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Inflammation Disrupts the LDL Receptor Pathway and Accelerates the Progression of Vascular Calcification in ESRD Patients  [PDF]
Jing Liu, Kun Ling Ma, Min Gao, Chang Xian Wang, Jie Ni, Yang Zhang, Xiao Liang Zhang, Hong Liu, Yan Li Wang, Bi Cheng Liu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047217
Abstract: Background Chronic inflammation plays a crucial role in the progression of vascular calcification (VC). This study was designed to investigate whether the low-density lipoprotein receptor (LDLr) pathway is involved in the progression of VC in patients with end-stage renal disease (ESRD) during inflammation. Methods and Results Twenty-eight ESRD patients were divided into control and inflamed groups according to plasma C-reactive protein (CRP) level. Surgically removed tissues from the radial arteries of patients receiving arteriovenostomy were used in the experiments. The expression of tumour necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1) of the radial artery were increased in the inflamed group. Hematoxylin-eosin and alizarin red S staining revealed parallel increases in foam cell formation and calcium deposit formation in continuous cross-sections of radial arteries in the inflamed group compared to the control, which were closely correlated with increased LDLr, sterol regulatory element binding protein-2 (SREBP-2), bone morphogenetic proteins-2 (BMP-2), and collagen I protein expression, as shown by immunohistochemical and immunofluorescent staining. Confocal microscopy confirmed that inflammation enhanced the translocation of the SREBP cleavage-activating protein (SCAP)/SREBP-2 complex from the endoplasmic reticulum to the Golgi, thereby activating LDLr gene transcription. Inflammation increased alkaline phosphatase protein expression and reduced α-smooth muscle actin protein expression, contributing to the conversion of the vascular smooth muscle cells in calcified vessels from the fibroblastic to the osteogenic phenotype; osteogenic cells are the main cellular components involved in VC. Further analysis showed that the inflammation-induced disruption of the LDLr pathway was significantly associated with enhanced BMP-2 and collagen I expression. Conclusions Inflammation accelerated the progression of VC in ESRD patients by disrupting the LDLr pathway, which may represent a novel mechanism involved in the progression of both VC and atherosclerosis.
The vascular phenotype in Pseudoxanthoma elasticum and related disorders: contribution of a genetic disease to the understanding of vascular calcification  [PDF]
Georges Lefthériotis,Loukman Omarjee,Olivier Le Saux,Daniel Henrion,Fabrice Prunier,Serge Willoteaux,Ludovic Martin
Frontiers in Genetics , 2013, DOI: 10.3389/fgene.2013.00004
Abstract: Vascular calcification is a complex and dynamic process occurring in various physiological conditions such as aging and exercise or in acquired metabolic disorders like diabetes or chronic renal insufficiency. Arterial calcifications are also observed in several genetic diseases revealing the important role of unbalanced or defective anti- or pro-calcifying factors. Pseudoxanthoma elasticum (PXE) is an inherited disease (OMIM 264800) characterized by elastic fiber fragmentation and calcification in various soft conjunctive tissues including the skin, eyes, and arterial media. The PXE disease results from mutations in the ABCC6 gene, encoding an ATP-binding cassette transporter primarily expressed in the liver, kidneys suggesting that it is a prototypic metabolic soft-tissue calcifying disease of genetic origin. The clinical expression of the PXE arterial disease is characterized by an increased risk for coronary (myocardial infarction), cerebral (aneurysm and stroke), and lower limb peripheral artery disease. However, the structural and functional changes in the arterial wall induced by PXE are still unexplained. The use of a recombinant mouse model inactivated for the Abcc6 gene is an important tool for the understanding of the PXE pathophysiology although the vascular impact in this model remains limited to date. Overlapping of the PXE phenotype with other inherited calcifying diseases could bring important informations to our comprehension of the PXE disease.
Induction of calcification by serum depletion in cell culture: a model for focal calcification in aortas related to atherosclerosis
Howard HT Hsu, Antonio Artigues, Maria T Villar
Lipids in Health and Disease , 2008, DOI: 10.1186/1476-511x-7-2
Abstract: Rabbit aortic smooth muscle cells were grown to confluence in a culture media containing 10 % fetal bovine serum (FBS). The confluent cells were then exposed to the media for 2 hrs with or without serum at a Ca × P ion product range of 4.5–9.4 mM2. In contrast to the cells cultured in the presence of FBS, confluent cells in its absence displayed marked mineral-positive alizarin red staining and infrared absorption of mineral phosphate. A kinetic parameter C1/2 was used to designate the concentration of serum or its protein constituents needed to reduce the deposition of Ca and P by half. The C1/2 for FBS and rabbit serum was 0.04–0.07 % The C1/2 value for rabbit serum proteins was 13.5 μg/ml corresponding to the protein concentration in 0.06 % of serum. This C1/2 was markedly smaller than 86.2 μg/ml for bovine serum albumin present in 0.37 % serum (p < 0.05). Serum depletion also caused marked membrane translocation as evidenced through a specific apoptosis dye uptake by cells. The proteomic analysis of calcifying vesicles, which can be released by serum depletion, revealed several calcification-related proteins.The aortic smooth muscle cell culture model suggests that serum depletion may play a role in the initiation of aortic calcification. The serum exhibits remarkable ability to inhibit cell-mediated calcification.Clinical and epidemiological studies have implicated vascular calcification in myocardial infarction [1], instability and rigidity of the arterial wall [2], bioprosthetic valve failures [3], etc. In spite of the evidence that both physiological and pathological calcification is regulated through gene expressions of osteopontin (OPN) [4], matrix γ-carboxyglutamate protein (MGP) [5], and osteoprotegerin (OPG) [6], the mechanisms whereby calcium phosphate minerals are initially deposited in the arterial wall remain uncertain [7-9]. The issue of the involvement of the active process vs. passive process in atherosclerosis-related calcification was reviewed
Vascular and Valvular Calcification in Chronic Peritoneal Dialysis Patients  [PDF]
Angela Yee-Moon Wang
International Journal of Nephrology , 2011, DOI: 10.4061/2011/198045
Abstract: Cardiovascular disease accounts over half of the total mortality in peritoneal dialysis (PD) patients. In addition, there is an increasing recognition of a high prevalence of vascular and valvular calcification that may contribute to the increased all-cause and cardiovascular mortality in the PD patients. Disturbed mineral metabolism in association with chronic kidney disease has been suggested as one of the major contributing factors to the increased vascular/valvular calcification in this population. In this paper, we provide an overview of the prevalence and importance of this complication in the PD patients. In addition, we review the contributing factors and some emerging mechanisms for this complication. Furthermore, we discuss some therapeutic strategies that may be useful in limiting the progression of vascular/valvular calcification in the PD population. 1. Introduction Cardiovascular disease is the leading cause of death in end-stage renal disease (ESRD) patients receiving long-term peritoneal dialysis (PD) therapy. Data from the Canada and United States (CANUSA) Peritoneal Dialysis Study showed that nearly half of the mortality in PD patients was due to cardiovascular disease [1]. According to data from the United State Renal Data System (USRDS), this trend has remained more or less the same in the recent years [2]. Vascular/valvular calcifications are important and highly prevalent complications in ESRD patients including those receiving PD therapy and very much contributed to the exceedingly high cardiovascular mortality in this population. Numerous observational cohort studies demonstrated the prognostic importance of vascular/valvular calcification in ESRD patients. Using plain radiographs to estimate number of arterial sites with calcification including carotid artery, abdominal aorta, and iliofemoral axis, both the presence and extent of vascular calcifications are strong predictors of cardiovascular and all-cause mortality in the ESRD patients [3]. Abdominal aortic calcification detected nonquantitatively using plain lateral abdominal radiographs has also been shown to be an independent predictor of all-cause mortality and cardiovascular death in hemodialysis patients [4]. Using multislice computed tomography (MSCT) that enables quantification of calcification, Block et al. demonstrated a significant mortality effect of the severity of coronary artery calcium score in incident hemodialysis patients [5]. Cardiac valvular calcification, detected using echocardiography, also predicts all-cause mortality and cardiovascular death in chronic
Bone metabolism and vascular calcification
Danilevicius, C.F.;Lopes, J.B.;Pereira, R.M.R.;
Brazilian Journal of Medical and Biological Research , 2007, DOI: 10.1590/S0100-879X2007000400001
Abstract: osteoporosis and atherosclerosis are chronic degenerative diseases which have been considered to be independent and whose common characteristic is increasing incidence with age. at present, growing evidence indicates the existence of a correlation between cardiovascular disease and osteoporosis, irrespective of age. the morbidity and mortality of osteoporosis is mainly related to the occurrence of fractures. atherosclerosis shows a high rate of morbidity and especially mortality because of its clinical repercussions such as angina pectoris, acute myocardial infarction, stroke, and peripheral vascular insufficiency. atherosclerotic disease is characterized by the accumulation of lipid material in the arterial wall resulting from autoimmune and inflammatory mechanisms. more than 90% of these fatty plaques undergo calcification. the correlation between osteoporosis and atherosclerosis is being established by studies of the underlying physiopathological mechanisms, which seem to coincide in many biochemical pathways, and of the risk factors for vascular disease, which have also been associated with a higher incidence of low-bone mineral density. in addition, there is evidence indicating an action of antiresorptive drugs on the reduction of cardiovascular risks and the effect of statins, antihypertensives and insulin on bone mass increase. the mechanism of arterial calcification resembles the process of osteogenesis, involving various cells, proteins and cytokines that lead to tissue mineralization. the authors review the factors responsible for atherosclerotic disease that correlate with low-bone mineral density.
Carotid artery calcification at the initiation of hemodialysis is a risk factor for cardiovascular events in patients with end-stage renal disease: a cohort study
Masaru Nakayama, Yoriko Ura, Masaharu Nagata, Yasushi Okada, Yoko Sumida, Kanako Nishida, Hirofumi Ikeda, Yoshiki Kaizu
BMC Nephrology , 2011, DOI: 10.1186/1471-2369-12-56
Abstract: One-hundred thirty-three patients who had been started on hemodialysis between 2004 and 2008 were included in this retrospective cohort study. These patients received multi-detector computed tomography to assess CAAC at the initiation of hemodialysis. Composite CV events, including ischemic heart disease, heart failure, cerebrovascular diseases, and CV deaths after the initiation of hemodialysis, were examined in each patient.CAAC was found in 94 patients (71%). At the end of follow-up, composite CV events were seen in 47 patients: ischemic heart disease in 20, heart failure in 8, cerebrovascular disease in 12, and CV deaths in 7. The incidence of CAAC was 87% in patients with CV events, which was significantly higher than the rate (62%) in those without. Kaplan-Meier analysis showed a significant increase in composite CV events in patients with CAAC compared with those without CAAC (p = 0.001, log-rank test). Univariate analysis using a Cox hazards model showed that age, smoking, common carotid artery intima-media thickness and CAAC were risk factors for composite CV events. In multivariate analysis, only CAAC was a significant risk factor for composite CV events (hazard ratio, 2.85; 95% confidence interval, 1.18-8.00; p = 0.02).CAAC is an independent risk factor for CV events in ESRD patients. The assessment of CAAC at the initiation of hemodialysis is useful for predicting the prognosis.The annual mortality rate due to cardiovascular (CV) disease in patients with end-stage renal disease (ESRD) is more than an order of magnitude greater than that in the population with normal kidney function [1]. Vascular calcification is a common complication of ESRD. Arterial disease in patients with ESRD is characterized by a high degree of intimal as well as medial calcification. Arterial intimal calcification is associated with atherosclerotic burden, resulting in arterial stenosis or occlusion; on the other hand, arterial medial calcification is related to arteriosclerosis,
The Effect of Paricalcitol on Vascular Calcification and Cardiovascular Disease in Uremia: Beyond PTH Control
Mario Cozzolino,Florjan Mehmeti,Paola Ciceri,Elisa Volpi,Andrea Stucchi,Irene Brenna,Daniele Cusi
International Journal of Nephrology , 2011, DOI: 10.4061/2011/269060
Abstract: Secondary hyperparathyroidism is a systemic disorder that associates with bone and cardiovascular disease, including arterial calcification. Treatment with calcitriol, the active form of vitamin D, reduces parathyroid hormone levels, but may result in elevations in serum calcium and phosphorus, increasing the risk of vascular calcification in dialysis patients. New vitamin D receptor activators (VDRAs) have been developed and investigated with the rationale to treat high serum PTH levels, with a reduced risk of hypercalcemia and hyperphosphatemia. Paricalcitol is a selective VDRA that suppresses PTH secretion with minimal increases on serum calcium and phosphate. Moreover, paricalcitol prevents vascular calcification in experimental models of renal failure, compared with calcitriol.
The Phosphorus and the Vascular Calcification in ESRD between Old Adventures and New Horizons  [PDF]
Biagio Raffaele Di Iorio,Markus Ketteler,Domenico Russo,Angela Wang
International Journal of Nephrology , 2011, DOI: 10.4061/2011/716526
Abstract:
The Phosphorus and the Vascular Calcification in ESRD between Old Adventures and New Horizons  [PDF]
Biagio Raffaele Di Iorio,Markus Ketteler,Domenico Russo,Angela Wang
International Journal of Nephrology , 2011, DOI: 10.4061/2011/716526
Abstract:
Evaluation of Peripheral Vascular Calcification and Serum Magnesium Level in a Group of Egyptian Hemodialysis Patients
K Okasha, A El Bendary, A Mourad
Arab Journal of Nephrology and Transplantation , 2010,
Abstract: Introduction: Vascular calcification is a risk factor for cardiovascular mortality in the general population. It is highly prevalent in end stage renal disease (ESRD) patients. Low magnesium (Mg) levels have been reported to have a strong association with vascular calcification in hemodialysis (HD) patients. The aims of this study were to evaluate the prevalence of vascular calcification and its relation to serum Mg concentration in a group of Egyptian HD patients. Methods: We studied 65 stable patients undergoing maintenance HD for more than 6 months. Vascular calcification was evaluated using hand roentgenography. Serum Mg, phosphorus, corrected calcium and intact parathyroid hormone (iPTH) levels were compared between patients with and without vascular calcification. Results: The study included 41 male and 24 female patients, aged 43-70 years. Vascular calcification was present in 38.5% of the patients. Mean serum Mg level was 2.88 ± 0.51 mg/dl. Male gender was more common in patients with vascular calcification, and they had significantly longer HD duration and significantly higher serum phosphorus and iPTH levels. Serum Mg level was significantly lower in patients with vascular calcification (2.36 ± 0.26 mg/dl vs.3.21 ± 0.32 mg/dl, p = 0.001). Serum Mg concentration remained as independent negative predictor of hand-artery vascular calcification after adjustment for age, gender, duration of HD, serum phosphorus and iPTH levels. Conclusion: Vascular calcification is common in the study population and is associated with a lower serum Mg level. High or sustained-normal Mg levels may have a protective role against the development of vascular calcification in HD patients.
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