Independent association between 1,25-dihydroxyvitamin D, 25-hydroxyvitamin D and the renin-angiotensin system The Ludwigshafen Risk and Cardiovascular Health (LURIC) study
ABSTRACT Antihypertensive and tissue-protective properties of vitamin D metabolites are increasingly attributed to the inhibition of renin synthesis by 1,25-dihydroxyvitamin D [1,25(OH)2D] in the kidney.
We aimed to document a potential association between 25-hydroxyvitamin D [25(OH)D], 1,25(OH)2D and the circulating renin-angiotensin system (RAS) in a large cohort of patients referred (n=3316) to coronary angiography.
Of the 3316 subjects, 3296 (median age: 63.5 (56.3-70.6)years; 30.2% women) had a baseline measurement of 25(OH)D [median: 15.6(10.1-23.0)microg/L)], 1,25(OH)2D [median: 33.2(25.2-42.9)pg/mL], plasma renin concentration [PRC; median: 11.4(6.0-24.6)pg/mL] and angiotensin 2 [median: 20.0(12.0-35.0)ng/L]. Multivariate adjusted ANCOVA showed a steady increase of PRC values across declining deciles of 25(OH)D and 1,25(OH)2D values (P=0.013 and P=0.045), respectively. Additionally, mean angiotensin 2 values increased significantly across decreasing 25(OH)D and 1,25(OH)2D values (P=0.020 and P=0.024, respectively). In contrast, multivariate adjusted ANCOVA revealed no significant associations between aldosterone, aldosterone-to-renin ratio and 25(OH)D/1,25(OH)2D values. In multivariate stepwise regression analyses both, 25(OH)D and 1,25(OH)2D emerged as independent predictors of plasma renin and angiotensin 2 concentrations.
Our data showed for the first time in humans that both, lower 25(OH)D and 1,25(OH)2D values are independently related to an upregulated circulating RAS.
- SourceAvailable from: James Dinicolantonio
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- "Also, even in individuals with normal kidney function, the effect of supplemental calcium on cardiovascular health has emerged as equivocal or even slightly negative in some recent studies   . This is a bit surprising in light of calcium's ability to decrease PTH and inhibit GI phosphate absorption, and evidence that calcium intake is not a determinant of risk for coronary artery calcification in the general population ; it has been proposed that supplemental calcium may up-regulate renin production by decreasing serum calcitriol   . Arguably, the optimal approach to moderating PTH in support of vascular and bone health may be to employ effective vitamin D supplementation, while keeping calcium intake moderate so that relatively high serum levels of both calcitriol and calcidiol are maintained. "
ABSTRACT: Increased fasting serum phosphate within the normal physiological range has been linked to increased cardiovascular risk in prospective epidemiology; increased production of fibroblast growth factor 23 (FGF23), and direct vascular effects of phosphate, may mediate this risk. Although dietary phosphate intake does not clearly influence fasting serum phosphate in those with normal renal function, increased phosphate intake can provoke an increase in FGF23, and in diurnal phosphate levels, and hence may adversely influence vascular health. Dietary phosphate absorption can be moderated by emphasizing plant-based dietary choices (which provide phosphate in less-bioavailable forms), avoidance of processed foods containing inorganic phosphate food additives, and by ingestion of phosphate-binder drugs, magnesium supplements, or niacin, which precipitate phosphate or suppress its gastrointestinal absorption. The propensity of dietary phosphate to promote vascular calcification may be opposed by optimal intakes of magnesium, vitamin K, and vitamin D; the latter should also counter the tendency of phosphate to elevate parathyroid hormone.Nutrition 01/2013; 30(7-8). DOI:10.1016/j.nut.2013.12.010 · 3.05 Impact Factor
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- "Secondary hyperparathyroidism is highly prevalent in severe heart failure, where hypovitaminosis D is contributory . Moreover, lower values of the vitamin D metabolites 25(OH)D and 1,25(OH) 2 D are both independently associated with an upregulated circulating renin angiotensin system . A better understanding of the role of vitamin D deficiency in cardiorenal syndromes and in CVD can only be achieved if in future studies both 25(OH)D and 1,25(OH) 2 D are measured. "
ABSTRACT: Evidence is accumulating that vitamin D status may influence the risk of cardiovascular disease (CVD). Final confirmation for a causal relationship between vitamin D and CVD is however still lacking. The present viewpoint article outlines several future research directions to close this gap. Future directions include the need of performing large randomised controlled supplementation trials with vitamin D in specific risk groups. In addition, large register sets of data on vitamin D supplementation can be used, provided that adequate statistical methods such as propensity score modelled analysis are applied. To better understand vitamin D-mediated effects on CVD risk, the routine measurement of circulating levels of the hormonal vitamin D form, 1,25-dihydroxyvitamin D, is also necessary, in addition to the determination of its precursor 25-hydroxyvitamin D. Further, genetic association studies may help in clarifying the contribution of vitamin D to the development of CVD. Finally, the interrelationship of vitamin D with physical activity should be considered when studying CVD risk. Overall, it can be expected that the next 10-15 years will provide an increased clarity concerning the role of vitamin D in CVD.Nutrition, metabolism, and cardiovascular diseases: NMCD 05/2012; 22(7):541-6. DOI:10.1016/j.numecd.2012.02.004 · 3.88 Impact Factor
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