scholarly journals Estrogen deficiency and low-calcium diet increased bone loss and urinary calcium excretion but did not alter arterial stiffness in young female rats

2008 ◽  
Vol 26 (3) ◽  
pp. 218-225 ◽  
Author(s):  
Jong-Hoon Park ◽  
Naomi Omi ◽  
Toshiya Nosaka ◽  
Ayako Kitajima ◽  
Ikuko Ezawa
1991 ◽  
Vol 55 ◽  
pp. 241
Author(s):  
Yuta Kobayashi ◽  
Keiko Shimoura ◽  
Youko Tanabe ◽  
Keisuke Hattori

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Sa'eed Bawa

Osteoporosis is defined as a progressive systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture. Although bone mass and quality is mainly determined genetically, many other factors, including lifestyle and nutrition also have an impact on bone health. It has been suggested that dietary protein intake may be a risk factor for osteoporosis, and high-protein diets are associated with increased bone loss. Many scientists have examined the relationship between types of protein and urinary calcium excretion, and found that although animal protein was associated with increased urinary calcium excretion, soy protein was not. There is sufficient evidence suggesting soy isoflavones may have potential benefits for bone. Soy protein with naturally occurring phytoestrogens, mainly isoflavones protect against bone loss and synthetic soy ipriflavone in some studies has been shown to favorably affect, but a cause and effect relationship has not been established between the consumption of ipriflavone and maintenance of bone mineral density in post-menopausal women. Therefore it is too early to recommend it as a supplement for this group of women.


1992 ◽  
Vol 83 (5) ◽  
pp. 561-565 ◽  
Author(s):  
Mario Barbagallo ◽  
Lawrence M. Resnick ◽  
R. Ernest Sosa ◽  
Mary Lou Corbett ◽  
John H. Laragh

1. To determine whether abnormal renal calcium excretion is unique to primary genetic hypertension, blood pressure and 24 h urinary excretion of calcium, magnesium, sodium and creatinine were measured in deoxycorticosterone—saline and two-kidney, one-clip Goldblatt hypertensive rats and in their respective controls on low (0.2%) and high (1.8%) dietary calcium intakes. 2. Calcium supplementation lowered blood pressure (P<0.05) in deoxycorticosterone—saline rats and in control saline-loaded rats, raised blood pressure in two-kidney, one clip rats, and had no effect in sham-operated control rats. 3. On both diets, calcium excretion was higher in hypertensive than in normotensive rats. The high calcium diet increased urinary calcium excretion in all rats, but the changes in urinary calcium excretion closely paralleled the diet-induced changes in blood pressure. Thus, urinary calcium excretion in deoxycorticosterone—saline animals, in whom calcium lowered blood pressure the most, rose the least (107%). Urinary calcium excretion rose the most in two-kidney, one-clip animals (1113%), whose blood pressure also rose the most. 4. Urinary magnesium excretion was also abnormal in hypertensive rats compared with normotensive rats, falling on the high compared with the low calcium diet in normotensive rats, but not in either hypertensive strain. Furthermore, urinary magnesium excretion was closely linked to urinary calcium excretion in saline-loaded control rats (r = 0.78; P = 0.008), but was dissociated from urinary calcium excretion in deoxycorticosterone—saline rats (r = 0.02; not significant). 5. We conclude (a) that the renal handling of both calcium and magnesium is altered in secondary hypertension, and (b) that dietary calcium supplementation may have different effects on blood pressure in different forms of hypertensive disease. We hypothesize that elevated blood pressure per se may be responsible for the exaggerated calciuresis of hypertension.


1998 ◽  
Vol 18 (3) ◽  
pp. 475-487 ◽  
Author(s):  
Susan J Whiting ◽  
Timothy J Green ◽  
Evelyn P MacKenzie ◽  
Shawna J Weeks

1991 ◽  
Vol 12 (2) ◽  
pp. 171
Author(s):  
Steven A. Abrams ◽  
Tomas J. Silber ◽  
Nora V. Esteban ◽  
Nancy E. Vieira ◽  
Mansoud Majd ◽  
...  

Author(s):  
Jing Liu ◽  
Maria Clarissa Tio ◽  
Ashish Verma ◽  
Insa M Schmidt ◽  
Titilayo O Ilori ◽  
...  

Abstract Context Abnormalities in calcium metabolism are common in chronic kidney disease (CKD). Diminished urinary calcium excretion may promote vascular calcification, and increased urinary calcium excretion may lead to nephrolithiasis and nephrocalcinosis, conditions associated with CKD. Objective To study predictors of urinary calcium excretion and its association with adverse clinical outcomes in CKD. Design, Setting and Patients This study assessed 3,768 non-dialysis participants in the Chronic Renal Insufficiency Cohort study from April 2003 to September 2008. Participants were followed up to October 2018. Exposure Clinically plausible predictors of urinary calcium excretion and 24-hour urinary calcium excretion at baseline. Main Outcome Measures Urinary calcium excretion; incident end stage kidney disease (ESKD), CKD progression (50% estimated glomerular filtration rate (eGFR) decline or incident ESKD), all-cause mortality, and atherosclerotic cardiovascular disease events. Results eGFR was positive correlated with 24-hour urinary calcium excretion. The variables most strongly associated with 24-hour urinary calcium excretion were 24-hour urinary sodium (β=0.19 and 0.28 in males and females), serum parathyroid hormone (β=-0.22 and -0.20), loop diuretics (β=0.36 and 0.26), thiazide diuretics (β=-0.49 and -0.53), and self-identified black race (β=-0.23 and -0.27). Lower urinary calcium excretion was associated with greater risks of outcomes, but these associations were greatly attenuated or nullified after adjustment for baseline eGFR. Conclusion Urinary calcium excretion is markedly lower in individuals with CKD compared to general population. Determinants of urinary calcium excretion differed between sexes and levels of CKD. Significant associations between urinary calcium excretion and adverse clinical events were substantially confounded by eGFR.


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