Effects of lα-Hydroxylated Vitamin-D Metabolites on Intestinal Radio-Calcium Absorption and Urinary Calcium Excretion in Short- and Long-Term Treatments of Postmenopausal Osteoporosis

Urolithiasis ◽  
1989 ◽  
pp. 615-615
Author(s):  
A. Caniggia ◽  
R. Nuti ◽  
F. Loré
1991 ◽  
Vol 12 (2) ◽  
pp. 171
Author(s):  
Steven A. Abrams ◽  
Tomas J. Silber ◽  
Nora V. Esteban ◽  
Nancy E. Vieira ◽  
Mansoud Majd ◽  
...  

2005 ◽  
Vol 90 (4) ◽  
pp. 2122-2126 ◽  
Author(s):  
Andrew Grey ◽  
Jenny Lucas ◽  
Anne Horne ◽  
Greg Gamble ◽  
James S. Davidson ◽  
...  

Abstract Vitamin D insufficiency is common in patients with primary hyperparathyroidism (PHPT) and may be associated with more severe and progressive disease. Uncertainty exists, however, as to whether repletion of vitamin D should be undertaken in patients with PHPT. Here we report the effects of vitamin D repletion on biochemical outcomes over 1 yr in a group of 21 patients with mild PHPT [serum calcium <12 mg/dl (3 mmol/liter)] and coexistent vitamin D insufficiency [serum 25 hydroxyvitamin D [25(OH)D] <20 μg/liter (50 nmol/liter)]. In response to vitamin D repletion to a serum 25(OH)D level greater than 20 μg/liter (50 nmol/liter), mean levels of serum calcium and phosphate did not change, and serum calcium did not exceed 12 mg/dl (3 mmol/liter) in any patient. Levels of intact PTH fell by 24% at 6 months (P < 0.01) and 26% at 12 months (P < 0.01). There was an inverse relationship between the change in serum 25(OH)D and that in intact PTH (r = −0.43, P = 0.056). At 12 months, total serum alkaline phosphatase was significantly lower, and urine N-telopeptides tended to be lower than baseline values (P = 0.02 and 0.13, respectively). In two patients, 24-h urinary calcium excretion rose to exceed 400 mg/d, but the group mean 24-h urinary calcium excretion did not change. These preliminary data suggest that vitamin D repletion in patients with PHPT does not exacerbate hypercalcemia and may decrease levels of PTH and bone turnover. Some patients with PHPT may experience an increase in urinary calcium excretion after vitamin D repletion.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Luigi Petramala ◽  
Laura Zinnamosca ◽  
Amina Settevendemmie ◽  
Cristiano Marinelli ◽  
Matteo Nardi ◽  
...  

Primary aldosteronism represents major cause of secondary hypertension, strongly associated with high cardiovascular morbidity and mortality. Aldosterone excess may influence mineral homeostasis, through higher urinary calcium excretion inducing secondary increase of parathyroid hormone. Recently, in a cohort of PA patients a significant increase of primary hyperparathyroidism was found, suggesting a bidirectional functional link between the adrenal and parathyroid glands. The aim of this study was to evaluate the impact of aldosterone excess on mineral metabolism and bone mass density. In 73 PA patients we evaluated anthropometric and biochemical parameters, renin-angiotensin-aldosterone system, calcium-phosphorus metabolism, and bone mineral density; control groups were 73 essential hypertension (EH) subjects and 40 healthy subjects. Compared to HS and EH, PA subjects had significantly lower serum calcium levels and higher urinary calcium excretion. Moreover, PA patients showed higher plasma PTH, lower serum 25(OH)-vitamin D levels, higher prevalence of vitamin D deficiency (65% versus 25% and 25%;P<0.001), and higher prevalence of osteopenia/osteoporosis (38.5 and 10.5%) than EH (28% and 4%) and NS (25% and 5%), respectively. This study supports the hypothesis that bone loss and fracture risk in PA patients are potentially the result of aldosterone mediated hypercalciuria and the consecutive secondary hyperparathyroidism.


2009 ◽  
Vol 104 (10) ◽  
pp. 1512-1516 ◽  
Author(s):  
Kristina L. Penniston ◽  
Andrea N. Jones ◽  
Stephen Y. Nakada ◽  
Karen E. Hansen

1971 ◽  
Vol 49 (5) ◽  
pp. 469-478 ◽  
Author(s):  
William H. Shaw

The relationship between urinary calcium excretion and serum calcium was studied at stable serum calcium levels, both normal and elevated. The linearity of this relationship being known, the slope of this line could be determined by sampling only at its lower and upper ends, that is, by measuring urine and serum calcium at a resting level and at a constant level of hypercalcemia produced by a calcium infusion. This method permitted three sets of measurements at each of the two levels, and also tended to eliminate the factor of renal delay time. The procedure was performed with normal subjects, with normals given vitamin D2 or parathyroid extract, and with subjects having hyperparathyroidism, sarcoidosis, and recurrent renal calculi. In the normal subjects the gradient of the slope appeared to indicate that there is no maximal tubular reabsorptive capacity for calcium, in the range sampled at any rate. The slopes of the various abnormal subjects mostly did not differ markedly from those of the normals. One incidental finding was that resting levels of urinary calcium excretion were significantly depressed 24 h following vitamin D2 administration, despite unchanged serum calcium levels.


2015 ◽  
Vol 9 (11-12) ◽  
pp. 403 ◽  
Author(s):  
Charles Hesswani ◽  
Yasser A Noureldin ◽  
Mohamed A Elkoushy ◽  
Sero Andonian

<p><strong>ABSTRACT </strong></p><p><strong>Introduction</strong>: We examined the effect of combined vitamin D and calcium supplementation (VDCS) on urinary calcium excretion and de novo stone formation in vitamin D inadequate (VDI) urolithiasis patients.</p><p><strong>Methods</strong>: We retrospectively reviewed the data of VDI patients (serum 25-hydroxyvitamin D&lt;75 nmol/L) followed at a tertiary stone centre between September 2009 and December 2014. VDI patients with history of urolithiasis, who were placed on VDCS for abnormal bone mineral density or hyperoxaliuria, were included. Hypercalciuric patients and patients on thiazide diuretics were excluded. Metabolic stone workup and two 24-hour urine collections were performed before and after VDCS.</p><p><strong> Results</strong>: In total, we inculded 34 patients, with a mean age of 54.8 years and a mean body mass index of 25.7 kg/m2. After VDCS, there was a significant increase in the mean serum 25-hydroxyvitamin D (52.0 vs. 66.4 nmol/L, p&lt;0.001) and the mean urinary calcium excretion (3.80 vs. 5.64 mmol/d, p&lt;0.001). Eight (23.5%) patients developed de novo hypercalciuria. After a median follow-up of 39 (range: 7-60) months, 50% of hypercalciuric patients developed stones compared with 11.5% of non-hypercalciuric patients (p=0.038).</p><p><strong>Conclusion</strong>: This study showed a significant effect of combined VDCS on mean urinary calcium excretion, de novo hypercalciuria, and stone development in VDI patients with history of urolithiasis. Therefore, VDI urolithiasis patients receiving VDCS are advised to have monitoring with 24-hour urine collections and imaging studies. Although small, the sample size is good enough to validate the statistical outcomes. Prospective studies are needed to confirm these results.</p>


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