Platelet-Leukocyte Aggregates During Hemodialysis: Effect of Membrane Type
Hemodialysis is associated with the formation of platelet‐leukocyte aggregates. Whether this phenomenon is hemodialysis (HD) membrane dependent is unclear. To evaluate this process, we examined respectively platelet activation (anti‐CD41, anti‐CD62, and antifibrinogen monoclonal antibodies [MoAb] bi...
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description | Hemodialysis is associated with the formation of platelet‐leukocyte aggregates. Whether this phenomenon is hemodialysis (HD) membrane dependent is unclear. To evaluate this process, we examined respectively platelet activation (anti‐CD41, anti‐CD62, and antifibrinogen monoclonal antibodies [MoAb] binding), leukocyte activation (CD11b expression), and the appearance of platelet specific antigens on leukocytes as an index of platelet‐leukocyte aggregation during HD using 3 different membrane materials, Cuprophan, Hemophan, and polysulfone. Flow cytometric techniques and specific MoAb were used. All parameters were assayed 5 min after initiation of HD to avoid the confounding variable of leukopenia and resultant cell subpopulation analysis. Platelet activation (anti‐CD62 and antifibrinogen binding) occurred only with Cuprophan. All 3 membranes induced equivalent increases in CD11b expression on neutrophils and similarly increased the binding of anti‐CD41 to neutrophils, reflecting an increment in the formation of platelet neutrophil aggregates. However, only Cuprophan induced an increase in anti‐CD62 binding to neutrophils, suggesting that the aggregated platelets linked to neutrophils were activated. Increased anti‐CD41 binding by monocytes was similarly observed with all 3 membranes. However, only polysulfone induced an increase in CD11b expression and fibrinogen binding to monocytes. We conclude that while the formation of platelet leukocyte aggregates appears to be a universal phenomenon in HD occurring with a variety of membrane types, subtypes of this phenomenon consisting of activated platelets and fibrinogen binding may be membrane dependent. This phenomenon may serve as a new biocompatibility parameter and may shed light on some of the biologic consequences of hemodialysis. |
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Whether this phenomenon is hemodialysis (HD) membrane dependent is unclear. To evaluate this process, we examined respectively platelet activation (anti‐CD41, anti‐CD62, and antifibrinogen monoclonal antibodies [MoAb] binding), leukocyte activation (CD11b expression), and the appearance of platelet specific antigens on leukocytes as an index of platelet‐leukocyte aggregation during HD using 3 different membrane materials, Cuprophan, Hemophan, and polysulfone. Flow cytometric techniques and specific MoAb were used. All parameters were assayed 5 min after initiation of HD to avoid the confounding variable of leukopenia and resultant cell subpopulation analysis. Platelet activation (anti‐CD62 and antifibrinogen binding) occurred only with Cuprophan. All 3 membranes induced equivalent increases in CD11b expression on neutrophils and similarly increased the binding of anti‐CD41 to neutrophils, reflecting an increment in the formation of platelet neutrophil aggregates. However, only Cuprophan induced an increase in anti‐CD62 binding to neutrophils, suggesting that the aggregated platelets linked to neutrophils were activated. Increased anti‐CD41 binding by monocytes was similarly observed with all 3 membranes. However, only polysulfone induced an increase in CD11b expression and fibrinogen binding to monocytes. We conclude that while the formation of platelet leukocyte aggregates appears to be a universal phenomenon in HD occurring with a variety of membrane types, subtypes of this phenomenon consisting of activated platelets and fibrinogen binding may be membrane dependent. This phenomenon may serve as a new biocompatibility parameter and may shed light on some of the biologic consequences of hemodialysis.</description><identifier>ISSN: 0160-564X</identifier><identifier>EISSN: 1525-1594</identifier><identifier>DOI: 10.1046/j.1525-1594.1999.06289.x</identifier><identifier>PMID: 9950176</identifier><language>eng</language><publisher>Boston, USA: Blackwell Science Inc</publisher><subject>Antibodies, Monoclonal ; Antigens - analysis ; Biocompatible Materials - chemistry ; Blood Platelets - immunology ; Blood Platelets - physiology ; CD11 Antigens - analysis ; Cell Aggregation - physiology ; Cellulose - analogs & derivatives ; Cellulose - chemistry ; Fibrinogen - analysis ; Flow Cytometry ; Humans ; Leukocytes - immunology ; Leukocytes - physiology ; Membranes, Artificial ; Neutrophil Activation - physiology ; Neutrophils - physiology ; P-Selectin - analysis ; Platelet ; Platelet Activation ; Platelet Aggregation - physiology ; Platelet Glycoprotein GPIIb-IIIa Complex - analysis ; Platelet-leukocyte coaggregates ; Polymers - chemistry ; Renal Dialysis - instrumentation ; Renal Dialysis - methods ; Sulfones - chemistry</subject><ispartof>Artificial organs, 1999-01, Vol.23 (1), p.29-36</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4029-faf02ec152b215d5a24695c2481fb29833c4736b51797f1773036110ff8475ba3</citedby><cites>FETCH-LOGICAL-c4029-faf02ec152b215d5a24695c2481fb29833c4736b51797f1773036110ff8475ba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1525-1594.1999.06289.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1525-1594.1999.06289.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9950176$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gawaz, Meinrad P.</creatorcontrib><creatorcontrib>Mujais, Salim K.</creatorcontrib><creatorcontrib>Schmidt, Bärbel</creatorcontrib><creatorcontrib>Blumenstein, Mathias</creatorcontrib><creatorcontrib>Gurland, Hans J.</creatorcontrib><title>Platelet-Leukocyte Aggregates During Hemodialysis: Effect of Membrane Type</title><title>Artificial organs</title><addtitle>Artificial Organs</addtitle><description>Hemodialysis is associated with the formation of platelet‐leukocyte aggregates. Whether this phenomenon is hemodialysis (HD) membrane dependent is unclear. To evaluate this process, we examined respectively platelet activation (anti‐CD41, anti‐CD62, and antifibrinogen monoclonal antibodies [MoAb] binding), leukocyte activation (CD11b expression), and the appearance of platelet specific antigens on leukocytes as an index of platelet‐leukocyte aggregation during HD using 3 different membrane materials, Cuprophan, Hemophan, and polysulfone. Flow cytometric techniques and specific MoAb were used. All parameters were assayed 5 min after initiation of HD to avoid the confounding variable of leukopenia and resultant cell subpopulation analysis. Platelet activation (anti‐CD62 and antifibrinogen binding) occurred only with Cuprophan. All 3 membranes induced equivalent increases in CD11b expression on neutrophils and similarly increased the binding of anti‐CD41 to neutrophils, reflecting an increment in the formation of platelet neutrophil aggregates. However, only Cuprophan induced an increase in anti‐CD62 binding to neutrophils, suggesting that the aggregated platelets linked to neutrophils were activated. Increased anti‐CD41 binding by monocytes was similarly observed with all 3 membranes. However, only polysulfone induced an increase in CD11b expression and fibrinogen binding to monocytes. We conclude that while the formation of platelet leukocyte aggregates appears to be a universal phenomenon in HD occurring with a variety of membrane types, subtypes of this phenomenon consisting of activated platelets and fibrinogen binding may be membrane dependent. This phenomenon may serve as a new biocompatibility parameter and may shed light on some of the biologic consequences of hemodialysis.</description><subject>Antibodies, Monoclonal</subject><subject>Antigens - analysis</subject><subject>Biocompatible Materials - chemistry</subject><subject>Blood Platelets - immunology</subject><subject>Blood Platelets - physiology</subject><subject>CD11 Antigens - analysis</subject><subject>Cell Aggregation - physiology</subject><subject>Cellulose - analogs & derivatives</subject><subject>Cellulose - chemistry</subject><subject>Fibrinogen - analysis</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Leukocytes - immunology</subject><subject>Leukocytes - physiology</subject><subject>Membranes, Artificial</subject><subject>Neutrophil Activation - physiology</subject><subject>Neutrophils - physiology</subject><subject>P-Selectin - analysis</subject><subject>Platelet</subject><subject>Platelet Activation</subject><subject>Platelet Aggregation - physiology</subject><subject>Platelet Glycoprotein GPIIb-IIIa Complex - analysis</subject><subject>Platelet-leukocyte coaggregates</subject><subject>Polymers - chemistry</subject><subject>Renal Dialysis - instrumentation</subject><subject>Renal Dialysis - methods</subject><subject>Sulfones - chemistry</subject><issn>0160-564X</issn><issn>1525-1594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMlOwzAURS0EgjJ8AlJW7BLseIqRWJSxQBmEQLCznPS5SkmaYiei-XsSWnXNypbvO9dPB6GA4IhgJk5nEeExDwlXLCJKqQiLOFHRcgsNNsE2GmAicMgF-9xD-97PMMaSYbGLdpXimEgxQPcvhamhgDocQ_NVZW0NwXA6dTDtnn1w1bh8Pg1GUFaT3BStz_1ZcG0tZHVQ2eARytSZOQRv7QIO0Y41hYej9XmA3m-u3y5H4fj59u5yOA4zhmMVWmNxDFm3ZhoTPuEmZkLxLGYJsWmsEkozJqlIOZFKWiIlxVQQgq1NmOSpoQfoZNW7cNV3A77WZe4zKIpukarxumsTUgncDSarwcxV3juweuHy0rhWE6x7jXqme1u6t6V7jfpPo1526PH6jyYtYbIB1966_HyV_-QFtP_u1cPn1_7W8eGKz30Nyw1v3JcWkkquP55u9YiOR_JBXugb-gt-ZY64</recordid><startdate>199901</startdate><enddate>199901</enddate><creator>Gawaz, Meinrad P.</creator><creator>Mujais, Salim K.</creator><creator>Schmidt, Bärbel</creator><creator>Blumenstein, Mathias</creator><creator>Gurland, Hans J.</creator><general>Blackwell Science Inc</general><scope>BSCLL</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>199901</creationdate><title>Platelet-Leukocyte Aggregates During Hemodialysis: Effect of Membrane Type</title><author>Gawaz, Meinrad P. ; Mujais, Salim K. ; Schmidt, Bärbel ; Blumenstein, Mathias ; Gurland, Hans J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4029-faf02ec152b215d5a24695c2481fb29833c4736b51797f1773036110ff8475ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Antibodies, Monoclonal</topic><topic>Antigens - analysis</topic><topic>Biocompatible Materials - chemistry</topic><topic>Blood Platelets - immunology</topic><topic>Blood Platelets - physiology</topic><topic>CD11 Antigens - analysis</topic><topic>Cell Aggregation - physiology</topic><topic>Cellulose - analogs & derivatives</topic><topic>Cellulose - chemistry</topic><topic>Fibrinogen - analysis</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Leukocytes - immunology</topic><topic>Leukocytes - physiology</topic><topic>Membranes, Artificial</topic><topic>Neutrophil Activation - physiology</topic><topic>Neutrophils - physiology</topic><topic>P-Selectin - analysis</topic><topic>Platelet</topic><topic>Platelet Activation</topic><topic>Platelet Aggregation - physiology</topic><topic>Platelet Glycoprotein GPIIb-IIIa Complex - analysis</topic><topic>Platelet-leukocyte coaggregates</topic><topic>Polymers - chemistry</topic><topic>Renal Dialysis - instrumentation</topic><topic>Renal Dialysis - methods</topic><topic>Sulfones - chemistry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gawaz, Meinrad P.</creatorcontrib><creatorcontrib>Mujais, Salim K.</creatorcontrib><creatorcontrib>Schmidt, Bärbel</creatorcontrib><creatorcontrib>Blumenstein, Mathias</creatorcontrib><creatorcontrib>Gurland, Hans J.</creatorcontrib><collection>Istex</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>Artificial organs</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gawaz, Meinrad P.</au><au>Mujais, Salim K.</au><au>Schmidt, Bärbel</au><au>Blumenstein, Mathias</au><au>Gurland, Hans J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet-Leukocyte Aggregates During Hemodialysis: Effect of Membrane Type</atitle><jtitle>Artificial organs</jtitle><addtitle>Artificial Organs</addtitle><date>1999-01</date><risdate>1999</risdate><volume>23</volume><issue>1</issue><spage>29</spage><epage>36</epage><pages>29-36</pages><issn>0160-564X</issn><eissn>1525-1594</eissn><abstract>Hemodialysis is associated with the formation of platelet‐leukocyte aggregates. Whether this phenomenon is hemodialysis (HD) membrane dependent is unclear. To evaluate this process, we examined respectively platelet activation (anti‐CD41, anti‐CD62, and antifibrinogen monoclonal antibodies [MoAb] binding), leukocyte activation (CD11b expression), and the appearance of platelet specific antigens on leukocytes as an index of platelet‐leukocyte aggregation during HD using 3 different membrane materials, Cuprophan, Hemophan, and polysulfone. Flow cytometric techniques and specific MoAb were used. All parameters were assayed 5 min after initiation of HD to avoid the confounding variable of leukopenia and resultant cell subpopulation analysis. Platelet activation (anti‐CD62 and antifibrinogen binding) occurred only with Cuprophan. All 3 membranes induced equivalent increases in CD11b expression on neutrophils and similarly increased the binding of anti‐CD41 to neutrophils, reflecting an increment in the formation of platelet neutrophil aggregates. However, only Cuprophan induced an increase in anti‐CD62 binding to neutrophils, suggesting that the aggregated platelets linked to neutrophils were activated. Increased anti‐CD41 binding by monocytes was similarly observed with all 3 membranes. However, only polysulfone induced an increase in CD11b expression and fibrinogen binding to monocytes. We conclude that while the formation of platelet leukocyte aggregates appears to be a universal phenomenon in HD occurring with a variety of membrane types, subtypes of this phenomenon consisting of activated platelets and fibrinogen binding may be membrane dependent. This phenomenon may serve as a new biocompatibility parameter and may shed light on some of the biologic consequences of hemodialysis.</abstract><cop>Boston, USA</cop><pub>Blackwell Science Inc</pub><pmid>9950176</pmid><doi>10.1046/j.1525-1594.1999.06289.x</doi><tpages>8</tpages></addata></record> |
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subjects | Antibodies, Monoclonal Antigens - analysis Biocompatible Materials - chemistry Blood Platelets - immunology Blood Platelets - physiology CD11 Antigens - analysis Cell Aggregation - physiology Cellulose - analogs & derivatives Cellulose - chemistry Fibrinogen - analysis Flow Cytometry Humans Leukocytes - immunology Leukocytes - physiology Membranes, Artificial Neutrophil Activation - physiology Neutrophils - physiology P-Selectin - analysis Platelet Platelet Activation Platelet Aggregation - physiology Platelet Glycoprotein GPIIb-IIIa Complex - analysis Platelet-leukocyte coaggregates Polymers - chemistry Renal Dialysis - instrumentation Renal Dialysis - methods Sulfones - chemistry |
title | Platelet-Leukocyte Aggregates During Hemodialysis: Effect of Membrane Type |
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