Oxidative stress, advanced glycation end product, and coronary artery calcification in hemodialysis patients
Coronary artery calcification is an index of the severity of atherosclerotic vascular disease, and may predict future adverse cardiovascular events in uremic patients undergoing hemodialysis (HD). HD patients are exposed to oxidative stress, and show high plasma levels of advanced glycation end prod...
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description | Coronary artery calcification is an index of the severity of atherosclerotic vascular disease, and may predict future adverse cardiovascular events in uremic patients undergoing hemodialysis (HD). HD patients are exposed to oxidative stress, and show high plasma levels of advanced glycation end products (AGEs). The association between oxidative stress, AGEs, established cardiovascular risk factors, and coronary artery calcification score (CACS) was studied in 225 HD patients (123 male, 102 female patients). CACS was measured by using multi-detector row computed tomography. Age, systolic blood pressure, calcium, calcium × phosphate, malondialdehyde, lipid peroxides, and pentosidine were significantly and positively correlated with CACS. Duration on HD tended to be positively correlated with CACS. From the independent variables included in the forward stepwise multiple linear regression analysis, only age, systolic blood pressure, lipid peroxides, calcium, and pentosidine were independently associated with CACS. The odds ratios for past history of coronary artery disease and the presence of diabetes mellitus for high CACS (≥100) were 6.25 (95% confidence interval; 1.83–21.4) and 2.03 (95% confidence interval; 1.02–4.05), respectively. The plasma pentosidine was significantly and positively correlated with indoxyl sulfate. In conclusion, in addition to such traditional cardiovascular risk factors as past history, diabetes mellitus, aging, systolic blood pressure and calcium overload, oxidative stress (lipid peroxides), and AGE (pentosidine) are associated with extensive coronary artery calcification in HD patients. Lipid peroxidation and glycoxidation may be involved in the pathogenesis of coronary artery calcification. |
doi_str_mv | 10.1038/sj.ki.5000330 |
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HD patients are exposed to oxidative stress, and show high plasma levels of advanced glycation end products (AGEs). The association between oxidative stress, AGEs, established cardiovascular risk factors, and coronary artery calcification score (CACS) was studied in 225 HD patients (123 male, 102 female patients). CACS was measured by using multi-detector row computed tomography. Age, systolic blood pressure, calcium, calcium × phosphate, malondialdehyde, lipid peroxides, and pentosidine were significantly and positively correlated with CACS. Duration on HD tended to be positively correlated with CACS. From the independent variables included in the forward stepwise multiple linear regression analysis, only age, systolic blood pressure, lipid peroxides, calcium, and pentosidine were independently associated with CACS. The odds ratios for past history of coronary artery disease and the presence of diabetes mellitus for high CACS (≥100) were 6.25 (95% confidence interval; 1.83–21.4) and 2.03 (95% confidence interval; 1.02–4.05), respectively. The plasma pentosidine was significantly and positively correlated with indoxyl sulfate. In conclusion, in addition to such traditional cardiovascular risk factors as past history, diabetes mellitus, aging, systolic blood pressure and calcium overload, oxidative stress (lipid peroxides), and AGE (pentosidine) are associated with extensive coronary artery calcification in HD patients. Lipid peroxidation and glycoxidation may be involved in the pathogenesis of coronary artery calcification.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/sj.ki.5000330</identifier><identifier>PMID: 16723988</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>advanced glycation end product ; Aged ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Arginine - analogs & derivatives ; Arginine - blood ; Biological and medical sciences ; Calcinosis - diagnosis ; coronary artery calcification ; Coronary Artery Disease - diagnosis ; Emergency and intensive care: renal failure. Dialysis management ; Female ; Glycation End Products, Advanced - blood ; hemodialysis ; Humans ; Indican - blood ; Intensive care medicine ; Lysine - analogs & derivatives ; Lysine - blood ; Male ; Medical sciences ; Middle Aged ; Nephrology. 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HD patients are exposed to oxidative stress, and show high plasma levels of advanced glycation end products (AGEs). The association between oxidative stress, AGEs, established cardiovascular risk factors, and coronary artery calcification score (CACS) was studied in 225 HD patients (123 male, 102 female patients). CACS was measured by using multi-detector row computed tomography. Age, systolic blood pressure, calcium, calcium × phosphate, malondialdehyde, lipid peroxides, and pentosidine were significantly and positively correlated with CACS. Duration on HD tended to be positively correlated with CACS. From the independent variables included in the forward stepwise multiple linear regression analysis, only age, systolic blood pressure, lipid peroxides, calcium, and pentosidine were independently associated with CACS. The odds ratios for past history of coronary artery disease and the presence of diabetes mellitus for high CACS (≥100) were 6.25 (95% confidence interval; 1.83–21.4) and 2.03 (95% confidence interval; 1.02–4.05), respectively. The plasma pentosidine was significantly and positively correlated with indoxyl sulfate. In conclusion, in addition to such traditional cardiovascular risk factors as past history, diabetes mellitus, aging, systolic blood pressure and calcium overload, oxidative stress (lipid peroxides), and AGE (pentosidine) are associated with extensive coronary artery calcification in HD patients. Lipid peroxidation and glycoxidation may be involved in the pathogenesis of coronary artery calcification.</description><subject>advanced glycation end product</subject><subject>Aged</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - blood</subject><subject>Biological and medical sciences</subject><subject>Calcinosis - diagnosis</subject><subject>coronary artery calcification</subject><subject>Coronary Artery Disease - diagnosis</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Female</subject><subject>Glycation End Products, Advanced - blood</subject><subject>hemodialysis</subject><subject>Humans</subject><subject>Indican - blood</subject><subject>Intensive care medicine</subject><subject>Lysine - analogs & derivatives</subject><subject>Lysine - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oxidative Stress</subject><subject>Prognosis</subject><subject>Renal Dialysis</subject><subject>Severity of Illness Index</subject><subject>Uremia - therapy</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kUFvEzEQhS0EoqFw5AhaVaK9sMFer9f2EVXQIlXqBc6WY8-C0806eLxR8-9xlBWRkOhpZM-nmXnvEfKW0SWjXH3C9fIhLAWllHP6jCyYaHjNpBDPyYJSJepGcHVGXiGuC6M0py_JGetkw7VSCzLcPwZvc9hBhTkB4sfK-p0dHfjq57B3pRXHCkZfbVP0k8ulXx4upjjatK9sylCKs4MLfZjxMFa_YBN9sMMeA1bb8g1jxtfkRW8HhDdzPSc_vn75fn1b393ffLv-fFc7IUSuYaWZk561WvVSU-pd16yolhpc17UUwEmxsl44wbhQylvft5pxC1a07UHZObk6zi03_54As9kEdDAMdoQ4oVFSCs1oywp5-STZKaG5blQBL_4B13FKY1FhGkYZo6o97K2PkEsRMUFvtilsik2GUXNIy-DaPAQzp1X49_PQabUBf6LneArwYQYsFov7VIIJeOKkVqxTBxnvjtxo85TgL3BaJI99KK7vAiSDriRSQg4JXDY-hv-c-AcKCrra</recordid><startdate>20060701</startdate><enddate>20060701</enddate><creator>Taki, K.</creator><creator>Takayama, F.</creator><creator>Tsuruta, Y.</creator><creator>Niwa, T.</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20060701</creationdate><title>Oxidative stress, advanced glycation end product, and coronary artery calcification in hemodialysis patients</title><author>Taki, K. ; Takayama, F. ; Tsuruta, Y. ; Niwa, T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c555t-eb91c7d1498f7900dc62b0979ec6640eec75bad5c513588dadf4913aea5446723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>advanced glycation end product</topic><topic>Aged</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - blood</topic><topic>Biological and medical sciences</topic><topic>Calcinosis - diagnosis</topic><topic>coronary artery calcification</topic><topic>Coronary Artery Disease - diagnosis</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Female</topic><topic>Glycation End Products, Advanced - blood</topic><topic>hemodialysis</topic><topic>Humans</topic><topic>Indican - blood</topic><topic>Intensive care medicine</topic><topic>Lysine - analogs & derivatives</topic><topic>Lysine - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Oxidative Stress</topic><topic>Prognosis</topic><topic>Renal Dialysis</topic><topic>Severity of Illness Index</topic><topic>Uremia - therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Taki, K.</creatorcontrib><creatorcontrib>Takayama, F.</creatorcontrib><creatorcontrib>Tsuruta, Y.</creatorcontrib><creatorcontrib>Niwa, T.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Taki, K.</au><au>Takayama, F.</au><au>Tsuruta, Y.</au><au>Niwa, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative stress, advanced glycation end product, and coronary artery calcification in hemodialysis patients</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2006-07-01</date><risdate>2006</risdate><volume>70</volume><issue>1</issue><spage>218</spage><epage>224</epage><pages>218-224</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Coronary artery calcification is an index of the severity of atherosclerotic vascular disease, and may predict future adverse cardiovascular events in uremic patients undergoing hemodialysis (HD). HD patients are exposed to oxidative stress, and show high plasma levels of advanced glycation end products (AGEs). The association between oxidative stress, AGEs, established cardiovascular risk factors, and coronary artery calcification score (CACS) was studied in 225 HD patients (123 male, 102 female patients). CACS was measured by using multi-detector row computed tomography. Age, systolic blood pressure, calcium, calcium × phosphate, malondialdehyde, lipid peroxides, and pentosidine were significantly and positively correlated with CACS. Duration on HD tended to be positively correlated with CACS. From the independent variables included in the forward stepwise multiple linear regression analysis, only age, systolic blood pressure, lipid peroxides, calcium, and pentosidine were independently associated with CACS. The odds ratios for past history of coronary artery disease and the presence of diabetes mellitus for high CACS (≥100) were 6.25 (95% confidence interval; 1.83–21.4) and 2.03 (95% confidence interval; 1.02–4.05), respectively. The plasma pentosidine was significantly and positively correlated with indoxyl sulfate. In conclusion, in addition to such traditional cardiovascular risk factors as past history, diabetes mellitus, aging, systolic blood pressure and calcium overload, oxidative stress (lipid peroxides), and AGE (pentosidine) are associated with extensive coronary artery calcification in HD patients. Lipid peroxidation and glycoxidation may be involved in the pathogenesis of coronary artery calcification.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>16723988</pmid><doi>10.1038/sj.ki.5000330</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | advanced glycation end product Aged Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Arginine - analogs & derivatives Arginine - blood Biological and medical sciences Calcinosis - diagnosis coronary artery calcification Coronary Artery Disease - diagnosis Emergency and intensive care: renal failure. Dialysis management Female Glycation End Products, Advanced - blood hemodialysis Humans Indican - blood Intensive care medicine Lysine - analogs & derivatives Lysine - blood Male Medical sciences Middle Aged Nephrology. Urinary tract diseases Oxidative Stress Prognosis Renal Dialysis Severity of Illness Index Uremia - therapy |
title | Oxidative stress, advanced glycation end product, and coronary artery calcification in hemodialysis patients |
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