Acute Kidney Injury in Decompensated Cirrhosis Is Associated With Both Hypo‐coagulable and Hyper‐coagulable Features

Background and Aims Recent evidence suggests that acute kidney injury (AKI) is the main predictor of postparacentesis bleeding in patients with cirrhosis. To assess the factors responsible for bleeding tendency in AKI, we performed a prospective study comparing all three aspects of hemostasis (plate...

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Veröffentlicht in:Hepatology (Baltimore, Md.) Md.), 2020-10, Vol.72 (4), p.1327-1340
Hauptverfasser: Zanetto, Alberto, Rinder, Henry M., Campello, Elena, Saggiorato, Graziella, Deng, Yanhong, Ciarleglio, Maria, Wilson, Francis P., Senzolo, Marco, Gavasso, Sabrina, Bulato, Cristiana, Simioni, Paolo, Garcia‐Tsao, Guadalupe
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container_end_page 1340
container_issue 4
container_start_page 1327
container_title Hepatology (Baltimore, Md.)
container_volume 72
creator Zanetto, Alberto
Rinder, Henry M.
Campello, Elena
Saggiorato, Graziella
Deng, Yanhong
Ciarleglio, Maria
Wilson, Francis P.
Senzolo, Marco
Gavasso, Sabrina
Bulato, Cristiana
Simioni, Paolo
Garcia‐Tsao, Guadalupe
description Background and Aims Recent evidence suggests that acute kidney injury (AKI) is the main predictor of postparacentesis bleeding in patients with cirrhosis. To assess the factors responsible for bleeding tendency in AKI, we performed a prospective study comparing all three aspects of hemostasis (platelets, coagulation, and fibrinolysis) in patients with decompensated cirrhosis with and without AKI. Approach and Results Primary hemostasis assessment included platelet aggregation and secretion (platelet function markers) and von Willebrand factor. Secondary hemostasis assessment included pro‐coagulant (factor VIII and factor XIII) and anti‐coagulant (protein C, protein S, and antithrombin) factors and thrombin generation. Tertiary hemostasis assessment included fibrinolytic factors and plasmin‐antiplasmin complex. Eighty patients with decompensated cirrhosis were recruited (40 each with and without AKI). Severity of cirrhosis and platelet count were comparable between groups. Median serum creatinine was 1.8 mg/dL and 0.8 mg/dL in patients with and without AKI, respectively. At baseline, patients with cirrhosis and AKI had lower platelet aggregation and secretion, indicative of impaired platelet function (increased bleeding tendency), without differences in von Willebrand factor. Regarding coagulation factors, factor VIII was higher, whereas protein C, protein S, and antithrombin were all lower, which, together with increased thrombin generation, indicate hypercoagulability. In contrast, factor XIII was lower in AKI (increased bleeding tendency). Finally, while both hypofibrinolytic and hyperfibrinolytic changes were present in AKI, a higher plasmin‐antiplasmin complex indicated a hyperfibrinolytic state. After AKI resolution (n = 23 of 40), platelet function and coagulation improved to levels observed in patients with cirrhosis patients without AKI; however, fibrinolysis remained hyperactivated. Conclusions In patients with decompensated cirrhosis, AKI is associated with both hypocoagulable and hypercoagulable features that can potentially increase the risk of both bleeding and thrombosis.
doi_str_mv 10.1002/hep.31443
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To assess the factors responsible for bleeding tendency in AKI, we performed a prospective study comparing all three aspects of hemostasis (platelets, coagulation, and fibrinolysis) in patients with decompensated cirrhosis with and without AKI. Approach and Results Primary hemostasis assessment included platelet aggregation and secretion (platelet function markers) and von Willebrand factor. Secondary hemostasis assessment included pro‐coagulant (factor VIII and factor XIII) and anti‐coagulant (protein C, protein S, and antithrombin) factors and thrombin generation. Tertiary hemostasis assessment included fibrinolytic factors and plasmin‐antiplasmin complex. Eighty patients with decompensated cirrhosis were recruited (40 each with and without AKI). Severity of cirrhosis and platelet count were comparable between groups. Median serum creatinine was 1.8 mg/dL and 0.8 mg/dL in patients with and without AKI, respectively. At baseline, patients with cirrhosis and AKI had lower platelet aggregation and secretion, indicative of impaired platelet function (increased bleeding tendency), without differences in von Willebrand factor. Regarding coagulation factors, factor VIII was higher, whereas protein C, protein S, and antithrombin were all lower, which, together with increased thrombin generation, indicate hypercoagulability. In contrast, factor XIII was lower in AKI (increased bleeding tendency). Finally, while both hypofibrinolytic and hyperfibrinolytic changes were present in AKI, a higher plasmin‐antiplasmin complex indicated a hyperfibrinolytic state. After AKI resolution (n = 23 of 40), platelet function and coagulation improved to levels observed in patients with cirrhosis patients without AKI; however, fibrinolysis remained hyperactivated. Conclusions In patients with decompensated cirrhosis, AKI is associated with both hypocoagulable and hypercoagulable features that can potentially increase the risk of both bleeding and thrombosis.</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.31443</identifier><identifier>PMID: 32614088</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Acute Kidney Injury - blood ; Acute Kidney Injury - complications ; Aged ; Antithrombin ; Bleeding ; Blood Coagulation Disorders - etiology ; Cirrhosis ; Coagulation factors ; Creatinine ; Factor VIII - analysis ; Female ; Fibrin ; Fibrinolysis ; Hemostasis ; Hepatology ; Humans ; Kidneys ; Liver cirrhosis ; Liver Cirrhosis - complications ; Male ; Middle Aged ; Plasmin ; Platelet aggregation ; Prospective Studies ; Protein C ; Protein S ; Proteins ; Secretion ; Thrombin ; Thrombosis ; Von Willebrand factor ; von Willebrand Factor - physiology</subject><ispartof>Hepatology (Baltimore, Md.), 2020-10, Vol.72 (4), p.1327-1340</ispartof><rights>2020 by the American Association for the Study of Liver Diseases.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4433-80aa1ed1793e2d30ea96caf43562746f592158e98e36f772b3a0172ea9300f823</citedby><cites>FETCH-LOGICAL-c4433-80aa1ed1793e2d30ea96caf43562746f592158e98e36f772b3a0172ea9300f823</cites><orcidid>0000-0001-6873-8026 ; 0000-0002-7261-6520 ; 0000-0002-6744-383X ; 0000-0002-3062-1268 ; 0000-0002-6591-3674 ; 0000-0002-0377-3741 ; 0000-0002-6734-7178 ; 0000-0001-7271-7447 ; 0000-0001-8371-4524 ; 0000-0002-2633-2412</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.31443$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.31443$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32614088$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zanetto, Alberto</creatorcontrib><creatorcontrib>Rinder, Henry M.</creatorcontrib><creatorcontrib>Campello, Elena</creatorcontrib><creatorcontrib>Saggiorato, Graziella</creatorcontrib><creatorcontrib>Deng, Yanhong</creatorcontrib><creatorcontrib>Ciarleglio, Maria</creatorcontrib><creatorcontrib>Wilson, Francis P.</creatorcontrib><creatorcontrib>Senzolo, Marco</creatorcontrib><creatorcontrib>Gavasso, Sabrina</creatorcontrib><creatorcontrib>Bulato, Cristiana</creatorcontrib><creatorcontrib>Simioni, Paolo</creatorcontrib><creatorcontrib>Garcia‐Tsao, Guadalupe</creatorcontrib><title>Acute Kidney Injury in Decompensated Cirrhosis Is Associated With Both Hypo‐coagulable and Hyper‐coagulable Features</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>Background and Aims Recent evidence suggests that acute kidney injury (AKI) is the main predictor of postparacentesis bleeding in patients with cirrhosis. To assess the factors responsible for bleeding tendency in AKI, we performed a prospective study comparing all three aspects of hemostasis (platelets, coagulation, and fibrinolysis) in patients with decompensated cirrhosis with and without AKI. Approach and Results Primary hemostasis assessment included platelet aggregation and secretion (platelet function markers) and von Willebrand factor. Secondary hemostasis assessment included pro‐coagulant (factor VIII and factor XIII) and anti‐coagulant (protein C, protein S, and antithrombin) factors and thrombin generation. Tertiary hemostasis assessment included fibrinolytic factors and plasmin‐antiplasmin complex. Eighty patients with decompensated cirrhosis were recruited (40 each with and without AKI). Severity of cirrhosis and platelet count were comparable between groups. Median serum creatinine was 1.8 mg/dL and 0.8 mg/dL in patients with and without AKI, respectively. At baseline, patients with cirrhosis and AKI had lower platelet aggregation and secretion, indicative of impaired platelet function (increased bleeding tendency), without differences in von Willebrand factor. Regarding coagulation factors, factor VIII was higher, whereas protein C, protein S, and antithrombin were all lower, which, together with increased thrombin generation, indicate hypercoagulability. In contrast, factor XIII was lower in AKI (increased bleeding tendency). Finally, while both hypofibrinolytic and hyperfibrinolytic changes were present in AKI, a higher plasmin‐antiplasmin complex indicated a hyperfibrinolytic state. After AKI resolution (n = 23 of 40), platelet function and coagulation improved to levels observed in patients with cirrhosis patients without AKI; however, fibrinolysis remained hyperactivated. Conclusions In patients with decompensated cirrhosis, AKI is associated with both hypocoagulable and hypercoagulable features that can potentially increase the risk of both bleeding and thrombosis.</description><subject>Acute Kidney Injury - blood</subject><subject>Acute Kidney Injury - complications</subject><subject>Aged</subject><subject>Antithrombin</subject><subject>Bleeding</subject><subject>Blood Coagulation Disorders - etiology</subject><subject>Cirrhosis</subject><subject>Coagulation factors</subject><subject>Creatinine</subject><subject>Factor VIII - analysis</subject><subject>Female</subject><subject>Fibrin</subject><subject>Fibrinolysis</subject><subject>Hemostasis</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Kidneys</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - complications</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Plasmin</subject><subject>Platelet aggregation</subject><subject>Prospective Studies</subject><subject>Protein C</subject><subject>Protein S</subject><subject>Proteins</subject><subject>Secretion</subject><subject>Thrombin</subject><subject>Thrombosis</subject><subject>Von Willebrand factor</subject><subject>von Willebrand Factor - physiology</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcFu1DAQhi1ERZfCgRdAkbjAIe3YTuL4grQsLbuiEhxAHC2vM-l6lbWDnQC58Qg8I0-Ct9tWFImLLf3z6dOMfkKeUTilAOxsg_0pp0XBH5AZLZnIOS_hIZkBE5BLyuUxeRzjFgBkwepH5JizihZQ1zPyY27GAbP3tnE4ZSu3HcOUWZe9ReN3PbqoB2yyhQ1h46ON2Spm8xi9sdf5Fztssjc-Pcup979__jJeX42dXneYadfsUwz34wvUwxgwPiFHre4iPr35T8jni_NPi2V--eHdajG_zE26h-c1aE2xoUJyZA0H1LIyui14WTFRVG0pGS1rlDXyqhWCrbkGKljCOEBbM35CXh-8_bjeYWPQDUF3qg92p8OkvLbq_sTZjbry31RdCcZhL3h5Iwj-64hxUDsbDXaddujHqFhBpaCFrKqEvvgH3foxuHReokoQklUCEvXqQJngYwzY3i1DQe37VKlPdd1nYp__vf0deVtgAs4OwHfb4fR_k1qefzwo_wBiZ6x0</recordid><startdate>202010</startdate><enddate>202010</enddate><creator>Zanetto, Alberto</creator><creator>Rinder, Henry M.</creator><creator>Campello, Elena</creator><creator>Saggiorato, Graziella</creator><creator>Deng, Yanhong</creator><creator>Ciarleglio, Maria</creator><creator>Wilson, Francis P.</creator><creator>Senzolo, Marco</creator><creator>Gavasso, Sabrina</creator><creator>Bulato, Cristiana</creator><creator>Simioni, Paolo</creator><creator>Garcia‐Tsao, Guadalupe</creator><general>Wiley Subscription Services, Inc</general><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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6873-8026</orcidid><orcidid>https://orcid.org/0000-0002-7261-6520</orcidid><orcidid>https://orcid.org/0000-0002-6744-383X</orcidid><orcidid>https://orcid.org/0000-0002-3062-1268</orcidid><orcidid>https://orcid.org/0000-0002-6591-3674</orcidid><orcidid>https://orcid.org/0000-0002-0377-3741</orcidid><orcidid>https://orcid.org/0000-0002-6734-7178</orcidid><orcidid>https://orcid.org/0000-0001-7271-7447</orcidid><orcidid>https://orcid.org/0000-0001-8371-4524</orcidid><orcidid>https://orcid.org/0000-0002-2633-2412</orcidid></search><sort><creationdate>202010</creationdate><title>Acute Kidney Injury in Decompensated Cirrhosis Is Associated With Both Hypo‐coagulable and Hyper‐coagulable Features</title><author>Zanetto, Alberto ; Rinder, Henry M. ; Campello, Elena ; Saggiorato, Graziella ; Deng, Yanhong ; Ciarleglio, Maria ; Wilson, Francis P. ; Senzolo, Marco ; Gavasso, Sabrina ; Bulato, Cristiana ; Simioni, Paolo ; Garcia‐Tsao, Guadalupe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4433-80aa1ed1793e2d30ea96caf43562746f592158e98e36f772b3a0172ea9300f823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acute Kidney Injury - blood</topic><topic>Acute Kidney Injury - complications</topic><topic>Aged</topic><topic>Antithrombin</topic><topic>Bleeding</topic><topic>Blood Coagulation Disorders - etiology</topic><topic>Cirrhosis</topic><topic>Coagulation factors</topic><topic>Creatinine</topic><topic>Factor VIII - analysis</topic><topic>Female</topic><topic>Fibrin</topic><topic>Fibrinolysis</topic><topic>Hemostasis</topic><topic>Hepatology</topic><topic>Humans</topic><topic>Kidneys</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis - complications</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Plasmin</topic><topic>Platelet aggregation</topic><topic>Prospective Studies</topic><topic>Protein C</topic><topic>Protein S</topic><topic>Proteins</topic><topic>Secretion</topic><topic>Thrombin</topic><topic>Thrombosis</topic><topic>Von Willebrand factor</topic><topic>von Willebrand Factor - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zanetto, Alberto</creatorcontrib><creatorcontrib>Rinder, Henry M.</creatorcontrib><creatorcontrib>Campello, Elena</creatorcontrib><creatorcontrib>Saggiorato, Graziella</creatorcontrib><creatorcontrib>Deng, Yanhong</creatorcontrib><creatorcontrib>Ciarleglio, Maria</creatorcontrib><creatorcontrib>Wilson, Francis P.</creatorcontrib><creatorcontrib>Senzolo, Marco</creatorcontrib><creatorcontrib>Gavasso, Sabrina</creatorcontrib><creatorcontrib>Bulato, Cristiana</creatorcontrib><creatorcontrib>Simioni, Paolo</creatorcontrib><creatorcontrib>Garcia‐Tsao, Guadalupe</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zanetto, Alberto</au><au>Rinder, Henry M.</au><au>Campello, Elena</au><au>Saggiorato, Graziella</au><au>Deng, Yanhong</au><au>Ciarleglio, Maria</au><au>Wilson, Francis P.</au><au>Senzolo, Marco</au><au>Gavasso, Sabrina</au><au>Bulato, Cristiana</au><au>Simioni, Paolo</au><au>Garcia‐Tsao, Guadalupe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acute Kidney Injury in Decompensated Cirrhosis Is Associated With Both Hypo‐coagulable and Hyper‐coagulable Features</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>2020-10</date><risdate>2020</risdate><volume>72</volume><issue>4</issue><spage>1327</spage><epage>1340</epage><pages>1327-1340</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><abstract>Background and Aims Recent evidence suggests that acute kidney injury (AKI) is the main predictor of postparacentesis bleeding in patients with cirrhosis. To assess the factors responsible for bleeding tendency in AKI, we performed a prospective study comparing all three aspects of hemostasis (platelets, coagulation, and fibrinolysis) in patients with decompensated cirrhosis with and without AKI. Approach and Results Primary hemostasis assessment included platelet aggregation and secretion (platelet function markers) and von Willebrand factor. Secondary hemostasis assessment included pro‐coagulant (factor VIII and factor XIII) and anti‐coagulant (protein C, protein S, and antithrombin) factors and thrombin generation. Tertiary hemostasis assessment included fibrinolytic factors and plasmin‐antiplasmin complex. Eighty patients with decompensated cirrhosis were recruited (40 each with and without AKI). Severity of cirrhosis and platelet count were comparable between groups. Median serum creatinine was 1.8 mg/dL and 0.8 mg/dL in patients with and without AKI, respectively. At baseline, patients with cirrhosis and AKI had lower platelet aggregation and secretion, indicative of impaired platelet function (increased bleeding tendency), without differences in von Willebrand factor. Regarding coagulation factors, factor VIII was higher, whereas protein C, protein S, and antithrombin were all lower, which, together with increased thrombin generation, indicate hypercoagulability. In contrast, factor XIII was lower in AKI (increased bleeding tendency). Finally, while both hypofibrinolytic and hyperfibrinolytic changes were present in AKI, a higher plasmin‐antiplasmin complex indicated a hyperfibrinolytic state. After AKI resolution (n = 23 of 40), platelet function and coagulation improved to levels observed in patients with cirrhosis patients without AKI; however, fibrinolysis remained hyperactivated. Conclusions In patients with decompensated cirrhosis, AKI is associated with both hypocoagulable and hypercoagulable features that can potentially increase the risk of both bleeding and thrombosis.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>32614088</pmid><doi>10.1002/hep.31443</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-6873-8026</orcidid><orcidid>https://orcid.org/0000-0002-7261-6520</orcidid><orcidid>https://orcid.org/0000-0002-6744-383X</orcidid><orcidid>https://orcid.org/0000-0002-3062-1268</orcidid><orcidid>https://orcid.org/0000-0002-6591-3674</orcidid><orcidid>https://orcid.org/0000-0002-0377-3741</orcidid><orcidid>https://orcid.org/0000-0002-6734-7178</orcidid><orcidid>https://orcid.org/0000-0001-7271-7447</orcidid><orcidid>https://orcid.org/0000-0001-8371-4524</orcidid><orcidid>https://orcid.org/0000-0002-2633-2412</orcidid><oa>free_for_read</oa></addata></record>
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subjects Acute Kidney Injury - blood
Acute Kidney Injury - complications
Aged
Antithrombin
Bleeding
Blood Coagulation Disorders - etiology
Cirrhosis
Coagulation factors
Creatinine
Factor VIII - analysis
Female
Fibrin
Fibrinolysis
Hemostasis
Hepatology
Humans
Kidneys
Liver cirrhosis
Liver Cirrhosis - complications
Male
Middle Aged
Plasmin
Platelet aggregation
Prospective Studies
Protein C
Protein S
Proteins
Secretion
Thrombin
Thrombosis
Von Willebrand factor
von Willebrand Factor - physiology
title Acute Kidney Injury in Decompensated Cirrhosis Is Associated With Both Hypo‐coagulable and Hyper‐coagulable Features
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