Biphasic effects of hemodialysis on platelet reactivity in patients with end-stage renal disease: A potential contributor to cardiovascular risk
Background: Cardiovascular disease is rampant in patients with end-stage renal disease (ESRD), and increased platelet reactivity may contribute. This study is designed to determine effects of hemodialysis in patients with ESRD on platelet reactivity per se. Methods: Platelet reactivity was determine...
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Veröffentlicht in: | American journal of kidney diseases 2002-08, Vol.40 (2), p.315-322 |
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description | Background: Cardiovascular disease is rampant in patients with end-stage renal disease (ESRD), and increased platelet reactivity may contribute. This study is designed to determine effects of hemodialysis in patients with ESRD on platelet reactivity per se. Methods: Platelet reactivity was determined by flow cytometry in 36 patients with ESRD undergoing hemodialysis. Blood was obtained from arterial and venous ends of the hemodialysis circuit at the beginning and end of the dialysis session. Platelet reactivity was defined with respect to capacity to bind fibrinogen (activation of glycoprotein IIb-IIIa) and expression of P-selectin in response to adenosine diphosphate (ADP; 0, 0.2, and 1.0 μmol/L). Comparison studies were performed with 55 patients with coronary artery disease (CAD) and 38 healthy subjects. Results: Platelet reactivity was increased by exposure to the dialysis circuit (capacity to bind fibrinogen: arterial, 28% ± 13%; venous, 47% ± 20%; P < 0.001). Despite this effect, surface expression of P-selectin in response to 1 μmol/L of ADP was lower at the end of the dialysis session (arterial blood at its onset, 40% ± 16%; arterial blood at its conclusion, 24% ± 15%; P < 0.05). Confocal microscopy showed increased nonspecific association of fibrinogen with platelets after dialysis, suggesting that increased aggregation after dialysis may be secondary to effects of dialysis on fibrinogen binding, rather than on platelet reactivity. Platelet reactivity was increased similarly in patients with ESRD and those with CAD compared with healthy subjects. Conclusion: Although interaction between platelets and the dialysis circuit increases platelet reactivity, continued dialysis decreases platelet reactivity. © 2002 by the National Kidney Foundation, Inc. |
doi_str_mv | 10.1053/ajkd.2002.34510 |
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This study is designed to determine effects of hemodialysis in patients with ESRD on platelet reactivity per se. Methods: Platelet reactivity was determined by flow cytometry in 36 patients with ESRD undergoing hemodialysis. Blood was obtained from arterial and venous ends of the hemodialysis circuit at the beginning and end of the dialysis session. Platelet reactivity was defined with respect to capacity to bind fibrinogen (activation of glycoprotein IIb-IIIa) and expression of P-selectin in response to adenosine diphosphate (ADP; 0, 0.2, and 1.0 μmol/L). Comparison studies were performed with 55 patients with coronary artery disease (CAD) and 38 healthy subjects. Results: Platelet reactivity was increased by exposure to the dialysis circuit (capacity to bind fibrinogen: arterial, 28% ± 13%; venous, 47% ± 20%; P < 0.001). Despite this effect, surface expression of P-selectin in response to 1 μmol/L of ADP was lower at the end of the dialysis session (arterial blood at its onset, 40% ± 16%; arterial blood at its conclusion, 24% ± 15%; P < 0.05). Confocal microscopy showed increased nonspecific association of fibrinogen with platelets after dialysis, suggesting that increased aggregation after dialysis may be secondary to effects of dialysis on fibrinogen binding, rather than on platelet reactivity. Platelet reactivity was increased similarly in patients with ESRD and those with CAD compared with healthy subjects. Conclusion: Although interaction between platelets and the dialysis circuit increases platelet reactivity, continued dialysis decreases platelet reactivity. © 2002 by the National Kidney Foundation, Inc.</description><identifier>ISSN: 0272-6386</identifier><identifier>EISSN: 1523-6838</identifier><identifier>DOI: 10.1053/ajkd.2002.34510</identifier><identifier>PMID: 12148104</identifier><language>eng</language><publisher>Orlando, FL: Elsevier Inc</publisher><subject>Adenosine Diphosphate - pharmacology ; Biological and medical sciences ; Coronary Artery Disease - blood ; coronary disease ; Female ; Fibrinogen - metabolism ; Flow Cytometry ; hemodialysis (HD) ; Humans ; kidney ; Kidney Failure, Chronic - blood ; Kidney Failure, Chronic - therapy ; Male ; Medical sciences ; Membranes, Artificial ; Microscopy, Confocal ; Middle Aged ; Myocardial Infarction - etiology ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; P-Selectin - metabolism ; Platelet Activation - drug effects ; Platelet Activation - physiology ; Platelet Aggregation - drug effects ; Platelet Aggregation - physiology ; Platelet Function Tests - methods ; Platelet Glycoprotein GPIIb-IIIa Complex - metabolism ; Platelets ; Protein Binding - drug effects ; Protein Binding - physiology ; Renal Dialysis - adverse effects ; Renal Dialysis - methods ; Renal failure ; Risk Factors</subject><ispartof>American journal of kidney diseases, 2002-08, Vol.40 (2), p.315-322</ispartof><rights>2002 National Kidney Foundation, Inc</rights><rights>2002 INIST-CNRS</rights><rights>Copyright 2002 by the National Kidney Foundation, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c373t-10ffc57dfd0db39264a47206c2407d4015d1cb9b98e7fedcb06a548cf5d9b7ef3</citedby><cites>FETCH-LOGICAL-c373t-10ffc57dfd0db39264a47206c2407d4015d1cb9b98e7fedcb06a548cf5d9b7ef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0272638602000458$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13835356$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12148104$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aggarwal, Atul</creatorcontrib><creatorcontrib>Kabbani, Samer S.</creatorcontrib><creatorcontrib>Rimmer, Jeffery M.</creatorcontrib><creatorcontrib>Gennari, F.John</creatorcontrib><creatorcontrib>Taatjes, Douglas J.</creatorcontrib><creatorcontrib>Sobel, Burton E.</creatorcontrib><creatorcontrib>Schneider, David J.</creatorcontrib><title>Biphasic effects of hemodialysis on platelet reactivity in patients with end-stage renal disease: A potential contributor to cardiovascular risk</title><title>American journal of kidney diseases</title><addtitle>Am J Kidney Dis</addtitle><description>Background: Cardiovascular disease is rampant in patients with end-stage renal disease (ESRD), and increased platelet reactivity may contribute. This study is designed to determine effects of hemodialysis in patients with ESRD on platelet reactivity per se. Methods: Platelet reactivity was determined by flow cytometry in 36 patients with ESRD undergoing hemodialysis. Blood was obtained from arterial and venous ends of the hemodialysis circuit at the beginning and end of the dialysis session. Platelet reactivity was defined with respect to capacity to bind fibrinogen (activation of glycoprotein IIb-IIIa) and expression of P-selectin in response to adenosine diphosphate (ADP; 0, 0.2, and 1.0 μmol/L). Comparison studies were performed with 55 patients with coronary artery disease (CAD) and 38 healthy subjects. Results: Platelet reactivity was increased by exposure to the dialysis circuit (capacity to bind fibrinogen: arterial, 28% ± 13%; venous, 47% ± 20%; P < 0.001). Despite this effect, surface expression of P-selectin in response to 1 μmol/L of ADP was lower at the end of the dialysis session (arterial blood at its onset, 40% ± 16%; arterial blood at its conclusion, 24% ± 15%; P < 0.05). Confocal microscopy showed increased nonspecific association of fibrinogen with platelets after dialysis, suggesting that increased aggregation after dialysis may be secondary to effects of dialysis on fibrinogen binding, rather than on platelet reactivity. Platelet reactivity was increased similarly in patients with ESRD and those with CAD compared with healthy subjects. Conclusion: Although interaction between platelets and the dialysis circuit increases platelet reactivity, continued dialysis decreases platelet reactivity. © 2002 by the National Kidney Foundation, Inc.</description><subject>Adenosine Diphosphate - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Coronary Artery Disease - blood</subject><subject>coronary disease</subject><subject>Female</subject><subject>Fibrinogen - metabolism</subject><subject>Flow Cytometry</subject><subject>hemodialysis (HD)</subject><subject>Humans</subject><subject>kidney</subject><subject>Kidney Failure, Chronic - blood</subject><subject>Kidney Failure, Chronic - therapy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membranes, Artificial</subject><subject>Microscopy, Confocal</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - etiology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>P-Selectin - metabolism</subject><subject>Platelet Activation - drug effects</subject><subject>Platelet Activation - physiology</subject><subject>Platelet Aggregation - drug effects</subject><subject>Platelet Aggregation - physiology</subject><subject>Platelet Function Tests - methods</subject><subject>Platelet Glycoprotein GPIIb-IIIa Complex - metabolism</subject><subject>Platelets</subject><subject>Protein Binding - drug effects</subject><subject>Protein Binding - physiology</subject><subject>Renal Dialysis - adverse effects</subject><subject>Renal Dialysis - methods</subject><subject>Renal failure</subject><subject>Risk Factors</subject><issn>0272-6386</issn><issn>1523-6838</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kb1uFDEUhS0EIkugpkNuSDcb_80fXYhCghSJJqmtO_Y162R2PNieRfsWPDJedqVUVJat7x75no-Qj5ytOavlJTw927VgTKylqjl7RVa8FrJqOtm9JismWlE1smvOyLuUnhhjvWyat-SMC646ztSK_Pnq5w0kbyg6hyYnGhzd4DZYD-M--XKf6DxCxhEzjQgm-53Pe-rLM2SPUxn57fOG4mSrlOEnFmqCkVqfEBJ-oVd0DrlwJZCaMOXohyWHSHOgBqL1YQfJLCNEGn16fk_eOBgTfjid5-Tx283D9V11_-P2-_XVfWVkK3PFmXOmbq2zzA6yF40C1QrWGKFYaxXjteVm6Ie-w9ahNQNroFadcbXthxadPCcXx9w5hl8Lpqy3PhkcR5gwLEm3vFeKM1HAyyNoYkgpotNz9FuIe82ZPkjQBwn6IEH_k1AmPp2il2GL9oU_tV6AzyegbA6jizAZn1442cla1k3h-iOHpYidx6iTKY0btD4WV9oG_99P_AWihKcU</recordid><startdate>20020801</startdate><enddate>20020801</enddate><creator>Aggarwal, Atul</creator><creator>Kabbani, Samer S.</creator><creator>Rimmer, Jeffery M.</creator><creator>Gennari, F.John</creator><creator>Taatjes, Douglas J.</creator><creator>Sobel, Burton E.</creator><creator>Schneider, David J.</creator><general>Elsevier Inc</general><general>Elsevier</general><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>7X8</scope></search><sort><creationdate>20020801</creationdate><title>Biphasic effects of hemodialysis on platelet reactivity in patients with end-stage renal disease: A potential contributor to cardiovascular risk</title><author>Aggarwal, Atul ; Kabbani, Samer S. ; Rimmer, Jeffery M. ; Gennari, F.John ; Taatjes, Douglas J. ; Sobel, Burton E. ; Schneider, David J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c373t-10ffc57dfd0db39264a47206c2407d4015d1cb9b98e7fedcb06a548cf5d9b7ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adenosine Diphosphate - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Coronary Artery Disease - blood</topic><topic>coronary disease</topic><topic>Female</topic><topic>Fibrinogen - metabolism</topic><topic>Flow Cytometry</topic><topic>hemodialysis (HD)</topic><topic>Humans</topic><topic>kidney</topic><topic>Kidney Failure, Chronic - blood</topic><topic>Kidney Failure, Chronic - therapy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membranes, Artificial</topic><topic>Microscopy, Confocal</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - etiology</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>P-Selectin - metabolism</topic><topic>Platelet Activation - drug effects</topic><topic>Platelet Activation - physiology</topic><topic>Platelet Aggregation - drug effects</topic><topic>Platelet Aggregation - physiology</topic><topic>Platelet Function Tests - methods</topic><topic>Platelet Glycoprotein GPIIb-IIIa Complex - metabolism</topic><topic>Platelets</topic><topic>Protein Binding - drug effects</topic><topic>Protein Binding - physiology</topic><topic>Renal Dialysis - adverse effects</topic><topic>Renal Dialysis - methods</topic><topic>Renal failure</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aggarwal, Atul</creatorcontrib><creatorcontrib>Kabbani, Samer S.</creatorcontrib><creatorcontrib>Rimmer, Jeffery M.</creatorcontrib><creatorcontrib>Gennari, F.John</creatorcontrib><creatorcontrib>Taatjes, Douglas J.</creatorcontrib><creatorcontrib>Sobel, Burton E.</creatorcontrib><creatorcontrib>Schneider, David J.</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>American journal of kidney diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aggarwal, Atul</au><au>Kabbani, Samer S.</au><au>Rimmer, Jeffery M.</au><au>Gennari, F.John</au><au>Taatjes, Douglas J.</au><au>Sobel, Burton E.</au><au>Schneider, David J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biphasic effects of hemodialysis on platelet reactivity in patients with end-stage renal disease: A potential contributor to cardiovascular risk</atitle><jtitle>American journal of kidney diseases</jtitle><addtitle>Am J Kidney Dis</addtitle><date>2002-08-01</date><risdate>2002</risdate><volume>40</volume><issue>2</issue><spage>315</spage><epage>322</epage><pages>315-322</pages><issn>0272-6386</issn><eissn>1523-6838</eissn><abstract>Background: Cardiovascular disease is rampant in patients with end-stage renal disease (ESRD), and increased platelet reactivity may contribute. This study is designed to determine effects of hemodialysis in patients with ESRD on platelet reactivity per se. Methods: Platelet reactivity was determined by flow cytometry in 36 patients with ESRD undergoing hemodialysis. Blood was obtained from arterial and venous ends of the hemodialysis circuit at the beginning and end of the dialysis session. Platelet reactivity was defined with respect to capacity to bind fibrinogen (activation of glycoprotein IIb-IIIa) and expression of P-selectin in response to adenosine diphosphate (ADP; 0, 0.2, and 1.0 μmol/L). Comparison studies were performed with 55 patients with coronary artery disease (CAD) and 38 healthy subjects. Results: Platelet reactivity was increased by exposure to the dialysis circuit (capacity to bind fibrinogen: arterial, 28% ± 13%; venous, 47% ± 20%; P < 0.001). Despite this effect, surface expression of P-selectin in response to 1 μmol/L of ADP was lower at the end of the dialysis session (arterial blood at its onset, 40% ± 16%; arterial blood at its conclusion, 24% ± 15%; P < 0.05). Confocal microscopy showed increased nonspecific association of fibrinogen with platelets after dialysis, suggesting that increased aggregation after dialysis may be secondary to effects of dialysis on fibrinogen binding, rather than on platelet reactivity. Platelet reactivity was increased similarly in patients with ESRD and those with CAD compared with healthy subjects. Conclusion: Although interaction between platelets and the dialysis circuit increases platelet reactivity, continued dialysis decreases platelet reactivity. © 2002 by the National Kidney Foundation, Inc.</abstract><cop>Orlando, FL</cop><pub>Elsevier Inc</pub><pmid>12148104</pmid><doi>10.1053/ajkd.2002.34510</doi><tpages>8</tpages></addata></record> |
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subjects | Adenosine Diphosphate - pharmacology Biological and medical sciences Coronary Artery Disease - blood coronary disease Female Fibrinogen - metabolism Flow Cytometry hemodialysis (HD) Humans kidney Kidney Failure, Chronic - blood Kidney Failure, Chronic - therapy Male Medical sciences Membranes, Artificial Microscopy, Confocal Middle Aged Myocardial Infarction - etiology Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure P-Selectin - metabolism Platelet Activation - drug effects Platelet Activation - physiology Platelet Aggregation - drug effects Platelet Aggregation - physiology Platelet Function Tests - methods Platelet Glycoprotein GPIIb-IIIa Complex - metabolism Platelets Protein Binding - drug effects Protein Binding - physiology Renal Dialysis - adverse effects Renal Dialysis - methods Renal failure Risk Factors |
title | Biphasic effects of hemodialysis on platelet reactivity in patients with end-stage renal disease: A potential contributor to cardiovascular risk |
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