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Association of Serum Phosphate and Related Factors in ESRD-Related Vascular Calcification  [PDF]
Cai-Mei Zheng,Kuo-Cheng Lu,Chia-Chao Wu,Yung-Ho Hsu,Yuh-Feng Lin
International Journal of Nephrology , 2011, DOI: 10.4061/2011/939613
Abstract: Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients. Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification. Hyperphosphatemia and vascular calcification become popular discussion among nephrologist environment more than five decades, and many researches have been evolved. Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications. 1. Introduction Vascular calcification is a kind of extraosseous calcification and is associated with aging physiologically, and a number of disorders including ESRD, diabetes mellitus, and cardiovascular disease pathologically. Multifactorial processes contribute to VC in which derangements in calcium and phosphorus homeostasis plays an important role and becomes popular therapeutic target nowadays. In ESRD patients with vascular calcification, a mixture of intimal and medial calcification has been observed in the effected vessels with dominant medial involvement. The risk of CVD mortality in ESRD patients with vascular calcification is 20 to 30 times higher than that of the general population [1–5]. Although phosphate is important for diverse cellular and physiological functions, impaired renal function with resultant phosphate accumulation with consequent bone and mineral disorders and vascular calcification are major problems among nephrologists. The increased risk of CVD mortality by hyperphosphatemia was partially explained by the predisposition of this population to vascular calcification [6–8]. (Figure 1) Even in early stage CKD, serum phosphorus level disturbances are proved to promote vascular calcification, hypertension, myocardial hypertrophy, and heart failure [9–11]. Current understanding of relationship between phosphorus and those disorders becomes popular in medical field, with the hope of halting or retarding the vascular calcification from the very early status in those patients. Figure 1: Mechanisms of VSMC osteogenesis during vascular calcification in chronic kidney disease. VSMC upregulate expression of transcription factors Osf2/Cbfa1 which were enhanced by ROS, leptin, vitamin D, increased CaxP product, or high PO 4 (Pi) levels induced by Pit-1. VSMC activation occurs in part as a result of the phenotypic switch of VSMCs into osteoblast-like cells. VSMCs that have acquired an osteogenic phenotype express ALP and produce hydroxyapatite crystals.
Study Of Cardic Valvular Calcification In ESRD Patients On Regular Hemodialysis (A Single Center Study)  [PDF]
Abdel-Bassit El Shaarawy1, Mona Hosny1, Manar Raafat2 and Nelly
Egyptian Journal of Hospital Medicine , 2012,
Abstract: Cardiac valve calcification are common among patients with chronic kidney disease (CKD). Risk factors include alterations in calcium and phosphorus metabolism, elevated calcium phosphorus product and persistent elevations in plasma parathyroid hormone (PTH). Echocardiography is a simple and inexpensive method for detection of valvular calcifications as suggested by KDIGO guidelines. 60 Patients on regular HD constituted group A (36 males and 24 females) and 25 healthy volunteers constituted group B. Group A was subdivided into: Group I: 21 patients with no valvular calcification, group 2: 26 patients with aortic valve calcification and group 3: 13 patients with aortic and mitral valve calcification. For all, the following was done: clinical examination, serum Ca, serum P, serum albumin, serum creatinine, BUN and PTH level in blood. M-mode echo cardiography was done for all. Age, duration of dialysis and duration of 1ry kidney disease was higher in group 2 and 3 compared to group 1 (p = 0.0001). Calcium was higher in group 2 than group 1 (p = 0.09) and group 3 (p = 0.004) than group I phosphorus was higher in group 2 and 3 than group 1 (P = 0.001). P was higher in group 3 than group 2 (p = 0.0001). Ca x P was higher in group 2 and 3 than group 1 (p = 0.0001), in group 3 than group 2 (p = 0.01) PTH was higher in group 1 than group 2 (p = 0.06). Cardiac dysfunction by echocardiography was least in group 1, increasing in group 2 and being highest in group 3. It was found that calcified valve groups has taken higher doses of Calcium and Vitamin D3 .We have to take care on prescribing Ca and vitamin D3 to ESRD patients on regular HD.
TRAIL-Deficiency Accelerates Vascular Calcification in Atherosclerosis via Modulation of RANKL  [PDF]
Belinda A. Di Bartolo, Sian P. Cartland, Hanis H. Harith, Yuri V. Bobryshev, Michael Schoppet, Mary M. Kavurma
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074211
Abstract: The osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) cytokine system, not only controls bone homeostasis, but has been implicated in regulating vascular calcification. TNF–related apoptosis-inducing ligand (TRAIL) is a second ligand for OPG, and although its effect in vascular calcification in vitro is controversial, its role in vivo is not yet established. This study aimed to investigate the role of TRAIL in vascular calcification in vitro using vascular smooth muscle cells (VSMCs) isolated from TRAIL?/? and wild-type mice, as well as in vivo, in advanced atherosclerotic lesions of TRAIL?/?ApoE?/? mice. The involvement of OPG and RANKL in this process was also examined. TRAIL dose-dependently inhibited calcium-induced calcification of human VSMCs, while TRAIL?/? VSMCs demonstrated accelerated calcification induced by multiple concentrations of calcium compared to wild-type cells. Consistent with this, RANKL mRNA was significantly elevated with 24 h calcium treatment, while OPG and TRAIL expression in human VSMCs was inhibited. Brachiocephalic arteries from TRAIL?/?ApoE?/? and ApoE?/? mice fed a high fat diet for 12 w demonstrated increased chondrocyte-like cells in atherosclerotic plaque, as well as increased aortic collagen II mRNA expression in TRAIL?/?ApoE?/? mice, with significant increases in calcification observed at 20 w. TRAIL?/?ApoE?/? aortas also had significantly elevated RANKL, BMP-2, IL-1β, and PPAR-γ expression at 12 w. Our data provides the first evidence that TRAIL deficiency results in accelerated cartilaginous metaplasia and calcification in atherosclerosis, and that TRAIL plays an important role in the regulation of RANKL and inflammatory markers mediating bone turn over in the vasculature.
Increased LDL susceptibility to oxidation accelerates future carotid artery atherosclerosis
Toshinari Aoki, Tsueko Abe, Eiji Yamada, Takayuki Matsuto, Masahiko Okada
Lipids in Health and Disease , 2012, DOI: 10.1186/1476-511x-11-4
Abstract: We selected 394 individuals (169 males and 225 females) who underwent a second carotid artery ultrasonographic examination in 2001 - 2002 for the present study. The susceptibility of LDL to oxidation was determined as the photometric absorbance and electrophoretic mobility of samples that had been collected in 1996 - 1997. The measurements were compared with ultrasonographic findings obtained in 2001 - 2002.The multivariate-adjusted model showed that age (odds ratio (OR), 1.034; 95% confidence interval (95%CI), 1.010 - 1.059), HbA1c (OR, 1.477; 95%CI, 0.980 - 2.225), and photometric O/N (OR, 2.012; 95%CI, 1.000 - 4.051) were significant variables that could independently predict the risk of new carotid artery atherosclerosis.The susceptibility of LDL to oxidation was a significant parameter that could predict new carotid artery atherosclerosis over a 5-year period, and higher susceptibility was associated with a higher incidence of new carotid artery atherosclerosis.The oxidation of low-density lipoprotein (LDL) is widely believed to be an important event in the pathogenesis of atherosclerosis. Macrophages endocytose oxidized LDL in an uncontrolled manner, which results in the generation of cholesterol-laden foam cells that characterize atherosclerotic lesions [1,2]. The oxidation of LDL in vitro can be mediated by cells or mimicked in a cell free system using transition metal ions such as copper or iron as prooxidants [3,4]. Metal ions are usually prerequisite for LDL oxidation, at least in vitro. Catalytically active copper and iron are also present in human atherosclerotic lesions [5].The initial step of LDL oxidation is the peroxidation of polyunsaturated fatty acids among LDL lipids. Fragments of modified fatty acids covalently attach to apolipoprotein B-100 (apoB-100) and neutralize its positively charged epsilon-amino acid group [2,6]. Another possible mechanism of the oxidation is that copper directly binds to apoB-100 at sites that are located at least on r
Ceramide Mediates Ox-LDL-Induced Human Vascular Smooth Muscle Cell Calcification via p38 Mitogen-Activated Protein Kinase Signaling  [PDF]
Lizhen Liao, Qin Zhou, Yan Song, Weikang Wu, Huimin Yu, Sheng Wang, Yanling Chen, Meihong Ye, Lihe Lu
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0082379
Abstract: Vascular calcification is associated with significant cardiovascular morbidity and mortality, and has been demonstrated as an actively regulated process resembling bone formation. Oxidized low density lipoprotein (Ox-LDL) has been identified as a regulatory factor involved in calcification of vascular smooth muscle cells (VSMCs). Additionally, over-expression of recombinant human neutral sphingomyelinase (N-SMase) has been shown to stimulate VSMC apoptosis, which plays an important role in the progression of vascular calcification. The aim of this study is to investigate whether ceramide regulates Ox-LDL-induced calcification of VSMCs via activation of p38 mitogen-activated protein kinase (MAPK) pathway. Ox-LDL increased the activity of N-SMase and the level of ceramide in cultured VSMCs. Calcification and the osteogenic transcription factor, Msx2 mRNA expression were reduced by N-SMase inhibitor, GW4869 in the presence of Ox-LDL. Usage of GW4869 inhibited Ox-LDL-induced apoptosis in VSMCs, an effect which was reversed by C2-ceramide. Additionally, C2-ceramide treatment accelerated VSMC calcification, with a concomitant increase in ALP activity. Furthermore, C2-ceramide treatment enhanced Ox-LDL-induced VSMC calcification. Addition of caspase inhibitor, ZVAD-fmk attenuated Ox-LDL-induced calcification. Both Ox-LDL and C2-ceramide treatment increased the phosphorylation of p38 MAPK. Inhibition of p38 MAPK by SB203580 attenuated Ox-LDL-induced calcification of VSMCs. These data suggest that Ox-LDL activates N-SMase-ceramide signaling pathway, and stimulates phosphorylation of p38 MAPK, leading to apoptosis in VSMCs, which initiates VSMC calcification.
Lactobacillus rhamnosus Accelerates Zebrafish Backbone Calcification and Gonadal Differentiation through Effects on the GnRH and IGF Systems  [PDF]
Matteo A. Avella, Allen Place, Shao-Jun Du, Ernest Williams, Stefania Silvi, Yonathan Zohar, Oliana Carnevali
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0045572
Abstract: Endogenous microbiota play essential roles in the host’s immune system, physiology, reproduction and nutrient metabolism. We hypothesized that a continuous administration of an exogenous probiotic might also influence the host’s development. Thus, we treated zebrafish from birth to sexual maturation (2-months treatment) with Lactobacillus rhamnosus, a probiotic species intended for human use. We monitored for the presence of L. rhamnosus during the entire treatment. Zebrafish at 6 days post fertilization (dpf) exhibited elevated gene expression levels for Insulin-like growth factors -I and -II, Peroxisome proliferator activated receptors -α and -β, VDR-α and RAR-γ when compared to untreated-10 days old zebrafish. Using a gonadotropin-releasing hormone 3 GFP transgenic zebrafish (GnRH3-GFP), higher GnRH3 expression was found at 6, 8 and 10 dpf upon L. rhamnosus treatment. The same larvae exhibited earlier backbone calcification and gonad maturation. Noteworthy in the gonad development was the presence of first testes differentiation at 3 weeks post fertilization in the treated zebrafish population -which normally occurs at 8 weeks- and a dramatic sex ratio modulation (93% females, 7% males in control vs. 55% females, 45% males in the treated group). We infer that administration of L. rhamnosus stimulated the IGF system, leading to a faster backbone calcification. Moreover we hypothesize a role for administration of L. rhamnosus on GnRH3 modulation during early larval development, which in turn affects gonadal development and sex differentiation. These findings suggest a significant role of the microbiota composition on the host organism development profile and open new perspectives in the study of probiotics usage and application.
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
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
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
The impact of losartan on the lifetime incidence of ESRD and costs in Mexico
Arredondo, Armando;Burke, Thomas A;Carides, George W;Lemus, Edith;Querol, Julio;
Revista de investigación clínica , 2005,
Abstract: background. the renaal (reduction of endpoints in type 2 diabetes with the angiotensin ii antagonist losartan) study demonstrated that treatment with losartan reduced the risk of esrd by 29% among hypertensive patients with type 2 diabetes and diabetic nephropathy. the objective of this study was to project the effect of losartan compared to placebo on the lifetime incidence of esrd and associated costs from a third-party payer perspective in mexico. methods. a competing risks method was used to estimate lifetime incidence of esrd, while accounting for the risk of death without esrd. the cost associated with esrd was estimated by combining the cumulative incidence of esrd with the lifetime cost associated with esrd. total cost was estimated as the sum of the cost associated with esrd from the three main public institutions in mexico, the lifetime cost of losartan therapy, and other costs (non-esrd/non-losartan) expected for patients with type 2 diabetes. survival was estimated by weighting the life expectancies with and without esrd by the cumulative risk of esrd. results. the projected lifetime incidence of esrd for losartan patients was lower (66%) compared with placebo patients (83%). this reduction in esrd resulted in a decrease in esrd-related cost of m$49,737 per patient and a discounted gain of 0.697 life years per patient. after accounting for the cost of losartan and the additional cost associated with greater survival, we projected that treatment with losartan would result in a net savings of m$24,073 per patient. conclusion. treatment with losartan in patients with type 2 diabetes and nephropathy not only reduced the within-trial incidence of esrd but is projected to result in lifetime reductions in esrd, increased survival, and overall cost savings to public institutions in mexico.
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