Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/26644
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dc.contributor.authorElitok, Saban-
dc.contributor.authorDevarajan, Prasad-
dc.contributor.authorBellomo, Rinaldo-
dc.contributor.authorIsermann, Berend-
dc.contributor.authorHaase, Michael-
dc.contributor.authorHaase-Fielitz, Anja-
dc.date2021-05-24-
dc.date.accessioned2021-05-31T22:59:22Z-
dc.date.available2021-05-31T22:59:22Z-
dc.date.issued2021-05-24-
dc.identifier.citationJournal of Nephrology 2021; online first: 24 Mayen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/26644-
dc.description.abstractAcute kidney injury (AKI) subtypes combining kidney functional parameters and injury biomarkers may have prognostic value. We aimed to determine whether neutrophil gelatinase-associated lipocalin (NGAL)/hepcidin-25 ratio (urinary concentrations of NGAL divided by that of hepcidin-25) defined subtypes are of prognostic relevance in cardiac surgery patients. We studied 198 higher-risk cardiac surgery patients. We allocated patients to four groups: Kidney Disease Improving Global Outcomes (KDIGO)-AKI-negative and NGAL/hepcidin-25 ratio-negative (no AKI), KDIGO AKI-negative and NGAL/hepcidin-25 ratio-positive (subclinical AKI), KDIGO AKI-positive and NGAL/hepcidin-25 ratio-negative (clinical AKI), KDIGO AKI-positive and NGAL/hepcidin-25 ratio-positive (combined AKI). Outcomes included in-hospital mortality (primary) and long-term mortality (secondary). We identified 127 (61.6%) patients with no AKI, 13 (6.6%) with subclinical, 40 (20.2%) with clinical and 18 (9.1%) with combined AKI. Subclinical AKI patients had a 23-fold greater in-hospital mortality than no AKI patients. For combined AKI vs. no AKI or clinical AKI, findings were stronger (odds ratios (ORs): 126 and 39, respectively). After adjusting for EuroScore, volume of intraoperative packed red blood cells, and aortic cross-clamp time, subclinical and combined AKI remained associated with greater in-hospital mortality than no AKI and clinical AKI (adjusted ORs: 28.118, 95% CI 1.465-539.703; 3.737, 95% CI 1.746-7.998). Cox proportional hazard models found a significant association of biomarker-informed AKI subtypes with long-term survival compared with no AKI (adjusted ORs: pooled subclinical and clinical AKI: 1.885, 95% CI 1.003-3.542; combined AKI: 1.792, 95% CI 1.367-2.350). In the presence or absence of KDIGO clinical criteria for AKI, the urinary NGAL/hepcidin-25-ratio appears to detect prognostically relevant AKI subtypes. NCT00672334, clinicaltrials.gov, date of registration: 6th May 2008, https://clinicaltrials.gov/ct2/show/NCT00672334 . Definition of AKI subtypes: subclinical AKI (KDIGO negative AND Ratio-positive), clinical AKI (KDIGO positive AND Ratio-negative) and combined AKI (KDIGO positive AND Ratio-positive) with urinary NGAL/hepcidin-25 ratio-positive cut-off at 85% specificity for in-hospital death. AKI, acute kidney injury. AUC, area under the curve. NGAL, neutrophil gelatinase-associated lipocalin. KDIGO, Kidney Disease Improving Global Outcomes Initiative AKI definition.en
dc.language.isoeng
dc.subjectCardiopulmonary bypassen
dc.subjectCardiorenal syndromeen
dc.subjectNGAL/hepcidin-25 ratioen
dc.subjectSubclinical AKIen
dc.titleNGAL/hepcidin-25 ratio and AKI subtypes in patients following cardiac surgery: a prospective observational study.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Nephrologyen
dc.identifier.affiliationMedical Faculty, Otto Von-Guericke-University Magdeburg, Leipziger Str. 44, 39120, Magdeburg, Germanyen
dc.identifier.affiliationDepartment of Nephrology and Hypertension, Cincinnati Children's Hospital, Cincinnati, OH, 45229, USAen
dc.identifier.affiliationDiaverum AB, Renal Care Center Potsdam, 21532, Malmö, Swedenen
dc.identifier.affiliationBrandenburg Medical School Theodor Fontane, 16816, Neuruppin, Germanyen
dc.identifier.affiliationFaculty of Health Sciences Brandenburg, Potsdam, Germanyen
dc.identifier.affiliationInstitute of Integrated Health Care Systems Research and Social Medicine, Otto Von-Guericke-University Magdeburg, 39120, Magdeburg, Germanyen
dc.identifier.affiliationDepartment of Cardiology, Brandenburg Heart Center, Immanuel Hospital, 16321, Bernau, Germanyen
dc.identifier.affiliationDepartment of Intensive Care, Royal Melbourne Hospital, Parkville, Melbourne, VIC, 3052, Australiaen
dc.identifier.affiliationIntensive Careen
dc.identifier.affiliationCenter for Integrated Critical Care, The University of Melbourne, Melbourne, Australiaen
dc.identifier.affiliationDepartment of Nephrology and Endocrinology, Ernst Von Bergmann Hospital Potsdam, 14467, Potsdam, Germanyen
dc.identifier.affiliationInstitute of Laboratory Medicine, Clinical Chemistry, and Molecular Diagnostic, Leipzig University Hospital, 04103, Leipzig, Germanyen
dc.identifier.doi10.1007/s40620-021-01063-5en
dc.type.contentTexten
dc.identifier.orcid0000-0002-1195-6871en
dc.identifier.orcid0000-0002-7847-8552en
dc.identifier.orcid0000-0002-1650-8939en
dc.identifier.orcid0000-0003-0714-6160en
dc.identifier.orcid0000-0001-8212-7416en
dc.identifier.orcid0000-0001-6881-2249en
dc.identifier.pubmedid34028701
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