Serum concentration of calcium, 1,25 vitamin D and parathyroid hormone are not correlated with coronary calcifications. An electron beam computed tomography study

Arad, Yadon; Spadaro, Louise A.; Roth, Marguerite; Scordo, Joan; Goodman, Ken; Sherman, Scott; Lerner, Gail; Newstein, David; Guerci, Alan D.

doi:10.1097/00019501-199809080-00007

Cited by 70 publications

(38 citation statements)

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“…Several clinical studies have also failed to find a relationship between circulating active vitamin D levels and calcifications. 26,27 In addition, these find- ings support the interpretation that the lower mortality associated with the use of less potent vitamin D analogues, such as paricalcitol and doxercalciferol, could be explained by less hyperphosphatemia. 11,28 Regardless, these studies are the first to show that restriction of dietary phosphate and lowering of the serum phosphate prevent vascular calcifications and improve survival in a hyperphosphatemic model.…”

supporting

confidence: 58%

Role of Hyperphosphatemia and 1,25-Dihydroxyvitamin D in Vascular Calcification and Mortality in Fibroblastic Growth Factor 23 Null Mice

Stubbs

Liu²,

Tang³

et al. 2007

Journal of the American Society of Nephrology

246

187

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Fibroblastic growth factor 23 (FGF23) regulates renal phosphate reabsorption and 1␣-hydroxylase activity. Ablation of FGF23 results in elevated serum phosphate, calcium, and 1,25-dihydroxyvitamin D3 [1,25(OH) 2 D] levels; vascular calcifications; and early death. For determination of the independent roles of hyperphosphatemia and excess vitamin D activity on the observed phenotypic abnormalities, FGF23 null mice were fed a phosphate-or vitamin D-deficient diet. The phosphate-deficient diet corrected the hyperphosphatemia, prevented vascular calcifications, and rescued the lethal phenotype in FGF23 null mice, despite persistent elevations of serum 1,25(OH) 2 D and calcium levels. This suggests that hyperphosphatemia, rather than excessive vitamin D activity, is the major stimulus for vascular calcifications and contributes to the increased mortality in the FGF23-null mouse model. In contrast, the vitamin D-deficient diet failed to correct either the hyperphosphatemia or the vascular calcifications in FGF23 null mice, indicating that FGF23 independently regulates renal phosphate excretion and that elevations in 1,25(OH) 2 D and calcium are not sufficient to induce vascular calcifications in the absence of hyperphosphatemia. The vitamin D-deficient diet also improved survival in FGF23 null mice in association with normalization of 1,25(OH) 2 D and calcium levels and despite persistent hyperphosphatemia and vascular calcifications, indicating that excessive vitamin D activity can also have adverse effects in the presence of hyperphosphatemia and absence of FGF23. Understanding the independent and context-dependent interactions between hyperphosphatemia and excessive vitamin D activity, as well as vascular calcifications and mortality in FGF23 null mice, may ultimately provide important insights into the management of clinical disorders of hyperphosphatemia and excess vitamin D activity. 18: 211618: -212418: , 200718: . doi: 10.1681 Disorders of mineral metabolism are nontraditional risk factors that are associated with high mortality in ESRD. 1,2 Epidemiologic studies have linked excessive cardiovascular mortality in ESRD with hyperphosphatemia, hypercalcemia, and elevated parathyroid hormone (PTH) levels. 2,3 Vascular calcifications, which are highly prevalent and directly correlated with mortality in this population, are the likely mechanism whereby disordered mineral metabolism contributes to cardiovascular mortality in ESRD. 3 Experimental models demonstrate that hyperphosphatemia is a major initiator of extracellular matrix mineralization and vascular calcification. 4 In addition, clinical data in ESRD show a strong association between hyperphosphatemia and mortality, as well as between phosphate levels and excess calcium with vascular calcifications. 2,5,6 The relationship among disordered mineral metabolism, the presence of vascular calcifications, and J Am Soc Nephrol

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supporting

confidence: 58%

Role of Hyperphosphatemia and 1,25-Dihydroxyvitamin D in Vascular Calcification and Mortality in Fibroblastic Growth Factor 23 Null Mice

Stubbs

Liu²,

Tang³

et al. 2007

Journal of the American Society of Nephrology

246

187

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“…Disturbances of Ca and PO 4 metabolism in chronic kidney disease are associated with PTH secretion and uremic bone disease, but their role in the pathogenesis of AC remains uncertain. Although considered a cause of AC, the association of hyperparathyroidism and AC is not constant, and according to the most recent data, serum PTH and AC scores were not associated, and serum PTH was lower in patients with high AC scores (1,2,18,19). Arterial media calcifications were observed more frequently in patients with ESRD after PTX, and patients with the highest AC scores had the lowest PTH levels (19).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, evidence indicates that many proteins involved in bone metabolism can be expressed in arterial tissue, reflecting changes in the phenotype of vascular smooth-muscle cells (11)(12)(13)(14)(15)(16)(17). Disturbances in calcium (Ca) and phosphate (PO 4 ) metabolism in ESRD are associated with changes of parathyroid hormone (PTH) secretion and uremic bone disease, but their role in the pathogenesis of AC remains uncertain (1,2,18,19). An inverse relationship between AC and bone density has been documented in uremic patients (20).…”

mentioning

confidence: 99%

Arterial Calcifications and Bone Histomorphometry in End-Stage Renal Disease

London¹,

Marty

Marchais³

et al. 2004

Journal of the American Society of Nephrology

541

392

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Abstract. Arterial calcification (AC) is a common complication of end-stage renal disease (ESRD). The mechanisms responsible are complex, including disturbances of mineral metabolism and active expression of various mineral-regulating proteins. An inverse relationship between AC and bone density has been documented in uremic patients. In the study presented here, which included 58 patients with ESRD on hemodialysis (HD), bone-histomorphometry characteristics were compared with the AC scores (0 to 4) determined according to the number of arterial sites with calcifications. Patients with AC scores of 0 (no calcifications), or 1 or 2 (mild calcifications) had similar serum parathyroid hormone levels and bone histomorphometry, with larger osteoclast resorption, higher osteoclast numbers, and larger osteoblastic and double tertracycline-labeled surfaces. In contrast, patients with high AC scores (3 and 4) were characterized by lower serum parathyroid hormone, low osteoclast numbers and osteoblastic surfaces, smaller or absent double tetracycline-labeled surfaces, and high percentages of aluminum-stained surfaces. According to multivariate analysis, AC score was positively associated with age (P Ͻ 0.0001), daily dose of calcium-containing phosphate binders (P ϭ 0.009), and bone aluminum-stained surfaces (P ϭ 0.037), and an inverse correlation was observed with osteoblastic surfaces (P ϭ 0.001). A high AC score is associated with bone histomorphometry suggestive of low bone activity and adynamic bone disease. These findings suggest that therapeutic interventions associated with excessive lowering of parathyroid activity (parathyroidectomy, excessive calcium or aluminum load) favor lower bone turnover and adynamic bone disease, which could influence the development and progression of AC.

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“…[10][11][12][13][14] This also pertains to the studies examining the associations of vitamin D metabolites and the vitamin D metabolism gene CYP24A1 with coronary artery calcification. 12,[15][16][17][18] See accompanying article on page 2467 © 2013 American Heart Association, Inc. Objective-Vitamin D deficiency has been implicated in cardiovascular disease and is associated with multiple cardiovascular risk factors. We investigated the serum 25-hydroxyvitamin D (25(OH)D) concentration in relation to latitude, baseline carotid intima-media thickness (IMT), and IMT progression, the carotid IMT measures being surrogate markers of subclinical atherosclerosis and cardiovascular disease risk.…”

mentioning

confidence: 99%

Serum 25-Hydroxyvitamin D Concentration in Subclinical Carotid Atherosclerosis

Deleskog

Piksasova

Silveira

et al. 2013

ATVB

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he role of vitamin D, most often measured as circulating 25-hydroxyvitamin D (25(OH)D), also designated calcidiol), in cardiovascular disease (CVD) remains much debated. Whereas the strongest support for the notion that low vitamin D levels promote CVD comes from some prospective studies of incident cardiovascular events or CVD mortality, [1][2][3] other prospective studies of the relationship between the circulating 25(OH)D concentration and risk of CVD have provided discrepant results. [4][5][6] Similarly, crosssectional studies, hitherto restricted to fairly small, diverse, and specific populations, on the relationship between 25(OH) D and carotid intima-media thickness (IMT), a widely used surrogate marker of subclinical atherosclerosis 7 and predictor of coronary and cerebrovascular events, 8,9 have shown contradictory results. [10][11][12][13][14] This also pertains to the studies examining the associations of vitamin D metabolites and the vitamin D metabolism gene CYP24A1 with coronary artery calcification. 12,[15][16][17][18] See accompanying article on page 2467 © 2013 American Heart Association, Inc. Objective-Vitamin D deficiency has been implicated in cardiovascular disease and is associated with multiple cardiovascular risk factors. We investigated the serum 25-hydroxyvitamin D (25(OH)D) concentration in relation to latitude, baseline carotid intima-media thickness (IMT), and IMT progression, the carotid IMT measures being surrogate markers of subclinical atherosclerosis and cardiovascular disease risk. Approach and Results-Serum 25(OH)D concentration was related to high-resolution carotid IMT measures in 3430middle-aged and elderly subjects with high cardiovascular risk but no prevalent disease, who were recruited at 7 centers in Finland, Sweden, The Netherlands, France, and Italy. Participants underwent carotid ultrasound examination at baseline and at months 15 and 30 after entry into the study, whereas blood samples, clinical data, and information about lifestyle were collected at baseline. Serum 25(OH)D levels were positively associated with latitude (Jonckheere-Terpstra χ=166.643; P<0.001) and, as previously reported, associated with a range of cardiovascular risk factors. There were no independent relationships between 25(OH)D and segment-specific or composite IMT measures in the entire cohort. In analyses stratified by sex, diabetes mellitus, and statin treatment, weak associations with some baseline and progression measures of carotid IMT were observed in males, diabetics, and nonstatin-treated individuals. 19 enabled us to explore whether potential latitude-related differences in vitamin D concentrations contribute to differences in subclinical atherosclerosis. By enrolling roughly the same numbers of male and female participants from different parts of Europe, this study allows results to be interpreted in a wider context than in previous studies. Finally, the present study, to the best of our knowledge, represents the first attempt to investigate 25(OH)D levels in relation to progressio...

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Serum concentration of calcium, 1,25 vitamin D and parathyroid hormone are not correlated with coronary calcifications. An electron beam computed tomography study

Cited by 70 publications

References 0 publications

Role of Hyperphosphatemia and 1,25-Dihydroxyvitamin D in Vascular Calcification and Mortality in Fibroblastic Growth Factor 23 Null Mice

Role of Hyperphosphatemia and 1,25-Dihydroxyvitamin D in Vascular Calcification and Mortality in Fibroblastic Growth Factor 23 Null Mice

Arterial Calcifications and Bone Histomorphometry in End-Stage Renal Disease

Serum 25-Hydroxyvitamin D Concentration in Subclinical Carotid Atherosclerosis

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