scholarly journals Disorders of renal calcium excretion

1983 ◽  
Vol 23 (5) ◽  
pp. 665-673 ◽  
Author(s):  
Roger A.L. Sutton
Keyword(s):  
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.

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.

scholarly journals Effects of furosemide on renal calcium handling

2007 ◽  
Vol 293 (4) ◽  
pp. F1231-F1237 ◽  
Author(s):  
Chien-Te Lee ◽  
Hung-Chun Chen ◽  
Li-Wen Lai ◽  
Kim-Chong Yong ◽  
Yeong-Hau H. Lien
Keyword(s):  
Calcium Transport ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Immunofluorescent Staining ◽  
Calcium Excretion ◽  
Mrna Levels ◽  
Calbindin D9k ◽  
Calbindin D28k ◽  
Transport Molecules ◽  
Renal Calcium Excretion

Furosemide is a loop diuretic agent that has been used to treat hypercalcemia because it increases renal calcium excretion. The effect of furosemide on calcium transport molecules in distal tubules has yet to be investigated. We conducted studies to examine the effects of furosemide on renal calcium excretion and expression of calcium transport molecules in mice. Mice were administered with a single dose of furosemide (15 mg/kg) and examined 4 h later or were given twice-daily furosemide injections for 3 days. To evaluate the effects of volume depletion, drinking water was supplemented with salt. Our results showed that, in acute experiments, furosemide enhanced urinary calcium excretion, which was associated with a significant increase in mRNA levels of TRPV5, TRPV6, and calbindin-D28k but not calbindin-D9k as measured by real-time PCR (TRPV5 and TRPV6 are transient receptor potential vanilloid 5 and 6). Chronic furosemide administration induced three- to fourfold increases in urinary calcium excretion and elevated mRNA levels of TRPV5, TRPV6, calbindin-D28k, and calbindin-D9k without or with salt supplement. Similar upregulation of calcium transport molecules was observed in mice with gentamicin-induced hypercalciuria. Coadministration of chlorothiazide decreased furosemide-induced calciuria, either acutely or chronically, although still accompanied by upregulation of these transport molecules. Immunofluorescent staining studies revealed comparably increased protein abundance in TRPV5 and calbindin-D28k. We conclude that furosemide treatment enhances urinary calcium excretion. Increased abundance of calcium transport molecules in the distal convoluted tubule represents a solute load-dependent effect in response to increased calcium delivery and serves as a compensatory adaptation in the downstream segment.

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