calcitriol and Vascular-Calcification

Topics: Calcium; Cardiovascular Diseases; Clinical Trials as Topic; Dietary Supplements; Humans; Renin-Angiotensin System; Risk Factors; Survival Analysis; Ultraviolet Rays; Vascular Calcification; Vitamin D; Vitamin D Deficiency

Vitamin D deficiency, low levels of fetuin-A, and fibroblast growth factor 23 (FGF-23) are related to vascular calcification, which is associated with cardiovascular disease. We hypothesized that omega-3 fatty acid (FA), which has cardioprotective properties, modifies vitamin D status, fetuin-A, and FGF-23 levels in dialysis patients. In a randomized, open-label, controlled study, a total of 47 patients treated with dialysis for at least 1 year were randomized to treatment for 6 months with omega-3 FAs (Omacor, 3 g/d; Pronova, Sandefjord, Norway) or a control group. Levels of fetuin-A and FGF-23 were measured by enzyme-linked immunoassay, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were measured by radioimmunoassay. The mean age of the enrolled patients was 57.4 ± 10.4 years, and mean dialysis duration was 46.5 ± 28.1 months. Twenty-seven hemodialysis patients and 16 peritoneal dialysis patients finished this trial. After 6 months, the levels of 1,25-dihydroxyvitamin D and fetuin-A were significantly increased in the group taking the omega-3 FA supplement compared with baseline. Levels of calcium, phosphorous, parathyroid hormone, 25-hydroxyvitamin D, FGF-23, and lipid profiles were not significantly changed in the omega-3 FA-supplemented group after 6 months compared with baseline. The erythrocyte membrane contents of eicosapentaenoic acid and docosahexaenoic acid were significantly increased, and oleic acid content was significantly decreased in the omega-3 FA-supplemented group after 6 months compared with baseline. Regarding vascular calcification and cardiovascular disease, omega-3 FA supplementation may have a clinical benefit caused by activating vitamin D, increasing fetuin-A levels, and modifying erythrocyte membrane FA contents in dialysis patients.

Topics: Adult; Aged; Aged, 80 and over; alpha-2-HS-Glycoprotein; Calcium; Cardiovascular Diseases; Diet; Dietary Supplements; Docosahexaenoic Acids; Drug Combinations; Eicosapentaenoic Acid; Energy Intake; Erythrocyte Membrane; Fatty Acids, Omega-3; Female; Fibroblast Growth Factor-23; Humans; Male; Middle Aged; Oleic Acid; Parathyroid Hormone; Peritoneal Dialysis; Phosphorus; Radioimmunoassay; Renal Dialysis; Vascular Calcification; Vitamin D

A 64-year-old man was hospitalized in 2002 with symptoms of stupor, weakness, and renal colic. The clinical examination indicated borderline hypertension, small masses in the glutei, and polyuria. Laboratory tests evidenced high serum concentrations of creatinine, calcium, and phosphate. Imaging assessments disclosed widespread vascular calcifications, gluteal calcifications, and pelvic ectasia. Subsequent lab tests indicated suppressed serum parathyroid hormone, extremely high serum 25-hydroxy vitamin D, and normal serum 1,25-dihydroxy vitamin D. Treatment was started with intravenous infusion of saline and furosemide due to the evidence of hypercalcemia. Prednisone and omeprazole were added given the evidence of hypervitaminosis D. The treatment improved serum calcium, kidney function, and consciousness. The medical history disclosed recent treatment with exceptionally high doses of slow-release intra-muscular cholecalciferol and the recent excretion of urinary stones. The patient was discharged when it was possible to stop the intravenous treatment. The post-discharge treatment included oral hydration, furosemide, prednisone and omeprazole for approximately 6 months up to complete resolution of the hypercalcemia. The patient came back 12 years later because of microhematuria. Lab tests were normal for calcium/phosphorus homeostasis and kidney function. Imaging tests indicated only minor vascular calcifications. This is the first evidence of reversible vascular calcifications secondary to hypervitaminosis D.

Topics: Biomarkers; Calcium; Cholecalciferol; Diuretics; Fluid Therapy; Furosemide; Glucocorticoids; Humans; Infusions, Intravenous; Injections, Intramuscular; Male; Middle Aged; Nutrition Disorders; Omeprazole; Prednisone; Proton Pump Inhibitors; Remission Induction; Sodium Chloride; Time Factors; Treatment Outcome; Up-Regulation; Vascular Calcification; Vitamin D

People with type 1 diabetes are at high risk of premature atherosclerosis. Existing evidence suggests that impaired vitamin D metabolism may contribute to the development of atherosclerosis. We tested associations of circulating vitamin D metabolite concentrations with subclinical atherosclerosis among 1,193 participants with type 1 diabetes in the DCCT/EDIC study.. We measured plasma concentrations of 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D, and 24,25-dihydroxyvitamin D by mass spectrometry at the end of the DCCT. In a staggered cross-sectional design, we tested associations with coronary artery calcium (CAC), measured by computed tomography a median of 10 years later, and with common and internal carotid intima-media thickness (IMT), measured by B-mode ultrasonography on two occasions a median of 4 years later and a median of 10 years later. We hypothesized that lower concentrations of each vitamin D metabolite would be associated with increased risk of CAC and greater carotid IMT. RESULTS At the time metabolites were measured, mean age was 32.4 years and mean duration of diabetes was 7.5 years. The prevalence and severity of CAC tended to be lower-not higher-with lower concentrations of each vitamin D metabolite. For instance, in a fully adjusted multinomial logistic model, a 25 nmol/L lower 25-hydroxyvitamin D was associated with a 0.8-fold decrease in the odds of having higher CAC (95% CI 0.68-0.96, P = 0.01). No vitamin D metabolite was associated with either common or internal mean IMT.. We did not find evidence linking impaired vitamin D metabolism with increased subclinical atherosclerosis in type 1 diabetes.

Topics: 24,25-Dihydroxyvitamin D 3; Adult; Atherosclerosis; Calcium; Carotid Artery Diseases; Carotid Intima-Media Thickness; Coronary Artery Disease; Coronary Vessels; Diabetes Mellitus, Type 1; Female; Humans; Male; Vascular Calcification; Vitamin D

The aim of this study was to determine the prevalence of vitamin D deficiency in hemodialysis (HD) patients and the relationship between seasonal variations in vitamin D levels and vascular calcification.. As a prospective observational study, we analyzed 289 HD patients. We have assessed serum 25-hydroxyvitamin D (25D) levels at the end of the summer (September) and winter (March) and analyzed the data to reveal the association of serum 25D level with vascular calcification scores (VCS) at the end of the summer, when vitamin D levels were found to peak. Plan X-ray images of lateral lumbar spine from all subjects were studied for calculation of semiquantitative VCS as described by Kauppila.. The prevalence of 25D deficiency was 86.2% at the end of the summer and increased to 96.2% at the end of the winter. Female gender and diabetes were associated with vitamin D deficiency. According to univariate analysis, 25D levels were inversely related to vascular calcification. However, after correcting for confounding factors, this relationship lost statistical significance. Multivariate analysis showed that age, systolic blood pressure, and LDL-cholesterol levels were directly associated with a higher VCS.. Vitamin D deficiency was highly prevalent in HD patients with marked seasonal variation. However, low 25D levels could not be identified as an independent predictor of vascular calcification in these patients.

Topics: Adult; Aged; Biomarkers; Chi-Square Distribution; Female; Humans; Logistic Models; Male; Middle Aged; Multivariate Analysis; Prevalence; Prospective Studies; Radiography; Renal Dialysis; Republic of Korea; Risk Assessment; Risk Factors; Seasons; Vascular Calcification; Vitamin D; Vitamin D Deficiency

Accumulated evidence suggest that the development of vascular calcification is similar to osteogenesis. Here we want to elucidate the effect of the common used osteo-regulatory factor 1,25(OH)2D3 on vascular calcification.. Adding 10(-9) mol/L to the culture media 1,25(OH)2D3 time dependently increased the calcium deposition on the in vitro calcification of bovine vascular smooth muscle cells (BVSMCs) induced by beta-GP. It also increased cellular alkaline phosphatase activity by 301.1% during the calcified process. Osteocalcin, one of the osteogenic specific metric proteins, was dramatically elevated by 58.3% during the calcified processes, which indicate the transformation of BVSMCs to osteoblastic cell. 1,25(OH)2D3 had no such effect on non-calcified BVSMCs.. These data suggest that 1,25(OH)2D3 exerts a stimulatory effect on vascular calcification through increasing the synthesis of ALP. This effect shares the same character as osteoblast cells. This effect is limited to the calcified prone vascular cell.

Topics: Animals; Calcitriol; Cattle; Cells, Cultured; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Osteocalcin; Vascular Calcification; Vitamin D