals unable to degrade active vitamin D, resulting in hypercalcemia due to increased intestinal calcium absorption, decreased renal calcium excretion, and increased osteoclastic bone activity. Clinicians should be aware that even therapeutic doses of vitamin D can prove harmful for patients with

Effects of endogenous estrogen on renal calcium and phosphate handling in elderly women

2005 ◽  
Vol 288 (2) ◽  
pp. E430-E435 ◽  
Author(s):  
I. M. Dick ◽  
A. Devine ◽  
J. Beilby ◽  
R. L. Prince
Keyword(s):  
Postmenopausal Women ◽  
Elderly Women ◽  
Calcium Supplementation ◽  
Calcium Excretion ◽  
Calcium Balance ◽  
Phosphate Excretion ◽  
Endogenous Estrogen ◽  
Serum Pth ◽  
Estradiol Concentration ◽  
Renal Calcium Excretion

High postmenopausal endogenous estrogen concentrations are an important determinant of preservation of bone mass and reduced fracture in elderly women. Calcium supplementation can also reduce bone loss in these patients, suggesting an interaction between estrogen deficiency and calcium balance. Potential mechanisms of estrogen on calcium transport include direct effects on the bone, the kidney, and the bowel. Previous studies have demonstrated effects of estrogen on renal phosphate handling. We have used a cross-sectional, population-based analysis of biochemical data obtained from ambulant elderly women to determine the association of endogenous estradiol with urine calcium and phosphorus excretion. The subjects were 293 postmenopausal women >70 yr old. Factors associated with renal calcium and phosphate excretion were measured, including the filtered calcium and phosphate load, parathyroid hormone (PTH), estradiol, and sex hormone-binding globulin (SHBG). The free estradiol concentration (FE) was calculated from a previously described formula. A high plasma estradiol concentration ( r2 = 0.023, P = 0.01) and a high FE ( r2 = 0.045, P = 0.001) were associated with reduced renal calcium excretion. The estradiol and FE effect on renal calcium excretion remained significant after adjusting for calcium filtered at the glomerulus and serum PTH. A high FE was associated with a reduced renal phosphate threshold in univariate analysis ( r2 = 0.023, P = 0.010). The effect remained significant after adjustment for serum PTH. The size of the effect of the FE was of the same order of magnitude as the effect of PTH on reducing renal calcium excretion and increasing renal phosphate excretion. These data support in vitro and animal data demonstrating an effect of estradiol on renal calcium and phosphate handling and indicate that, in elderly postmenopausal women, the effect is of a similar magnitude to the well-recognized effects of PTH on these physiologically regulated parameters.

scholarly journals MON-492 A Case of Gitelman’s Syndrome with Hyperphosphatemia That Responded Effectively to Single Oral Administration of Magnesium Oxide

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Aika Miya ◽  
Akinobu Nakamura ◽  
Hiraku Kameda ◽  
Kandai Nozu ◽  
Hideaki Miyoshi ◽  
...  
Keyword(s):  
Oral Administration ◽  
Magnesium Oxide ◽  
Gitelman's Syndrome ◽  
Single Oral Administration

Effect of dietary calcium on bone density in growing rabbits

1991 ◽  
Vol 260 (3) ◽  
pp. E471-E476 ◽  
Author(s):  
V. Gilsanz ◽  
T. F. Roe ◽  
J. Antunes ◽  
M. Carlson ◽  
M. L. Duarte ◽  
...  
Keyword(s):  
Bone Density ◽  
Bone Mass ◽  
Calcium Intake ◽  
Peak Bone Mass ◽  
Skeletal Maturity ◽  
Dietary Calcium ◽  
Calcium Excretion ◽  
Vertebral Bone ◽  
Epiphyseal Closure ◽  
Renal Calcium Excretion

Reductions in peak bone mass at skeletal maturity may increase the risk for the subsequent development of osteoporosis. Although changes in calcium intake can modify the rate of decline in bone density in the mature skeleton, longitudinal assessments of the effect of dietary calcium supplementation during skeletal growth on peak bone mass have not been done in humans or experimental animals. Thus quantitative computed tomography (QCT) was used to monitor changes in vertebral bone density at 6-wk intervals during growth from 8 wk of age until skeletal maturity at 35 wk in male New Zealand White rabbits maintained on diets containing 0.15% (low Ca), 0.45% (normal Ca), or 1.35% (high Ca) calcium. Serum parathyroid hormone (PTH) and calcitriol levels increased, and renal calcium excretion decreased in low Ca compared with normal Ca; in contrast, serum calcitriol levels decreased and renal calcium excretion increased from control values in high Ca. Vertebral bone density by QCT did not differ during growth between high Ca and normal Ca, and peak values at epiphyseal closure also did not differ in these two groups. Vertebral bone density was lower, however, throughout the study in low Ca, and peak values at epiphyseal closure remained below those in either normal Ca or high Ca. Quantitative bone histology revealed decreases in cortical thickness in the third lumbar vertebra in low Ca, whereas trabecular bone area did not differ among groups; there was no histological evidence of osteomalacia in low Ca. Thus dietary calcium restriction during growth reduces peak bone mass at skeletal maturity, but raising dietary calcium intake above normal levels does not increase peak bone mass in this experimental model.

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