Cell-Free DNA, Neutrophil extracellular traps Associated Acute Kidney Injury
Introduction: Neutrophil extracellular traps (NETs) release (i.e., NETosis) has been recently implicated in the pathomechanism underlying severe end-organ damage in Coronavirus Disease 2019 (COVID-19) and could present a novel therapeutic target. We aimed to determine whether circulating levels of c...
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| Veröffentlicht in: | Mediators of inflammation 2022-04, Vol.2022 |
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| container_title | Mediators of inflammation |
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| creator | Henry, Brandon Michael de Oliveira, Maria Helena Santos Cheruiyot, Isaac Benoit, Justin Rose, James Favaloro, Emmanuel J Lippi, Giuseppe |
| description | Introduction: Neutrophil extracellular traps (NETs) release (i.e., NETosis) has been recently implicated in the pathomechanism underlying severe end-organ damage in Coronavirus Disease 2019 (COVID-19) and could present a novel therapeutic target. We aimed to determine whether circulating levels of cell-free DNA (cfDNA), a surrogate for NETosis, may be associated with the development of acute kidney injury (AKI), a major contributor to poor outcomes and mortality in COVID-19. Methods: Blood samples were collected prospectively from adult patients infected with SARS-CoV-2 presenting to the emergency department (ED). Circulating levels of cfDNA were quantified from patients' serum. Further assessment of correlations between cfDNA levels and markers of AKI (i.e., serum creatinine (SCr), cystatin C, neutrophil gelatinase-associated lipocalin (NGAL)), biomarkers of thrombotic microangiopathy and of inflammation in patients' serum was performed. Results: Fifty-one COVID-19 patients were enrolled. cfDNA levels were found to be significantly higher in those who developed severe AKI (p |
| doi_str_mv | 10.1155/2022/9339411 |
| format | Article |
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We aimed to determine whether circulating levels of cell-free DNA (cfDNA), a surrogate for NETosis, may be associated with the development of acute kidney injury (AKI), a major contributor to poor outcomes and mortality in COVID-19. Methods: Blood samples were collected prospectively from adult patients infected with SARS-CoV-2 presenting to the emergency department (ED). Circulating levels of cfDNA were quantified from patients' serum. Further assessment of correlations between cfDNA levels and markers of AKI (i.e., serum creatinine (SCr), cystatin C, neutrophil gelatinase-associated lipocalin (NGAL)), biomarkers of thrombotic microangiopathy and of inflammation in patients' serum was performed. Results: Fifty-one COVID-19 patients were enrolled. cfDNA levels were found to be significantly higher in those who developed severe AKI (p<0.001) and those needing renal replacement therapy (p=0.020). cfDNA positively correlated with ED SCr, NGAL, cystatin C, neutrophil count, neutrophil-to-lymphocyte ratio, C3a, C5a, Scb5-9, IL-6, IL-8, IL-10, TNF-α , LDH, CRP, ferritin, and fibrinogen and negatively correlated with ADAMTS13/von-Willebrand factor ratio and lymphocyte count. In a multivariate logistic regression, a one-unit increase in cfDNA value was associated with 4.6% increased odds of severe AKI (OR=1.046; p=0.040). Finally, cfDNA significantly correlated with established NETs components, myeloperoxidase, and neutrophil elastase. Conclusion: Intravascular NETosis could be an important contributing factor in the development of microthrombosis and COVID-19-associated AKI. Further research is urgently needed to understand the role of NETosis in COVID-19 and evaluate therapeutic avenues for targeting this process.</description><identifier>ISSN: 0962-9351</identifier><identifier>DOI: 10.1155/2022/9339411</identifier><language>eng</language><publisher>John Wiley & Sons, Inc</publisher><subject>Coronaviruses ; DNA ; Endothelium ; Ethylenediaminetetraacetic acid ; Fibrin ; Health aspects ; Mortality ; Ohio</subject><ispartof>Mediators of inflammation, 2022-04, Vol.2022</ispartof><rights>COPYRIGHT 2022 John Wiley & Sons, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27901,27902</link.rule.ids></links><search><creatorcontrib>Henry, Brandon Michael</creatorcontrib><creatorcontrib>de Oliveira, Maria Helena Santos</creatorcontrib><creatorcontrib>Cheruiyot, Isaac</creatorcontrib><creatorcontrib>Benoit, Justin</creatorcontrib><creatorcontrib>Rose, James</creatorcontrib><creatorcontrib>Favaloro, Emmanuel J</creatorcontrib><creatorcontrib>Lippi, Giuseppe</creatorcontrib><title>Cell-Free DNA, Neutrophil extracellular traps Associated Acute Kidney Injury</title><title>Mediators of inflammation</title><description>Introduction: Neutrophil extracellular traps (NETs) release (i.e., NETosis) has been recently implicated in the pathomechanism underlying severe end-organ damage in Coronavirus Disease 2019 (COVID-19) and could present a novel therapeutic target. We aimed to determine whether circulating levels of cell-free DNA (cfDNA), a surrogate for NETosis, may be associated with the development of acute kidney injury (AKI), a major contributor to poor outcomes and mortality in COVID-19. Methods: Blood samples were collected prospectively from adult patients infected with SARS-CoV-2 presenting to the emergency department (ED). Circulating levels of cfDNA were quantified from patients' serum. Further assessment of correlations between cfDNA levels and markers of AKI (i.e., serum creatinine (SCr), cystatin C, neutrophil gelatinase-associated lipocalin (NGAL)), biomarkers of thrombotic microangiopathy and of inflammation in patients' serum was performed. Results: Fifty-one COVID-19 patients were enrolled. cfDNA levels were found to be significantly higher in those who developed severe AKI (p<0.001) and those needing renal replacement therapy (p=0.020). cfDNA positively correlated with ED SCr, NGAL, cystatin C, neutrophil count, neutrophil-to-lymphocyte ratio, C3a, C5a, Scb5-9, IL-6, IL-8, IL-10, TNF-α , LDH, CRP, ferritin, and fibrinogen and negatively correlated with ADAMTS13/von-Willebrand factor ratio and lymphocyte count. In a multivariate logistic regression, a one-unit increase in cfDNA value was associated with 4.6% increased odds of severe AKI (OR=1.046; p=0.040). Finally, cfDNA significantly correlated with established NETs components, myeloperoxidase, and neutrophil elastase. Conclusion: Intravascular NETosis could be an important contributing factor in the development of microthrombosis and COVID-19-associated AKI. Further research is urgently needed to understand the role of NETosis in COVID-19 and evaluate therapeutic avenues for targeting this process.</description><subject>Coronaviruses</subject><subject>DNA</subject><subject>Endothelium</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Fibrin</subject><subject>Health aspects</subject><subject>Mortality</subject><subject>Ohio</subject><issn>0962-9351</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNptT8tOwzAQ9AEkSuHGB1jiSlqvH4l9jAItFVG59F4l9rq4SpMqTiT69wTBgQPaw45mZ0azhDwAWwAoteSM86URwkiAKzJjJuWJEQpuyG2MR8aYklLPSFlg0ySrHpE-b_MnusVx6LvzR2gofg59Zafz2FQ9nfA50jzGzoZqQEdzOw5I34Jr8UI37XHsL3fk2ldNxPvfPSe71cuueE3K9_WmyMvkkGY6QQVCp8ZzppysnfYpgDA1VxwM2ExkNa-VS41kxlpMQUrPpQbMHHMuw0rMyeNP7KFqcB9a330XPYVo93k2vc2N5npSLf5RTePwFGzXog8T_8fwBe6sWsY</recordid><startdate>20220422</startdate><enddate>20220422</enddate><creator>Henry, Brandon Michael</creator><creator>de Oliveira, Maria Helena Santos</creator><creator>Cheruiyot, Isaac</creator><creator>Benoit, Justin</creator><creator>Rose, James</creator><creator>Favaloro, Emmanuel J</creator><creator>Lippi, Giuseppe</creator><general>John Wiley & Sons, Inc</general><scope/></search><sort><creationdate>20220422</creationdate><title>Cell-Free DNA, Neutrophil extracellular traps Associated Acute Kidney Injury</title><author>Henry, Brandon Michael ; de Oliveira, Maria Helena Santos ; Cheruiyot, Isaac ; Benoit, Justin ; Rose, James ; Favaloro, Emmanuel J ; Lippi, Giuseppe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g678-e513869f205d4bd8f61139b252191c737b2b5d69409cce6144f2481e7d0dd7ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Coronaviruses</topic><topic>DNA</topic><topic>Endothelium</topic><topic>Ethylenediaminetetraacetic acid</topic><topic>Fibrin</topic><topic>Health aspects</topic><topic>Mortality</topic><topic>Ohio</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Henry, Brandon Michael</creatorcontrib><creatorcontrib>de Oliveira, Maria Helena Santos</creatorcontrib><creatorcontrib>Cheruiyot, Isaac</creatorcontrib><creatorcontrib>Benoit, Justin</creatorcontrib><creatorcontrib>Rose, James</creatorcontrib><creatorcontrib>Favaloro, Emmanuel J</creatorcontrib><creatorcontrib>Lippi, Giuseppe</creatorcontrib><jtitle>Mediators of inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Henry, Brandon Michael</au><au>de Oliveira, Maria Helena Santos</au><au>Cheruiyot, Isaac</au><au>Benoit, Justin</au><au>Rose, James</au><au>Favaloro, Emmanuel J</au><au>Lippi, Giuseppe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cell-Free DNA, Neutrophil extracellular traps Associated Acute Kidney Injury</atitle><jtitle>Mediators of inflammation</jtitle><date>2022-04-22</date><risdate>2022</risdate><volume>2022</volume><issn>0962-9351</issn><abstract>Introduction: Neutrophil extracellular traps (NETs) release (i.e., NETosis) has been recently implicated in the pathomechanism underlying severe end-organ damage in Coronavirus Disease 2019 (COVID-19) and could present a novel therapeutic target. We aimed to determine whether circulating levels of cell-free DNA (cfDNA), a surrogate for NETosis, may be associated with the development of acute kidney injury (AKI), a major contributor to poor outcomes and mortality in COVID-19. Methods: Blood samples were collected prospectively from adult patients infected with SARS-CoV-2 presenting to the emergency department (ED). Circulating levels of cfDNA were quantified from patients' serum. Further assessment of correlations between cfDNA levels and markers of AKI (i.e., serum creatinine (SCr), cystatin C, neutrophil gelatinase-associated lipocalin (NGAL)), biomarkers of thrombotic microangiopathy and of inflammation in patients' serum was performed. Results: Fifty-one COVID-19 patients were enrolled. cfDNA levels were found to be significantly higher in those who developed severe AKI (p<0.001) and those needing renal replacement therapy (p=0.020). cfDNA positively correlated with ED SCr, NGAL, cystatin C, neutrophil count, neutrophil-to-lymphocyte ratio, C3a, C5a, Scb5-9, IL-6, IL-8, IL-10, TNF-α , LDH, CRP, ferritin, and fibrinogen and negatively correlated with ADAMTS13/von-Willebrand factor ratio and lymphocyte count. In a multivariate logistic regression, a one-unit increase in cfDNA value was associated with 4.6% increased odds of severe AKI (OR=1.046; p=0.040). Finally, cfDNA significantly correlated with established NETs components, myeloperoxidase, and neutrophil elastase. Conclusion: Intravascular NETosis could be an important contributing factor in the development of microthrombosis and COVID-19-associated AKI. Further research is urgently needed to understand the role of NETosis in COVID-19 and evaluate therapeutic avenues for targeting this process.</abstract><pub>John Wiley & Sons, Inc</pub><doi>10.1155/2022/9339411</doi></addata></record> |
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| source | Wiley-Blackwell Open Access Titles; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access |
| subjects | Coronaviruses DNA Endothelium Ethylenediaminetetraacetic acid Fibrin Health aspects Mortality Ohio |
| title | Cell-Free DNA, Neutrophil extracellular traps Associated Acute Kidney Injury |
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