In severe alcohol-related hepatitis, acute kidney injury is prevalent, associated with mortality independent of liver disease severity, and can be predicted using IL-8 and micro-RNAs
The prevalence, prediction and impact of acute kidney injury (AKI) in alcohol-related hepatitis (AH) is uncertain. We aimed to determine AKI incidence; association with mortality; evaluate serum biomarkers and the modifying effects of prednisolone and pentoxifylline in the largest AH cohort to date....
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| Veröffentlicht in: | Alimentary pharmacology & therapeutics 2023-12, Vol.58 (11-12), p.1217-1229 |
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| creator | Tyson, Luke D Atkinson, Stephen Hunter, Robert W Allison, Michael Austin, Andrew Dear, James W Forrest, Ewan Liu, Tong Lord, Emma Masson, Steven Nunes, Joao Richardson, Paul Ryder, Stephen D Wright, Mark Thursz, Mark Vergis, Nikhil |
| description | The prevalence, prediction and impact of acute kidney injury (AKI) in alcohol-related hepatitis (AH) is uncertain.
We aimed to determine AKI incidence; association with mortality; evaluate serum biomarkers and the modifying effects of prednisolone and pentoxifylline in the largest AH cohort to date.
Participants in the Steroids or Pentoxifylline for Alcoholic Hepatitis trial with day zero (D0) creatinine available were included. AKI was defined by modified International Club of Ascites criteria; incident AKI as day 7 (D7) AKI without D0-AKI. Survival was compared by Kaplan-Meier; mortality associations by Cox regression; associations with AKI by binary logistic regression; biomarkers by AUROC analyses.
D0-AKI was present in 198/1051 (19%) participants; incident AKI developed in a further 119/571 (21%) with available data. Participants with D0-AKI had higher 90-day mortality than those without (32% vs. 25%, p = 0.008), as did participants with incident AKI compared to those without D0-AKI or incident AKI (47% vs. 25%, p |
| doi_str_mv | 10.1111/apt.17733 |
| format | Article |
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We aimed to determine AKI incidence; association with mortality; evaluate serum biomarkers and the modifying effects of prednisolone and pentoxifylline in the largest AH cohort to date.
Participants in the Steroids or Pentoxifylline for Alcoholic Hepatitis trial with day zero (D0) creatinine available were included. AKI was defined by modified International Club of Ascites criteria; incident AKI as day 7 (D7) AKI without D0-AKI. Survival was compared by Kaplan-Meier; mortality associations by Cox regression; associations with AKI by binary logistic regression; biomarkers by AUROC analyses.
D0-AKI was present in 198/1051 (19%) participants; incident AKI developed in a further 119/571 (21%) with available data. Participants with D0-AKI had higher 90-day mortality than those without (32% vs. 25%, p = 0.008), as did participants with incident AKI compared to those without D0-AKI or incident AKI (47% vs. 25%, p < 0.001). Incident AKI was associated with D90 mortality adjusted for age and discriminant function (AHR 2.15, 1.56-2.97, p < 0.001); D0-AKI was not. Prednisolone therapy reduced incident AKI (AOR 0.55, 0.36-0.85, p = 0.007) but not mortality. D0 bilirubin and IL-8 combined, miR-6826-5p, and miR-6811-3p predicted incident AKI (AUROCs 0.726, 0.821, 0.770, p < 0.01).
Incident AKI is associated with 90-day mortality independent of liver function. Prednisolone therapy was associated with reduced incident AKI. IL-8 and several miRNAs are potential biomarkers to predict AKI. Novel therapies to prevent incident AKI should be evaluated in AH to reduce mortality.</description><identifier>ISSN: 0269-2813</identifier><identifier>ISSN: 1365-2036</identifier><identifier>EISSN: 1365-2036</identifier><identifier>DOI: 10.1111/apt.17733</identifier><identifier>PMID: 37781965</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Acute Kidney Injury ; Acute Kidney Injury in Alcohol‐related Hepatitis ; Ascites ; Bilirubin ; Biomarkers ; Creatinine ; Hepatitis ; Hepatitis, Alcoholic - diagnosis ; Hepatitis, Alcoholic - drug therapy ; Humans ; Interleukin-8 ; Kidneys ; Liver diseases ; MicroRNAs - genetics ; Mortality ; Original ; Patient Acuity ; Pentoxifylline ; Prednisolone ; Prednisolone - adverse effects ; Steroid hormones</subject><ispartof>Alimentary pharmacology & therapeutics, 2023-12, Vol.58 (11-12), p.1217-1229</ispartof><rights>2023 The Authors. Alimentary Pharmacology & Therapeutics published by John Wiley & Sons Ltd.</rights><rights>2023. This article is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 The Authors. published by John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-6f8d350b5cb4609c4963b879d54e7a6d2c66456bb43854edd3a6b1ea53899c4e3</citedby><cites>FETCH-LOGICAL-c404t-6f8d350b5cb4609c4963b879d54e7a6d2c66456bb43854edd3a6b1ea53899c4e3</cites><orcidid>0000-0002-7293-2574 ; 0000-0002-8630-8625 ; 0000-0003-2745-0282 ; 0000-0003-1041-9844</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37781965$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tyson, Luke D</creatorcontrib><creatorcontrib>Atkinson, Stephen</creatorcontrib><creatorcontrib>Hunter, Robert W</creatorcontrib><creatorcontrib>Allison, Michael</creatorcontrib><creatorcontrib>Austin, Andrew</creatorcontrib><creatorcontrib>Dear, James W</creatorcontrib><creatorcontrib>Forrest, Ewan</creatorcontrib><creatorcontrib>Liu, Tong</creatorcontrib><creatorcontrib>Lord, Emma</creatorcontrib><creatorcontrib>Masson, Steven</creatorcontrib><creatorcontrib>Nunes, Joao</creatorcontrib><creatorcontrib>Richardson, Paul</creatorcontrib><creatorcontrib>Ryder, Stephen D</creatorcontrib><creatorcontrib>Wright, Mark</creatorcontrib><creatorcontrib>Thursz, Mark</creatorcontrib><creatorcontrib>Vergis, Nikhil</creatorcontrib><title>In severe alcohol-related hepatitis, acute kidney injury is prevalent, associated with mortality independent of liver disease severity, and can be predicted using IL-8 and micro-RNAs</title><title>Alimentary pharmacology & therapeutics</title><addtitle>Aliment Pharmacol Ther</addtitle><description>The prevalence, prediction and impact of acute kidney injury (AKI) in alcohol-related hepatitis (AH) is uncertain.
We aimed to determine AKI incidence; association with mortality; evaluate serum biomarkers and the modifying effects of prednisolone and pentoxifylline in the largest AH cohort to date.
Participants in the Steroids or Pentoxifylline for Alcoholic Hepatitis trial with day zero (D0) creatinine available were included. AKI was defined by modified International Club of Ascites criteria; incident AKI as day 7 (D7) AKI without D0-AKI. Survival was compared by Kaplan-Meier; mortality associations by Cox regression; associations with AKI by binary logistic regression; biomarkers by AUROC analyses.
D0-AKI was present in 198/1051 (19%) participants; incident AKI developed in a further 119/571 (21%) with available data. Participants with D0-AKI had higher 90-day mortality than those without (32% vs. 25%, p = 0.008), as did participants with incident AKI compared to those without D0-AKI or incident AKI (47% vs. 25%, p < 0.001). Incident AKI was associated with D90 mortality adjusted for age and discriminant function (AHR 2.15, 1.56-2.97, p < 0.001); D0-AKI was not. Prednisolone therapy reduced incident AKI (AOR 0.55, 0.36-0.85, p = 0.007) but not mortality. D0 bilirubin and IL-8 combined, miR-6826-5p, and miR-6811-3p predicted incident AKI (AUROCs 0.726, 0.821, 0.770, p < 0.01).
Incident AKI is associated with 90-day mortality independent of liver function. Prednisolone therapy was associated with reduced incident AKI. IL-8 and several miRNAs are potential biomarkers to predict AKI. Novel therapies to prevent incident AKI should be evaluated in AH to reduce mortality.</description><subject>Acute Kidney Injury</subject><subject>Acute Kidney Injury in Alcohol‐related Hepatitis</subject><subject>Ascites</subject><subject>Bilirubin</subject><subject>Biomarkers</subject><subject>Creatinine</subject><subject>Hepatitis</subject><subject>Hepatitis, Alcoholic - diagnosis</subject><subject>Hepatitis, Alcoholic - drug therapy</subject><subject>Humans</subject><subject>Interleukin-8</subject><subject>Kidneys</subject><subject>Liver diseases</subject><subject>MicroRNAs - genetics</subject><subject>Mortality</subject><subject>Original</subject><subject>Patient Acuity</subject><subject>Pentoxifylline</subject><subject>Prednisolone</subject><subject>Prednisolone - adverse effects</subject><subject>Steroid hormones</subject><issn>0269-2813</issn><issn>1365-2036</issn><issn>1365-2036</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdktuOFCEQhjtG446rF76AIfFGE3uF5tD01Waz8TDJRBOj14SGmh1GBlqgx-yL-XwyM-tG5YJKqI-_quBvmucEX5C63uqpXJC-p_RBsyBU8LbDVDxsFrgTQ9tJQs-aJzlvMcaix93j5oz2vSSD4Ivm1zKgDHtIgLQ3cRN9m8DrAhZtYNLFFZffIG3mAui7swFukQvbOdWQ0ZRgrz2EUomco3HHez9d2aBdTEV7Vw64hQnqFgqKa-RdLYasy6AznEpXqgoEi4wOaISDrHXmIDVnF27QctXKY37nTIrtl09X-WnzaK19hmd38bz59v7d1-uP7erzh-X11ao1DLPSirW0lOORm5EJPBg2CDrKfrCcQa-F7YwQjItxZFTWI2upFiMBzakcKg30vLk86U7zuANr6hBJezUlt9PpVkXt1L-Z4DbqJu4VwQMTksmq8OpOIcUfM-Sidi4b8F4HiHNWneyJ4ELgvqIv_0O3cU6hzlepgQ68Z5hX6vWJqm-Rc4L1fTcEq4MdVLWDOtqhsi_-bv-e_PP_9DdAEbP2</recordid><startdate>20231201</startdate><enddate>20231201</enddate><creator>Tyson, Luke D</creator><creator>Atkinson, Stephen</creator><creator>Hunter, Robert W</creator><creator>Allison, Michael</creator><creator>Austin, Andrew</creator><creator>Dear, James W</creator><creator>Forrest, Ewan</creator><creator>Liu, Tong</creator><creator>Lord, Emma</creator><creator>Masson, Steven</creator><creator>Nunes, Joao</creator><creator>Richardson, Paul</creator><creator>Ryder, Stephen D</creator><creator>Wright, Mark</creator><creator>Thursz, Mark</creator><creator>Vergis, Nikhil</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons 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>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7293-2574</orcidid><orcidid>https://orcid.org/0000-0002-8630-8625</orcidid><orcidid>https://orcid.org/0000-0003-2745-0282</orcidid><orcidid>https://orcid.org/0000-0003-1041-9844</orcidid></search><sort><creationdate>20231201</creationdate><title>In severe alcohol-related hepatitis, acute kidney injury is prevalent, associated with mortality independent of liver disease severity, and can be predicted using IL-8 and micro-RNAs</title><author>Tyson, Luke D ; 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We aimed to determine AKI incidence; association with mortality; evaluate serum biomarkers and the modifying effects of prednisolone and pentoxifylline in the largest AH cohort to date.
Participants in the Steroids or Pentoxifylline for Alcoholic Hepatitis trial with day zero (D0) creatinine available were included. AKI was defined by modified International Club of Ascites criteria; incident AKI as day 7 (D7) AKI without D0-AKI. Survival was compared by Kaplan-Meier; mortality associations by Cox regression; associations with AKI by binary logistic regression; biomarkers by AUROC analyses.
D0-AKI was present in 198/1051 (19%) participants; incident AKI developed in a further 119/571 (21%) with available data. Participants with D0-AKI had higher 90-day mortality than those without (32% vs. 25%, p = 0.008), as did participants with incident AKI compared to those without D0-AKI or incident AKI (47% vs. 25%, p < 0.001). Incident AKI was associated with D90 mortality adjusted for age and discriminant function (AHR 2.15, 1.56-2.97, p < 0.001); D0-AKI was not. Prednisolone therapy reduced incident AKI (AOR 0.55, 0.36-0.85, p = 0.007) but not mortality. D0 bilirubin and IL-8 combined, miR-6826-5p, and miR-6811-3p predicted incident AKI (AUROCs 0.726, 0.821, 0.770, p < 0.01).
Incident AKI is associated with 90-day mortality independent of liver function. Prednisolone therapy was associated with reduced incident AKI. IL-8 and several miRNAs are potential biomarkers to predict AKI. Novel therapies to prevent incident AKI should be evaluated in AH to reduce mortality.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37781965</pmid><doi>10.1111/apt.17733</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-7293-2574</orcidid><orcidid>https://orcid.org/0000-0002-8630-8625</orcidid><orcidid>https://orcid.org/0000-0003-2745-0282</orcidid><orcidid>https://orcid.org/0000-0003-1041-9844</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Kidney Injury Acute Kidney Injury in Alcohol‐related Hepatitis Ascites Bilirubin Biomarkers Creatinine Hepatitis Hepatitis, Alcoholic - diagnosis Hepatitis, Alcoholic - drug therapy Humans Interleukin-8 Kidneys Liver diseases MicroRNAs - genetics Mortality Original Patient Acuity Pentoxifylline Prednisolone Prednisolone - adverse effects Steroid hormones |
| title | In severe alcohol-related hepatitis, acute kidney injury is prevalent, associated with mortality independent of liver disease severity, and can be predicted using IL-8 and micro-RNAs |
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