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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.
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.
Association of Serum Phosphorus Variability with Coronary Artery Calcification among Hemodialysis Patients  [PDF]
Mengjing Wang, Haiming Li, Li You, Xiaoling Yu, Min Zhang, Ruijiang Zhu, Chuanming Hao, Zhijie Zhang, Jing Chen
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0093360
Abstract: Coronary artery calcification (CAC) is associated with increased mortality in patients on maintenance hemodialysis (MHD), but the pathogenesis of this condition is not well understood. We evaluated the relationship of CAC score (CACs) and variability in serum phosphorus in MHD patients. Seventy-seven adults on MHD at Huashan Hospital (Shanghai) were enrolled in July, 2010. CAC of all the patients were measured by computed tomography and CACs was calculated by the Agatston method at the entry of enrollment. Patients were divided into three categories according to their CACs (0~10, 11~400, and >400). Blood chemistry was recorded every 3 months from January 2008 to July 2010. Phosphorus variation was defined by the standard deviation (SD) or coefficient of variation (CV) and it was calculated from the past records. The ordinal multivariate logistic regression analysis was used to analyze the predictors of CAC. The mean patient age (± SD) was 61.7 years (±11.3) and 51% of patients were men. The mean CACs was 609.6 (±1062.9), the median CACs was 168.5, and 78% of patients had CACs more than 0. Multivariate analysis indicated that female gender (OR = 0.20, 95% CI = 0.07–0.55), age (OR = 2.31, 95% CI = 1.32–4.04), serum fibroblast growth factor 23 (OR = 2.25, 95% CI = 1.31–3.85), SD-phosphorus calculated from the most recent 6 measurements (OR = 2.12; 95% CI = 1.23–3.63), and CV-phosphorus calculated from the most recent 6 measurements (OR = 1.90, 95% CI = 1.16–3.11) were significantly and independently associated with CACs. These associations persisted for phosphorus variation calculated from past 7, 8, 9, 10, and 11 follow-up values. Variability of serum phosphorus may contribute significantly to CAC and keeping serum phosphorus stable may decrease coronary calcification and associated morbidity and mortality in MHD patients.
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.
Horizons  [PDF]
Olaf Müller
Physics , 2011,
Abstract: We define different notions of black holes, event horizons and Killing horizons for a general time-oriented manifold $(M,g)$ extending previous notions but without the assumption of asymptotical flatness. The notions of 'horizon' are always conformally invariant while the notions of 'black hole' are genuinely geometric. Some connections between the different notions are found. Finally, we put the definitions into the context of the weak cosmic censorship conjecture.
Relationship between Calcium-Phosphorus Product and Severity of Valvular Heart Insufficiency in Patients Undergoing Chronic Hemodialysis
Masoumeh Kahnooji,Mohammad Masoomi,Ali Naderinasab,Akram Zaeem
Journal of Tehran University Heart Center , 2010,
Abstract: Background: Recent interests have mainly focused on the roles of serum calcium and phosphorus and their product (Ca-P product) in the development of valvular heart disease. The present study assessed the relationship between the Ca-P product and the severity of valvular heart disease in end-stage renal disease (ESRD) patients undergoing chronic hemodialysis.Methods: This cross-sectional study reviewed the clinical course of 72 consecutive patients with the final diagnosis of ESRD candidated for chronic hemodialysis. The severity of valvular heart disease was determined using M-mode two-dimensional echocardiography. The serum calcium and phosphate values adopted were those values measured on the day between the two consecutive dialyses, and the Ca-P product was calculated.Results: The most common causes of ESRD were diabetic nephropathy, malignant hypertension, and chronic glomerulonephritis. The mean Ca-P product level in the dialysis patients was 50.44 ± 17.78 mg2/dL2. The receiver-operator characteristic (ROC) curve illustrated that a Ca-P product level > 42 mg2/dL2 was the optimal value in terms of sensitivity and specificity for predicting the presence of valvular insufficiency. Aortic insufficiency was directly associated with a high Ca-P product value after adjustment for age, gender, serum albumin, diabetes, hypertension, hyperlipidemia, coronary artery disease, and serum creatinine (β = 0.412, SE = 158, p value= 0.011).Conclusion: A positive relationship between the Ca-P product value and the severity of aortic insufficiency is expected. Achieving an appropriate control of the Ca-P product level may decrease aortic valve calcification and improve the survival of patients on chronic hemodialysis.
microRNA在高磷诱导血管平滑肌细胞钙化早期的动态变化
Dynamic alteration of microRNA in high phosphorus induced calcification of vascular smooth muscle cell
 [PDF]

肖洋,杜瑶瑶,高成,孔炜
- , 2016, DOI: 10.3969/j.issn.1671-167X.2016.05.002
Abstract: 目的:观察高磷诱导的血管平滑肌细胞钙化早期microRNA表达变化,分析其可能参与的信号通路途径。方法:采用高磷(无机磷 2.6 mmol/L)刺激大鼠血管平滑肌细胞系A7r5钙化7 d,邻甲酚酞络合酮比色法和考马斯亮蓝法检测细胞内钙含量,RTPCR法检测平滑肌细胞表型和钙化相关基因的表达变化,茜素红染色观察钙结节。microRNA microarray 法检测高磷刺激后0、3、12 h,680种microRNA表达变化。采用TAM软件分析不同时间点间信号激活情况。结果:高磷诱导的A7r5细胞钙盐含量升高9.6倍(P<0.05),平滑肌细胞表型mRNA(SM-α actin,SM22)下调(P<0.05), 钙化相关mRNA(BMP2、MSX2、Runx2)上调(P<0.05),茜素红染色后可见高磷刺激组有明显钙结节。680种microRNA在3个时间点的表达各不相同,只有6种microRNA分别逐级上调或渐渐下调。26种信号通路被明显激活,其中包括细胞凋亡、分化增殖等已知与钙化相关的信号通路。结论:microRNA参与调节血管钙化是一种动态微调的过程,为血管钙化研究带来新的思路。
Objective:To study the change of microRNA during the early stage of high phosphorus induced vascular smooth muscle cell (VSMC) calcification and its related mechanism.Methods:The in vitro calcification model was created through stimulating VSMC cell line A7r5 with high Pi (2.6 mmol/L) for 7 d. The calcification was validated through ocresolphthalein complexone colorimetry to detect the cellular calcium content, real-time PCR to measure the calcification-related gene expression and alizarin red staining to observe the formation of calcium nodules. Based on the cell calcification model, microRNA microarray array was applied to screen the profiles of microRNA expression in VSMC following high Pi stimulation for different periods (0, 3 and 12 h). The array data were analyzed by TAM tool to explore the activated signaling pathway.Results: The calcium content of A7r5 cells induced by high Pi was increased 9.6 times high as cells without Pi treatment (P<0.05). VSMC contractile phenotype genes (SM-α actin, SM22) were down-regulated (P<0.05), while calcification-related genes (BMP2, MSX2, Runx2) were up-regulated (P<0.05) in VSMC stimulated by high Pi. The calcium nodules were obviously formed in cells after 7 d high Pi treatment. In microarray experiment, 680 individual microRNAs were detected in high Pi-treated VSMCs at different time points (0, 3 and 12 h). Among these genes, miR-183, miR-664 and miR-9* were increased whereas miR-542-5P, let-7f and miR-29a were decreased in time-dependent manners. Twenty-six kinds of signaling pathways, including cell apoptosis, differentiation and proliferation, were significantly activated. All these activated pathways were associated with calcification. Conclusion:This study implies that microRNA changed in high Pi-induced VSMCs may involve in the process of calcification.
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 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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