Increased arterial inflammation in individuals with stage 3 chronic kidney disease
Purpose While it is well known that patients with chronic kidney disease (CKD) are at increased risk for the development and progression of atherosclerosis, it is not known whether arterial inflammation is increased in mild CKD. The aim of this study was to compare arterial inflammation using 18 F-F...
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| Veröffentlicht in: | European journal of nuclear medicine and molecular imaging 2016-02, Vol.43 (2), p.333-339 |
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| creator | Takx, Richard A. P. MacNabb, Megan H. Emami, Hamed Abdelbaky, Amr Singh, Parmanand Lavender, Zachary R. di Carli, Marcelo Taqueti, Viviany Foster, Courtney Mann, Jessica Comley, Robert A. Weber, Chek Ing Kiu Tawakol, Ahmed |
| description | Purpose
While it is well known that patients with chronic kidney disease (CKD) are at increased risk for the development and progression of atherosclerosis, it is not known whether arterial inflammation is increased in mild CKD. The aim of this study was to compare arterial inflammation using
18
F-FDG PET/CT in patients with CKD and in matched controls.
Methods
This restrospective study included 128 patients undergoing FDG PET/CT imaging for clinical indications, comprising 64 patients with stage 3 CKD and 64 control patients matched by age, gender, and cancer history. CKD was defined according to guidelines using a calculated glomerular filtration rate (eGFR). Arterial inflammation was measured in the ascending aorta as FDG uptake on PET. Background FDG uptake (venous, subcutaneous fat and muscle) were recorded. Coronary artery calcification (CAC) was assessed using the CT images. The impact of CKD on arterial inflammation and CAC was then assessed.
Results
Arterial inflammation was higher in patients with CKD than in matched controls (standardized uptake value, SUV: 2.41 ± 0.49 vs. 2.16 ± 0.43;
p
= 0.002). Arterial SUV correlated inversely with eGFR (
r
= −0.299,
p
= 0.001). Venous SUV was also significantly elevated in patients with CKD, while subcutaneous fat and muscle tissue SUVs did not differ between groups. Moreover, arterial SUV remained significantly elevated in patients with CKD compared to controls after correcting for muscle and fat background, and also remained significant after adjusting for clinical risk factors. Further, CKD was associated with arterial inflammation (SUV) independent of the presence of subclinical atherosclerosis (CAC).
Conclusion
Moderate CKD is associated with increased arterial inflammation beyond that of controls. Further, the increased arterial inflammation is independent of presence of subclinical atherosclerosis. Current risk stratification tools may underestimate the presence of atherosclerosis in patients with CKD and thereby the risk of cardiovascular events. |
| doi_str_mv | 10.1007/s00259-015-3203-6 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4833679</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3911274171</sourcerecordid><originalsourceid>FETCH-LOGICAL-c573t-1bc711ec10b6393ab87673293ba50f6091966cb9b16c32c8266a74083934f30f3</originalsourceid><addsrcrecordid>eNqFkV1L5TAQhoMofv8Ab5aCN950nUnapLkRFlFXEATR65Cm6TnRNtWkVfz3m3L04C4sQmAS5pl3JvMScoTwEwHEaQSgpcwBy5xRYDnfILvIUeYCKrm5vgvYIXsxPgJgRSu5TXYoL3gBotgld9feBKujbTIdRhuc7jLn2073vR7d4NMjnca9umbSXcze3LjM4qgXNmOZWYbBO5M9ucbb96xxcVY6IFttQu3hR9wnD5cX9-e_85vbq-vzXze5KQUbc6yNQLQGoeZMMl1XggtGJat1CS0HiZJzU8sauWHUVJRzLQqoElu0DFq2T85Wus9T3dvGWD8G3ann4Hod3tWgnfo7491SLYZXVVSMcSGTwMmHQBheJhtH1btobNdpb4cpKpx7MkDk36OCU5a2XkJCj_9BH4cp-LSJRJUMq4JTkShcUSYMMQbbrudGULO5amWuSuaq2Vw1D_Hj64fXFZ9uJoCugJhSfmHDl9b_Vf0D8RuuXA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1753184627</pqid></control><display><type>article</type><title>Increased arterial inflammation in individuals with stage 3 chronic kidney disease</title><source>SpringerLink</source><creator>Takx, Richard A. P. ; MacNabb, Megan H. ; Emami, Hamed ; Abdelbaky, Amr ; Singh, Parmanand ; Lavender, Zachary R. ; di Carli, Marcelo ; Taqueti, Viviany ; Foster, Courtney ; Mann, Jessica ; Comley, Robert A. ; Weber, Chek Ing Kiu ; Tawakol, Ahmed</creator><creatorcontrib>Takx, Richard A. P. ; MacNabb, Megan H. ; Emami, Hamed ; Abdelbaky, Amr ; Singh, Parmanand ; Lavender, Zachary R. ; di Carli, Marcelo ; Taqueti, Viviany ; Foster, Courtney ; Mann, Jessica ; Comley, Robert A. ; Weber, Chek Ing Kiu ; Tawakol, Ahmed</creatorcontrib><description>Purpose
While it is well known that patients with chronic kidney disease (CKD) are at increased risk for the development and progression of atherosclerosis, it is not known whether arterial inflammation is increased in mild CKD. The aim of this study was to compare arterial inflammation using
18
F-FDG PET/CT in patients with CKD and in matched controls.
Methods
This restrospective study included 128 patients undergoing FDG PET/CT imaging for clinical indications, comprising 64 patients with stage 3 CKD and 64 control patients matched by age, gender, and cancer history. CKD was defined according to guidelines using a calculated glomerular filtration rate (eGFR). Arterial inflammation was measured in the ascending aorta as FDG uptake on PET. Background FDG uptake (venous, subcutaneous fat and muscle) were recorded. Coronary artery calcification (CAC) was assessed using the CT images. The impact of CKD on arterial inflammation and CAC was then assessed.
Results
Arterial inflammation was higher in patients with CKD than in matched controls (standardized uptake value, SUV: 2.41 ± 0.49 vs. 2.16 ± 0.43;
p
= 0.002). Arterial SUV correlated inversely with eGFR (
r
= −0.299,
p
= 0.001). Venous SUV was also significantly elevated in patients with CKD, while subcutaneous fat and muscle tissue SUVs did not differ between groups. Moreover, arterial SUV remained significantly elevated in patients with CKD compared to controls after correcting for muscle and fat background, and also remained significant after adjusting for clinical risk factors. Further, CKD was associated with arterial inflammation (SUV) independent of the presence of subclinical atherosclerosis (CAC).
Conclusion
Moderate CKD is associated with increased arterial inflammation beyond that of controls. Further, the increased arterial inflammation is independent of presence of subclinical atherosclerosis. Current risk stratification tools may underestimate the presence of atherosclerosis in patients with CKD and thereby the risk of cardiovascular events.</description><identifier>ISSN: 1619-7070</identifier><identifier>EISSN: 1619-7089</identifier><identifier>DOI: 10.1007/s00259-015-3203-6</identifier><identifier>PMID: 26464074</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Cardiology ; Imaging ; Medicine ; Medicine & Public Health ; Nuclear Medicine ; Oncology ; Original Article ; Orthopedics ; Radiology</subject><ispartof>European journal of nuclear medicine and molecular imaging, 2016-02, Vol.43 (2), p.333-339</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c573t-1bc711ec10b6393ab87673293ba50f6091966cb9b16c32c8266a74083934f30f3</citedby><cites>FETCH-LOGICAL-c573t-1bc711ec10b6393ab87673293ba50f6091966cb9b16c32c8266a74083934f30f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00259-015-3203-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00259-015-3203-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26464074$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Takx, Richard A. P.</creatorcontrib><creatorcontrib>MacNabb, Megan H.</creatorcontrib><creatorcontrib>Emami, Hamed</creatorcontrib><creatorcontrib>Abdelbaky, Amr</creatorcontrib><creatorcontrib>Singh, Parmanand</creatorcontrib><creatorcontrib>Lavender, Zachary R.</creatorcontrib><creatorcontrib>di Carli, Marcelo</creatorcontrib><creatorcontrib>Taqueti, Viviany</creatorcontrib><creatorcontrib>Foster, Courtney</creatorcontrib><creatorcontrib>Mann, Jessica</creatorcontrib><creatorcontrib>Comley, Robert A.</creatorcontrib><creatorcontrib>Weber, Chek Ing Kiu</creatorcontrib><creatorcontrib>Tawakol, Ahmed</creatorcontrib><title>Increased arterial inflammation in individuals with stage 3 chronic kidney disease</title><title>European journal of nuclear medicine and molecular imaging</title><addtitle>Eur J Nucl Med Mol Imaging</addtitle><addtitle>Eur J Nucl Med Mol Imaging</addtitle><description>Purpose
While it is well known that patients with chronic kidney disease (CKD) are at increased risk for the development and progression of atherosclerosis, it is not known whether arterial inflammation is increased in mild CKD. The aim of this study was to compare arterial inflammation using
18
F-FDG PET/CT in patients with CKD and in matched controls.
Methods
This restrospective study included 128 patients undergoing FDG PET/CT imaging for clinical indications, comprising 64 patients with stage 3 CKD and 64 control patients matched by age, gender, and cancer history. CKD was defined according to guidelines using a calculated glomerular filtration rate (eGFR). Arterial inflammation was measured in the ascending aorta as FDG uptake on PET. Background FDG uptake (venous, subcutaneous fat and muscle) were recorded. Coronary artery calcification (CAC) was assessed using the CT images. The impact of CKD on arterial inflammation and CAC was then assessed.
Results
Arterial inflammation was higher in patients with CKD than in matched controls (standardized uptake value, SUV: 2.41 ± 0.49 vs. 2.16 ± 0.43;
p
= 0.002). Arterial SUV correlated inversely with eGFR (
r
= −0.299,
p
= 0.001). Venous SUV was also significantly elevated in patients with CKD, while subcutaneous fat and muscle tissue SUVs did not differ between groups. Moreover, arterial SUV remained significantly elevated in patients with CKD compared to controls after correcting for muscle and fat background, and also remained significant after adjusting for clinical risk factors. Further, CKD was associated with arterial inflammation (SUV) independent of the presence of subclinical atherosclerosis (CAC).
Conclusion
Moderate CKD is associated with increased arterial inflammation beyond that of controls. Further, the increased arterial inflammation is independent of presence of subclinical atherosclerosis. Current risk stratification tools may underestimate the presence of atherosclerosis in patients with CKD and thereby the risk of cardiovascular events.</description><subject>Cardiology</subject><subject>Imaging</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nuclear Medicine</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Orthopedics</subject><subject>Radiology</subject><issn>1619-7070</issn><issn>1619-7089</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkV1L5TAQhoMofv8Ab5aCN950nUnapLkRFlFXEATR65Cm6TnRNtWkVfz3m3L04C4sQmAS5pl3JvMScoTwEwHEaQSgpcwBy5xRYDnfILvIUeYCKrm5vgvYIXsxPgJgRSu5TXYoL3gBotgld9feBKujbTIdRhuc7jLn2073vR7d4NMjnca9umbSXcze3LjM4qgXNmOZWYbBO5M9ucbb96xxcVY6IFttQu3hR9wnD5cX9-e_85vbq-vzXze5KQUbc6yNQLQGoeZMMl1XggtGJat1CS0HiZJzU8sauWHUVJRzLQqoElu0DFq2T85Wus9T3dvGWD8G3ann4Hod3tWgnfo7491SLYZXVVSMcSGTwMmHQBheJhtH1btobNdpb4cpKpx7MkDk36OCU5a2XkJCj_9BH4cp-LSJRJUMq4JTkShcUSYMMQbbrudGULO5amWuSuaq2Vw1D_Hj64fXFZ9uJoCugJhSfmHDl9b_Vf0D8RuuXA</recordid><startdate>20160201</startdate><enddate>20160201</enddate><creator>Takx, Richard A. P.</creator><creator>MacNabb, Megan H.</creator><creator>Emami, Hamed</creator><creator>Abdelbaky, Amr</creator><creator>Singh, Parmanand</creator><creator>Lavender, Zachary R.</creator><creator>di Carli, Marcelo</creator><creator>Taqueti, Viviany</creator><creator>Foster, Courtney</creator><creator>Mann, Jessica</creator><creator>Comley, Robert A.</creator><creator>Weber, Chek Ing Kiu</creator><creator>Tawakol, Ahmed</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160201</creationdate><title>Increased arterial inflammation in individuals with stage 3 chronic kidney disease</title><author>Takx, Richard A. P. ; MacNabb, Megan H. ; Emami, Hamed ; Abdelbaky, Amr ; Singh, Parmanand ; Lavender, Zachary R. ; di Carli, Marcelo ; Taqueti, Viviany ; Foster, Courtney ; Mann, Jessica ; Comley, Robert A. ; Weber, Chek Ing Kiu ; Tawakol, Ahmed</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c573t-1bc711ec10b6393ab87673293ba50f6091966cb9b16c32c8266a74083934f30f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Cardiology</topic><topic>Imaging</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Nuclear Medicine</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Orthopedics</topic><topic>Radiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takx, Richard A. P.</creatorcontrib><creatorcontrib>MacNabb, Megan H.</creatorcontrib><creatorcontrib>Emami, Hamed</creatorcontrib><creatorcontrib>Abdelbaky, Amr</creatorcontrib><creatorcontrib>Singh, Parmanand</creatorcontrib><creatorcontrib>Lavender, Zachary R.</creatorcontrib><creatorcontrib>di Carli, Marcelo</creatorcontrib><creatorcontrib>Taqueti, Viviany</creatorcontrib><creatorcontrib>Foster, Courtney</creatorcontrib><creatorcontrib>Mann, Jessica</creatorcontrib><creatorcontrib>Comley, Robert A.</creatorcontrib><creatorcontrib>Weber, Chek Ing Kiu</creatorcontrib><creatorcontrib>Tawakol, Ahmed</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science 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)</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Database (1962 - current)</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Biological Science Journals</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest advanced technologies & aerospace journals</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European journal of nuclear medicine and molecular imaging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takx, Richard A. P.</au><au>MacNabb, Megan H.</au><au>Emami, Hamed</au><au>Abdelbaky, Amr</au><au>Singh, Parmanand</au><au>Lavender, Zachary R.</au><au>di Carli, Marcelo</au><au>Taqueti, Viviany</au><au>Foster, Courtney</au><au>Mann, Jessica</au><au>Comley, Robert A.</au><au>Weber, Chek Ing Kiu</au><au>Tawakol, Ahmed</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased arterial inflammation in individuals with stage 3 chronic kidney disease</atitle><jtitle>European journal of nuclear medicine and molecular imaging</jtitle><stitle>Eur J Nucl Med Mol Imaging</stitle><addtitle>Eur J Nucl Med Mol Imaging</addtitle><date>2016-02-01</date><risdate>2016</risdate><volume>43</volume><issue>2</issue><spage>333</spage><epage>339</epage><pages>333-339</pages><issn>1619-7070</issn><eissn>1619-7089</eissn><abstract>Purpose
While it is well known that patients with chronic kidney disease (CKD) are at increased risk for the development and progression of atherosclerosis, it is not known whether arterial inflammation is increased in mild CKD. The aim of this study was to compare arterial inflammation using
18
F-FDG PET/CT in patients with CKD and in matched controls.
Methods
This restrospective study included 128 patients undergoing FDG PET/CT imaging for clinical indications, comprising 64 patients with stage 3 CKD and 64 control patients matched by age, gender, and cancer history. CKD was defined according to guidelines using a calculated glomerular filtration rate (eGFR). Arterial inflammation was measured in the ascending aorta as FDG uptake on PET. Background FDG uptake (venous, subcutaneous fat and muscle) were recorded. Coronary artery calcification (CAC) was assessed using the CT images. The impact of CKD on arterial inflammation and CAC was then assessed.
Results
Arterial inflammation was higher in patients with CKD than in matched controls (standardized uptake value, SUV: 2.41 ± 0.49 vs. 2.16 ± 0.43;
p
= 0.002). Arterial SUV correlated inversely with eGFR (
r
= −0.299,
p
= 0.001). Venous SUV was also significantly elevated in patients with CKD, while subcutaneous fat and muscle tissue SUVs did not differ between groups. Moreover, arterial SUV remained significantly elevated in patients with CKD compared to controls after correcting for muscle and fat background, and also remained significant after adjusting for clinical risk factors. Further, CKD was associated with arterial inflammation (SUV) independent of the presence of subclinical atherosclerosis (CAC).
Conclusion
Moderate CKD is associated with increased arterial inflammation beyond that of controls. Further, the increased arterial inflammation is independent of presence of subclinical atherosclerosis. Current risk stratification tools may underestimate the presence of atherosclerosis in patients with CKD and thereby the risk of cardiovascular events.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26464074</pmid><doi>10.1007/s00259-015-3203-6</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1619-7070 1619-7089 |
| language | eng |
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| source | SpringerLink |
| subjects | Cardiology Imaging Medicine Medicine & Public Health Nuclear Medicine Oncology Original Article Orthopedics Radiology |
| title | Increased arterial inflammation in individuals with stage 3 chronic kidney disease |
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