Plasminogen activator inhibitor-1 activity and 4G/5G polymorphism in hemodialysis
Chronic insufficiency alters homeostasis, in part due to endothelial inflammation. Plasminogen activator inhibitor-1 (PAI-1) is increased in renal disease, contributing to vascular damage. We assessed PAI-1 activity and PAI-1 4G/5G polymorphism in hemodialysis (HD) subjects and any association betwe...
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| Veröffentlicht in: | The journal of vascular access 2008-04, Vol.9 (2), p.142-147 |
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| creator | Trimarchi, H Duboscq, C Genoud, V Lombi, F Muryan, A Young, P Schwab, M Castanon, M Rodriguez-Reimundes, E Forrester, M Pereyra, H Campolo-Girard, V Seminario, O Alonso, M Kordich, L |
| description | Chronic insufficiency alters homeostasis, in part due to endothelial inflammation. Plasminogen activator inhibitor-1 (PAI-1) is increased in renal disease, contributing to vascular damage. We assessed PAI-1 activity and PAI-1 4G/5G polymorphism in hemodialysis (HD) subjects and any association between thrombotic vascular access (VA) events and PAI-1 polymorphism.
Prospective, observational study in 36 HD patients: mean age: 66.6 +/- 12.5 yr, males n=26 (72%), time on HD: 28.71 +/- 22.45 months. Vascular accesses: 10 polytetrafluoroethylene grafts (PTFEG), 22 arteriovenous fistulae (AVF), four dual lumen catheters (CAT). Control group (CG): 40 subjects; mean age: 60.0 +/- 15 yrs, males n=30 (75%). Group A (GA): thrombotic events (n=12), and group B (GB): No events (n=24). Groups were no different according to age (69.2 +/- 9.12 vs. 65.3 +/- 14.5 yrs), gender (males: 7; 58.3% vs. 18; 81.8%), time on HD (26.1 +/- 14.7 vs. 30.1 +/- 38.7 months), causes of renal failure. Time to follow-up for access thrombosis: 12 months.
PAI-1 levels in HD: 7.21 +/- 2.13 vs. CG: 0.42 +/- 0.27 U/ml (p |
| doi_str_mv | 10.1177/112972980800900212 |
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Prospective, observational study in 36 HD patients: mean age: 66.6 +/- 12.5 yr, males n=26 (72%), time on HD: 28.71 +/- 22.45 months. Vascular accesses: 10 polytetrafluoroethylene grafts (PTFEG), 22 arteriovenous fistulae (AVF), four dual lumen catheters (CAT). Control group (CG): 40 subjects; mean age: 60.0 +/- 15 yrs, males n=30 (75%). Group A (GA): thrombotic events (n=12), and group B (GB): No events (n=24). Groups were no different according to age (69.2 +/- 9.12 vs. 65.3 +/- 14.5 yrs), gender (males: 7; 58.3% vs. 18; 81.8%), time on HD (26.1 +/- 14.7 vs. 30.1 +/- 38.7 months), causes of renal failure. Time to follow-up for access thrombosis: 12 months.
PAI-1 levels in HD: 7.21 +/- 2.13 vs. CG: 0.42 +/- 0.27 U/ml (p<0.0001). PAI-1 4G/5G polymorphic variant distribution in HD: 5G/5G: 6 (17%), 4G/5G: 23 (64%); 4G/4G: 7 (19%) and in CG: 5G/5G: 14 (35%); 4G/5G: 18 (45%); 4G/4G: 8 (20%). C-reactive protein (CRP) in HD: 24.5 +/- 15.2 mg/L vs. in CG 2.3 +/- 0.2 mg/L (p<0.0001). PAI-1 4G/5G variants: GA: 5G/5G: 3; 4G/5G: 8; 4G/4G: 1; GB: 5G/5G: 3; 4G/5G: 15; 4G/4G: 6. Thrombosis occurred in 8/10 patients (80%) with PTFEG, 3/22 (9%) in AVF, and 1/4 (25%) in CAT. Among the eight PTFEG patients with thrombosis, seven were PAI 4G/5G.
PAI-1 levels were elevated in HD patients, independent of their polymorphic variants, 4G/5G being the most prevalent variant. Our data suggest that in patients with PTFEG the 4G/5G variant might be associated with an increased thrombosis risk.</description><identifier>ISSN: 1129-7298</identifier><identifier>EISSN: 1724-6032</identifier><identifier>DOI: 10.1177/112972980800900212</identifier><identifier>PMID: 18609532</identifier><language>eng</language><publisher>United States</publisher><subject>Aged ; Arteriovenous Shunt, Surgical ; Blood Vessel Prosthesis ; C-Reactive Protein - metabolism ; Chi-Square Distribution ; Female ; Graft Occlusion, Vascular - genetics ; Humans ; Male ; Middle Aged ; Plasminogen Activator Inhibitor 1 - blood ; Plasminogen Activator Inhibitor 1 - genetics ; Polymorphism, Genetic ; Polytetrafluoroethylene ; Prospective Studies ; Renal Dialysis ; Statistics, Nonparametric ; Thrombosis - genetics</subject><ispartof>The journal of vascular access, 2008-04, Vol.9 (2), p.142-147</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c301t-8f39ba7513880854fb3d010a2c9ea14eb3ab1d4860b11466b3b81aeb109bba303</citedby><cites>FETCH-LOGICAL-c301t-8f39ba7513880854fb3d010a2c9ea14eb3ab1d4860b11466b3b81aeb109bba303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18609532$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Trimarchi, H</creatorcontrib><creatorcontrib>Duboscq, C</creatorcontrib><creatorcontrib>Genoud, V</creatorcontrib><creatorcontrib>Lombi, F</creatorcontrib><creatorcontrib>Muryan, A</creatorcontrib><creatorcontrib>Young, P</creatorcontrib><creatorcontrib>Schwab, M</creatorcontrib><creatorcontrib>Castanon, M</creatorcontrib><creatorcontrib>Rodriguez-Reimundes, E</creatorcontrib><creatorcontrib>Forrester, M</creatorcontrib><creatorcontrib>Pereyra, H</creatorcontrib><creatorcontrib>Campolo-Girard, V</creatorcontrib><creatorcontrib>Seminario, O</creatorcontrib><creatorcontrib>Alonso, M</creatorcontrib><creatorcontrib>Kordich, L</creatorcontrib><title>Plasminogen activator inhibitor-1 activity and 4G/5G polymorphism in hemodialysis</title><title>The journal of vascular access</title><addtitle>J Vasc Access</addtitle><description>Chronic insufficiency alters homeostasis, in part due to endothelial inflammation. Plasminogen activator inhibitor-1 (PAI-1) is increased in renal disease, contributing to vascular damage. We assessed PAI-1 activity and PAI-1 4G/5G polymorphism in hemodialysis (HD) subjects and any association between thrombotic vascular access (VA) events and PAI-1 polymorphism.
Prospective, observational study in 36 HD patients: mean age: 66.6 +/- 12.5 yr, males n=26 (72%), time on HD: 28.71 +/- 22.45 months. Vascular accesses: 10 polytetrafluoroethylene grafts (PTFEG), 22 arteriovenous fistulae (AVF), four dual lumen catheters (CAT). Control group (CG): 40 subjects; mean age: 60.0 +/- 15 yrs, males n=30 (75%). Group A (GA): thrombotic events (n=12), and group B (GB): No events (n=24). Groups were no different according to age (69.2 +/- 9.12 vs. 65.3 +/- 14.5 yrs), gender (males: 7; 58.3% vs. 18; 81.8%), time on HD (26.1 +/- 14.7 vs. 30.1 +/- 38.7 months), causes of renal failure. Time to follow-up for access thrombosis: 12 months.
PAI-1 levels in HD: 7.21 +/- 2.13 vs. CG: 0.42 +/- 0.27 U/ml (p<0.0001). PAI-1 4G/5G polymorphic variant distribution in HD: 5G/5G: 6 (17%), 4G/5G: 23 (64%); 4G/4G: 7 (19%) and in CG: 5G/5G: 14 (35%); 4G/5G: 18 (45%); 4G/4G: 8 (20%). C-reactive protein (CRP) in HD: 24.5 +/- 15.2 mg/L vs. in CG 2.3 +/- 0.2 mg/L (p<0.0001). PAI-1 4G/5G variants: GA: 5G/5G: 3; 4G/5G: 8; 4G/4G: 1; GB: 5G/5G: 3; 4G/5G: 15; 4G/4G: 6. Thrombosis occurred in 8/10 patients (80%) with PTFEG, 3/22 (9%) in AVF, and 1/4 (25%) in CAT. Among the eight PTFEG patients with thrombosis, seven were PAI 4G/5G.
PAI-1 levels were elevated in HD patients, independent of their polymorphic variants, 4G/5G being the most prevalent variant. Our data suggest that in patients with PTFEG the 4G/5G variant might be associated with an increased thrombosis risk.</description><subject>Aged</subject><subject>Arteriovenous Shunt, Surgical</subject><subject>Blood Vessel Prosthesis</subject><subject>C-Reactive Protein - metabolism</subject><subject>Chi-Square Distribution</subject><subject>Female</subject><subject>Graft Occlusion, Vascular - genetics</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Plasminogen Activator Inhibitor 1 - blood</subject><subject>Plasminogen Activator Inhibitor 1 - genetics</subject><subject>Polymorphism, Genetic</subject><subject>Polytetrafluoroethylene</subject><subject>Prospective Studies</subject><subject>Renal Dialysis</subject><subject>Statistics, Nonparametric</subject><subject>Thrombosis - genetics</subject><issn>1129-7298</issn><issn>1724-6032</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNplkEFLxDAQhYMo7rr6BzxIT97qziRpmxxl0VVYUEHPJWlTN9I2NekK_fdm2QUPnuYxfO8x8wi5RrhDLIolIpUFlQIEgASgSE_IHAvK0xwYPY06AumemJGLEL4iIjPk52SGIgeZMTonb6-tCp3t3afpE1WN9keNzie231pto0rxsLXjlKi-Tvh6ma2TwbVT5_ywtaGLbLI1nautaqdgwyU5a1QbzNVxLsjH48P76indvKyfV_ebtGKAYyoaJrUqMmQiPpDxRrMaEBStpFHIjWZKY83joRqR57lmWqAyGkFqrRiwBbk95A7efe9MGMvOhsq0reqN24UylwyooDKC9ABW3oXgTVMO3nbKTyVCuS-y_F9kNN0c03e6M_Wf5dgc-wUcPm15</recordid><startdate>20080401</startdate><enddate>20080401</enddate><creator>Trimarchi, H</creator><creator>Duboscq, C</creator><creator>Genoud, V</creator><creator>Lombi, F</creator><creator>Muryan, A</creator><creator>Young, P</creator><creator>Schwab, M</creator><creator>Castanon, M</creator><creator>Rodriguez-Reimundes, E</creator><creator>Forrester, M</creator><creator>Pereyra, H</creator><creator>Campolo-Girard, V</creator><creator>Seminario, O</creator><creator>Alonso, M</creator><creator>Kordich, L</creator><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>7X8</scope></search><sort><creationdate>20080401</creationdate><title>Plasminogen activator inhibitor-1 activity and 4G/5G polymorphism in hemodialysis</title><author>Trimarchi, H ; Duboscq, C ; Genoud, V ; Lombi, F ; Muryan, A ; Young, P ; Schwab, M ; Castanon, M ; Rodriguez-Reimundes, E ; Forrester, M ; Pereyra, H ; Campolo-Girard, V ; Seminario, O ; Alonso, M ; Kordich, L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c301t-8f39ba7513880854fb3d010a2c9ea14eb3ab1d4860b11466b3b81aeb109bba303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Aged</topic><topic>Arteriovenous Shunt, Surgical</topic><topic>Blood Vessel Prosthesis</topic><topic>C-Reactive Protein - metabolism</topic><topic>Chi-Square Distribution</topic><topic>Female</topic><topic>Graft Occlusion, Vascular - genetics</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Plasminogen Activator Inhibitor 1 - blood</topic><topic>Plasminogen Activator Inhibitor 1 - genetics</topic><topic>Polymorphism, Genetic</topic><topic>Polytetrafluoroethylene</topic><topic>Prospective Studies</topic><topic>Renal Dialysis</topic><topic>Statistics, Nonparametric</topic><topic>Thrombosis - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Trimarchi, H</creatorcontrib><creatorcontrib>Duboscq, C</creatorcontrib><creatorcontrib>Genoud, V</creatorcontrib><creatorcontrib>Lombi, F</creatorcontrib><creatorcontrib>Muryan, A</creatorcontrib><creatorcontrib>Young, P</creatorcontrib><creatorcontrib>Schwab, M</creatorcontrib><creatorcontrib>Castanon, M</creatorcontrib><creatorcontrib>Rodriguez-Reimundes, E</creatorcontrib><creatorcontrib>Forrester, M</creatorcontrib><creatorcontrib>Pereyra, H</creatorcontrib><creatorcontrib>Campolo-Girard, V</creatorcontrib><creatorcontrib>Seminario, O</creatorcontrib><creatorcontrib>Alonso, M</creatorcontrib><creatorcontrib>Kordich, L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The journal of vascular access</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Trimarchi, H</au><au>Duboscq, C</au><au>Genoud, V</au><au>Lombi, F</au><au>Muryan, A</au><au>Young, P</au><au>Schwab, M</au><au>Castanon, M</au><au>Rodriguez-Reimundes, E</au><au>Forrester, M</au><au>Pereyra, H</au><au>Campolo-Girard, V</au><au>Seminario, O</au><au>Alonso, M</au><au>Kordich, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasminogen activator inhibitor-1 activity and 4G/5G polymorphism in hemodialysis</atitle><jtitle>The journal of vascular access</jtitle><addtitle>J Vasc Access</addtitle><date>2008-04-01</date><risdate>2008</risdate><volume>9</volume><issue>2</issue><spage>142</spage><epage>147</epage><pages>142-147</pages><issn>1129-7298</issn><eissn>1724-6032</eissn><abstract>Chronic insufficiency alters homeostasis, in part due to endothelial inflammation. Plasminogen activator inhibitor-1 (PAI-1) is increased in renal disease, contributing to vascular damage. We assessed PAI-1 activity and PAI-1 4G/5G polymorphism in hemodialysis (HD) subjects and any association between thrombotic vascular access (VA) events and PAI-1 polymorphism.
Prospective, observational study in 36 HD patients: mean age: 66.6 +/- 12.5 yr, males n=26 (72%), time on HD: 28.71 +/- 22.45 months. Vascular accesses: 10 polytetrafluoroethylene grafts (PTFEG), 22 arteriovenous fistulae (AVF), four dual lumen catheters (CAT). Control group (CG): 40 subjects; mean age: 60.0 +/- 15 yrs, males n=30 (75%). Group A (GA): thrombotic events (n=12), and group B (GB): No events (n=24). Groups were no different according to age (69.2 +/- 9.12 vs. 65.3 +/- 14.5 yrs), gender (males: 7; 58.3% vs. 18; 81.8%), time on HD (26.1 +/- 14.7 vs. 30.1 +/- 38.7 months), causes of renal failure. Time to follow-up for access thrombosis: 12 months.
PAI-1 levels in HD: 7.21 +/- 2.13 vs. CG: 0.42 +/- 0.27 U/ml (p<0.0001). PAI-1 4G/5G polymorphic variant distribution in HD: 5G/5G: 6 (17%), 4G/5G: 23 (64%); 4G/4G: 7 (19%) and in CG: 5G/5G: 14 (35%); 4G/5G: 18 (45%); 4G/4G: 8 (20%). C-reactive protein (CRP) in HD: 24.5 +/- 15.2 mg/L vs. in CG 2.3 +/- 0.2 mg/L (p<0.0001). PAI-1 4G/5G variants: GA: 5G/5G: 3; 4G/5G: 8; 4G/4G: 1; GB: 5G/5G: 3; 4G/5G: 15; 4G/4G: 6. Thrombosis occurred in 8/10 patients (80%) with PTFEG, 3/22 (9%) in AVF, and 1/4 (25%) in CAT. Among the eight PTFEG patients with thrombosis, seven were PAI 4G/5G.
PAI-1 levels were elevated in HD patients, independent of their polymorphic variants, 4G/5G being the most prevalent variant. Our data suggest that in patients with PTFEG the 4G/5G variant might be associated with an increased thrombosis risk.</abstract><cop>United States</cop><pmid>18609532</pmid><doi>10.1177/112972980800900212</doi><tpages>6</tpages></addata></record> |
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| subjects | Aged Arteriovenous Shunt, Surgical Blood Vessel Prosthesis C-Reactive Protein - metabolism Chi-Square Distribution Female Graft Occlusion, Vascular - genetics Humans Male Middle Aged Plasminogen Activator Inhibitor 1 - blood Plasminogen Activator Inhibitor 1 - genetics Polymorphism, Genetic Polytetrafluoroethylene Prospective Studies Renal Dialysis Statistics, Nonparametric Thrombosis - genetics |
| title | Plasminogen activator inhibitor-1 activity and 4G/5G polymorphism in hemodialysis |
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