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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
Association of Fetuin-A Levels with Carotid Intima Media Thickness and Valvular Calcification in Hemodialysis and Peritoneal Dialysis Patients  [PDF]
Solak, Yal??n,?nal, Ali,Atalay, Hüseyin,Kayrak, Mehmet
The Turkish Nephrology, Dialysis and Transplantation Journal , 2013, DOI: 10.5262/tndt.2013.1001.07
Abstract: BACKGROUND: Fetuin-A is a negative acute-phase reactant which prevents vascular calcification. Coronary artery disease (CAD) is the most important cause of mortality in patients undergoing renal replacement therapy (RRT). The key element of cardiovascular disease (CVD) seen in end-stage renal disease patients who are on dialysis treatment is accelerated calcific atherosclerosis. There are a limited number of studies in which HD and PD is compared in terms of fetuin-A level.OBJECTIVE: We aimed to investigate the association of serum fetuin-A level with valvular calcification and predictors of CAD in hemodialysis (HD) and peritoneal dialysis (PD) patients.MATERIAL and METHODS: 39 HD (24 males, 15 females) and 39 PD (25 males, 14 females) patients were included in the study. We determined carotid artery intima media thickness (CIMT) and evaluated heart valve calcification via echocardiography. We also measured serum fetuin-A level, CRP, ferritin, fibrinogen and serum albumin level. According to fetuin-A level, patients were stratified into quartiles.RESULTS: Fetuin-A level was significantly lower in HD patients when compared with that of PD patients (28.6±5.934 ng/ml, 32±4.8 ng/ml respectively p<0.001). There was a significant negative correlation between CIMT and fetuin-A level. CIMT was found to be lower in PD patients than in HD patients. We found a positive correlation between fetuin-A and dialysis adequacy and albumin level. There was a negative correlation of fetuin-A with age, fibrinogen, ferritin and CRP. Fetuin-A level was lower in patients with aortic calcification.CONCLUSION: Fetuin-A level was found to be lower in HD patients. Fetuin-A may be a novel marker for CVD in patients undergoing RRT.BACKGROUND: Fetuin-A is a negative acute-phase reactant which prevents vascular calcification. Coronary artery disease (CAD) is the most important cause of mortality in patients undergoing renal replacement therapy (RRT). The key element of cardiovascular disease (CVD) seen in end-stage renal disease patients who are on dialysis treatment is accelerated calcific atherosclerosis. There are a limited number of studies in which HD and PD is compared in terms of fetuin-A level.OBJECTIVE: We aimed to investigate the association of serum fetuin-A level with valvular calcification and predictors of CAD in hemodialysis (HD) and peritoneal dialysis (PD) patients.MATERIAL and METHODS: 39 HD (24 males, 15 females) and 39 PD (25 males, 14 females) patients were included in the study. We determined carotid artery intima media thickness (CIMT) and evaluated heart valve c
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.
Valvular heart disease in patients undergoing chronic hemodialysis  [PDF]
Loncar Daniela,Tabakovic Mithat,Mulic-Bacic Suada,Hadzovic Djani
Cardiologia Croatica , 2013,
Abstract: Valvular heart disease is a common phenomenon in patients undergoing chronic hemodialysis. Abnormalities include valvular and annular thickening and calcification of any of the heart valves, causing regurgitation and/or stenosis. Valvular thickening or sclerosis in patients undergoing chronic dialysis treatment usually affects the aortic and mitral valve. Aortic valve calcification is recorded in up to a half of hemodialyzed patients, occurring from 10 to 20 years earlier than in the general population. Valvular regurgitation occurs mostly in mitral, tricuspid and less commonly in aortic valve. The aim of the article was to determine the incidence of valvular heart disease in asymptomatic patients undergoing chronic dialysis.The analysis involves a total of 50 patients, of whom 35 (70%) are treated by hemodialysis and 15 (30%) by continuous ambulatory peritoneal dialysis. Valvular thickening or sclerosis was diagnosed in 20 (40%) patients. Sclerosis of mitral cusps was diagnosed in 9 (18%) patients and sclerosis of aortic cusps was diagnosed in 11 (22%) patients. Heart valve calcifications were diagnosed in 12 (31%) patients. Mild aortic stenosis was present in 3 (6%) patients. Mitral regurgitation was diagnosed in 38 (76%) patients, aortic regurgitation in 14 (28%), and tricuspid regurgitation in 24 (48%) patients.The evaluation of the valve apparatus for all patients undergoing chronic dialysis program requires echocardiographic examination that is to be performed, considering the high prevalence of valvular heart diseases.
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.
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,
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.
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.
Secondary hyperparathyroidism: Risk factor for development of cardiovascular complications in patients on hemodialysis  [PDF]
Petrovi? Dejan,Stojimirovi? Biljana
Medicinski Pregled , 2010, DOI: 10.2298/mpns1010674p
Abstract: Introduction. Cardiovascular disease is a leading cause of death among hemodialysis patients. Secondary hyperparathyroidism. Secondary hyperparathyroidism is one of the main factors for the development of cardiovascular complications among these patients. A high concentration of parathormone, hypercalcemia, hyperphosphatemia and high calcium x phosphate product among dialysis patients play a crucial role in the development of vascular (calcification of coronary artery) and valvular calcifications. Discussion and conclusion. With every new patient on hemodialysis it is necessary to see if there is a vascular/valvular calcification in order to single out the patients at risk of progression of coronary artery calcification and to use non-calcium containing binder phosphate in due time. Noncalcium containing binder phosphate, new active vitamin D agents and calcimimetics prevent the development of secondary hyperparathyroidism as well as cardiovascular complications and decrease the rate of cardiovascular morbidity and mortality of these patients.
Valvular and perivalvular involvement in patients with chronic kidney disease
Neelavathi Senkottaiyan,Saad Hafidh,Farrin A Manian,Martin A Alpert,
Neelavathi Senkottaiyan
,Saad Hafidh,Farrin A. Manian,Martin A. Alpert

老年心脏病学杂志(英文版) , 2005,
Abstract: Mitral annular calcification (MAC) and aortic valve calcification (AVC) are the most common valvular and perivalvular abnormalities in patients with chronic kidney disease (CKD). Both MAC and AVC occur at a younger age in CKD patients than in the general population. AVC progresses to aortic stenosis and mild aortic stenosis progresses to severe aortic stenosis at a more rapid rate in patients with CKD than in the general population. The use of calcium-free phosphate binders in such patients may reduce the calcium burden in valvular and perivalvular structures and retard the rate of progression of aortic stenosis. Despite high rates of morbidity and mortality, the prognosis associated with valve surgery in patients with CKD is better than without valve surgery. Infective endocarditis remains an important complication of CKD, particularly in those treated with hemodialysis.
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