

{"id":2785,"date":"2020-03-24T19:16:11","date_gmt":"2020-03-25T00:16:11","guid":{"rendered":"https:\/\/staging.advancedrenaleducation.com\/wparep\/?post_type=article&#038;p=1139"},"modified":"2025-05-21T12:58:08","modified_gmt":"2025-05-21T17:58:08","slug":"endothelial-protection","status":"publish","type":"article","link":"https:\/\/staging.advancedrenaleducation.com\/wparep\/asiapacific\/article\/endothelial-protection\/","title":{"rendered":"Endothelial Protection"},"content":{"rendered":"<p>Cardiovascular causes \u2014including arrhythmias, cardiac arrest, congestive heart failure (CHF), acute myocardial infarction (AMI), and atherosclerotic heart disease (ASHD)\u2014are the leading cause of mortality in end-stage kidney disease (ESKD) patients on hemodialysis. The etiology of ESKD is complex and multifactorial \u2013 volume and pressure overload, abnormalities in cardiac morphology and function, dyslipidemias, atherosclerosis, and nutritional derangements all play a role.<\/p>\n<p>At the heart of atherosclerosis is an abnormal and dysfunctional endothelium, which is consistently observed in ESKD patients<sup>1,2<\/sup>. Bone marrow-derived endothelial progenitor cells (EPCs) are important for endothelial maintenance. EPCs mediate repair of damaged vascular endothelium, promote angiogenesis, and protect the blood vessel from atherosclerosis development<sup>3<\/sup>. Several reports in the literature describe qualitative and quantitative abnormalities of EPCs in uremic and dialyzed patients<sup>4\u20138<\/sup>.<\/p>\n<p>Intensifying the HD prescription does not appear to have a direct effect on endothelial progenitor cell numbers; however, Chan et al<sup>9<\/sup> hypothesized that improved uremic toxin removal during daily, nocturnal hemodialysis can result in improved EPC number and function, improving overall cardiovascular parameters in dialysis patients. EPCs were isolated from 3 groups of age- and gender-matched subjects (normal control, n=10; conventional, thrice weekly HD (CHD), n=12; and daily, nocturnal HD (NHD), n=10 patients). None of the patients had symptomatic cardiovascular disease. EPC function was assessed by\u00a0<em>in vitro<\/em>\u00a0testing of the migratory response to 50 ng\/mL of vascular endothelial growth factor. Left ventricular mass index (LVMI) was derived using 2D echocardiography. EPC number and function were markedly impaired in CHD patients despite higher doses of erythropoietin (Figure 1). In contrast, NHD patients had similar EPC biology to normal controls, and EPC number and function inversely correlated to pre-dialysis urea concentration and LVMI.<\/p>\n<p>&nbsp;<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter  wp-image-7608\" src=\"https:\/\/staging.advancedrenaleducation.com\/wparep\/wp-content\/uploads\/2020\/03\/EP1-1024x438.png\" alt=\"\" width=\"823\" height=\"352\" \/><\/p>\n<h6><strong>Figure 1: <\/strong>Endothelial precursor cell (EPC) number (left) and migratory function (right) in normal controls, conventional HD (CHD) and daily nocturnal HD (NHD). HPF: high-power field. * denotes p &lt; 0.05 compared with normal and NHD (Adapted from Chan et al<sup>9<\/sup>).<\/h6>\n<p>&nbsp;<\/p>\n<p>In addition to EPC parameters, several papers have described improvement in dyslipidemia with intensified hemodialysis. Since this also could not be a direct effect, it is assumed that intensified HD better removes one or more solutes of larger size that impairs normal lipid metabolism. Bugeja et al<sup>10<\/sup> conducted a prospective cohort study of 11 ESKD patients before and after conversion from conventional to daily nocturnal hemodialysis (5-6 times\/week), and obtained a 12-hour fasting lipid profile while on CHD and after switching to NHD. Three months after converting to NHD, and without dietary restriction, the authors reported a significant decrease in triglyceride (TG) levels, an increase in high density lipoprotein (HDL), and an increase in HDL\/total cholesterol (TC) ratio (Figure 2). TC and low-density lipoprotein (LDL) levels were unchanged.<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter  wp-image-7609\" src=\"https:\/\/staging.advancedrenaleducation.com\/wparep\/wp-content\/uploads\/2020\/03\/EP2-1024x573.png\" alt=\"\" width=\"703\" height=\"393\" \/><\/p>\n<h6><strong>Figure 2: <\/strong>Plasma lipid profile on conventional HD (CHD) and 3 months after conversion to nocturnal HD (NHD). TC: total cholesterol; TG: triglyceride; HDL: high density lipoprotein; LDL: low density lipoprotein; * denotes p &lt; 0.001 (Adapted from Bugeja et al<sup>10<\/sup>).<\/h6>\n<p>&nbsp;<\/p>\n<p>Although changes of this magnitude in lipid profile might be considered as a clinically significant response to any other lipid lowering therapy, it must be noted that randomized controlled trials with lipid lowering drugs (statins) have not shown any improvement in clinical outcomes in patients on maintenance HD<sup>11,12<\/sup>.<\/p>\n<p>More recently, Jin et al<sup>1<\/sup> performed a non-randomized control study to examine the effects of longer nocturnal HD sessions (8 hours, thrice weekly) on endothelial dysfunction compared with conventional HD sessions (4 hours, thrice weekly). The authors used vascular ultrasound to measure flow-mediated dilation (FMD) of the brachial artery, finding that nocturnal HD is associated with an improvement in endothelial function as determined by FMD. Further, Jin et al<sup>1<\/sup> found a negative correlation between serum phosphate and FMD, implicating the improved removal of phosphorus with nocturnal HD with improved endothelial function. It is worth noting that while both treatment groups in this study received their HD treatments in-center, longer nocturnal treatments may be more easily performed at home.<\/p>\n<div class=\"vcex-spacing\" style=\"height:30px\"><\/div><div class=\"vcex-module vcex-divider vcex-divider-solid\" style=\"width:100%;margin-top:20px;margin-bottom:20px;border-top-width:1px;border-color:#dddddd;\"><\/div>\n<h4>References:<\/h4>\n<ol>\n<li>Jin X, Rong S, Mei C, Ye C, Chen J, Chen X. Effects of In\u2010Center Nocturnal Versus Conventional Hemodialysis on Endothelial Dysfunction. <em>Therapeutic Apheresis and Dialysis<\/em>. 2012;16(4):334-340.<\/li>\n<li>Roumeliotis S, Mallamaci F, Zoccali C. Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update. <em>J Clin Med<\/em>. 2020;9(8):2359.<\/li>\n<li>Hill JM, Zalos G, Halcox JPJ, et al. Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. <em>N Engl J Med<\/em>. 2003;348(7):593-600. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/12584367.<\/li>\n<li>Bahlmann FH, DeGroot K, Duckert T, et al. Endothelial progenitor cell proliferation and differentiation is regulated by erythropoietin. <em>Kidney Int<\/em>. 2003;64(5):1648-1652. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/14531796.<\/li>\n<li>Chen Y-LY-T, Cheng B-C, Ko S-F, et al. Value and level of circulating endothelial progenitor cells, angiogenesis factors and mononuclear cell apoptosis in patients with chronic kidney disease. <em>Clin Exp Nephrol<\/em>. 2013;17(1):83-91. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/22814956.<\/li>\n<li>Jourde-Chiche N, Dou L, Sabatier F, et al. Levels of circulating endothelial progenitor cells are related to uremic toxins and vascular injury in hemodialysis patients. <em>J Thromb Haemost<\/em>. 2009;7(9):1576-1584. Available from: https:\/\/pubmed.ncbi.nlm.nih.gov\/19583820\/.<\/li>\n<li>Krieter DH, Fischer R, Merget K, et al. Endothelial progenitor cells in patients on extracorporeal maintenance dialysis therapy. <em>Nephrol Dial Transplant<\/em>. 2010;25(12):4023-4031.<\/li>\n<li>Kun-Ying Z, Hui-Lan L, Xiao-Feng D, Guo-Gang L. Association between Circulating Endothelial Cells and Carotid Atherosclerosis in Patients Receiving Maintenance Hemodialysis. Published online 2014. Available from: http:\/\/dx.doi.org\/10.1155\/2014\/753759.<\/li>\n<li>Chan CT, Li SH, Verma S. Nocturnal hemodialysis is associated with restoration of impaired endothelial progenitor cell biology in end-stage renal disease. <em>Am J Physiol Renal Physiol<\/em>. 2005;289(4):F679-84. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/15928211.<\/li>\n<li>Bugeja AL, Chan CT. Improvement in lipid profile by nocturnal hemodialysis in patients with end-stage renal disease. <em>ASAIO J<\/em>. 2004;50(4):328-331. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/15307542.<\/li>\n<li>Fellstr\u00f6m BC, Jardine AG, Schmieder RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. <em>N Engl J Med<\/em>. 2009;360(14):1395-1407. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/19332456.<\/li>\n<li>Wanner C, Krane V, M\u00e4rz W, et al. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. <em>N Engl J Med<\/em>. 2005;353(3):238-248. Available from: http:\/\/www.ncbi.nlm.nih.gov\/pubmed\/16034009.<\/li>\n<\/ol>\n<p><span style=\"font-size: 16px\">GMO-001403\u00a0 Rev C\u00a0 11\/2024<\/span><\/p>\n<div class=\"vcex-spacing\" style=\"height:30px\"><\/div>\n","protected":false},"featured_media":0,"template":"","format":"standard","meta":{"_acf_changed":false},"categories":[128],"tags":[151],"language":[41],"articles":[231],"class_list":["post-2785","article","type-article","status-publish","format-standard","hentry","category-articles","tag-hhd1","language-english","articles-home-hemodialysis","entry","no-media"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v26.2 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Endothelial Protection - AREP Asia Pacific<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/staging.advancedrenaleducation.com\/wparep\/article\/endothelial-protection\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Endothelial Protection - AREP Asia Pacific\" \/>\n<meta property=\"og:description\" content=\"Cardiovascular causes \u2014including arrhythmias, cardiac arrest, congestive heart failure (CHF), acute myocardial infarction (AMI), and atherosclerotic heart disease (ASHD)\u2014are the leading cause of mortality in end-stage kidney disease (ESKD) patients on hemodialysis. 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