Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/35063
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dc.contributor.authorSadjadi, Mahan-
dc.contributor.authorvon Groote, Thilo-
dc.contributor.authorWeiss, Raphael-
dc.contributor.authorStrauß, Christian-
dc.contributor.authorWempe, Carola-
dc.contributor.authorAlbert, Felix-
dc.contributor.authorLangenkämper, Marie-
dc.contributor.authorLandoni, Giovanni-
dc.contributor.authorBellomo, Rinaldo-
dc.contributor.authorKhanna, Ashish K-
dc.contributor.authorCoulson, Tim G-
dc.contributor.authorMeersch, Melanie-
dc.contributor.authorZarbock, Alexander-
dc.date2024-
dc.date.accessioned2024-02-07T04:14:31Z-
dc.date.available2024-02-07T04:14:31Z-
dc.date.issued2024-01-30-
dc.identifier.citationAnesthesia and Analgesia 2024-01-30en_US
dc.identifier.issn1526-7598-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/35063-
dc.description.abstractVasoplegia is common after cardiac surgery, is associated with hyperreninemia, and can lead to acute kidney stress. We aimed to conduct a pilot study to test the hypothesis that, in vasoplegic cardiac surgery patients, angiotensin-II (AT-II) may not increase kidney stress (measured by [TIMP-2]*[IGFBP7]). We randomly assigned patients with vasoplegia (cardiac index [CI] > 2.1l/min, postoperative hypotension requiring vasopressors) and Δ-renin (4-hour postoperative-preoperative value) ≥3.7 µU/mL, to AT-II or placebo targeting a mean arterial pressure ≥65 mm Hg for 12 hours. The primary end point was the incidence of kidney stress defined as the difference between baseline and 12 hours [TIMP-2]*[IGFBP7] levels. Secondary end points included serious adverse events (SAEs). We randomized 64 patients. With 1 being excluded, 31 patients received AT-II, and 32 received placebo. No significant difference was observed between AT-II and placebo groups for kidney stress (Δ-[TIMP-2]*[IGFBP7] 0.06 [ng/mL]2/1000 [Q1-Q3, -0.24 to 0.28] vs -0.08 [ng/mL]2/1000 [Q1-Q3, -0.35 to 0.14]; P = .19; Hodges-Lehmann estimation of the location shift of 0.12 [ng/mL]2/1000 [95% confidence interval, CI, -0.1 to 0.36]). AT-II patients received less fluid during treatment than placebo patients (2946 vs 3341 mL, P = .03), and required lower doses of norepinephrine equivalent (0.19 mg vs 4.18mg, P < .001). SAEs were reported in 38.7% of patients in the AT-II group and in 46.9% of patients in the placebo group. The infusion of AT-II for 12 hours appears feasible and did not lead to an increase in kidney stress in a high-risk cohort of cardiac surgery patients. These findings support the cautious continued investigation of AT-II as a vasopressor in hyperreninemic cardiac surgery patients.en_US
dc.language.isoeng-
dc.titleA Pilot Study of Renin-Guided Angiotensin-II Infusion to Reduce Kidney Stress After Cardiac Surgery.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleAnesthesia and Analgesiaen_US
dc.identifier.affiliationFrom the Department of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, Münster, Germany.en_US
dc.identifier.affiliationIntensive Careen_US
dc.identifier.affiliationInstitute of Biostatistics and Clinical Research, University of Münster, Münster, Germany.en_US
dc.identifier.affiliationDepartment of Intensive Care and Anesthesia, IRCCS San Raffaele Scientific Institute, Milan, Italy.;Department of Anesthesia and Intensive Care, School of Medicine, Vita-Salute San Raffaele University, Milan, Italy.en_US
dc.identifier.affiliationDepartment of Critical Care, The University of Melbourne, Melbourne, Australia.;Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia.en_US
dc.identifier.affiliationDepartment of Anesthesiology, Section on Critical Care Medicine, School of Medicine, Wake Forest University, Atrium Health Wake Forest Baptist Medical Center, Winston-Salem, North Carolina.;Outcomes Research Consortium, Cleveland, Ohio.;Perioperative Outcomes and Informatics Collaborative (POIC), Winston-Salem, North Carolina; and.en_US
dc.identifier.affiliationDepartment of Anesthesiology and Perioperative Medicine, The Alfred Hospital, Melbourne, Victoria, Australia; Department of Critical Care, University of Melbourne, Melbourne, Victoria, Australia.en_US
dc.identifier.affiliationDepartment of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, Münster, Germany.en_US
dc.identifier.doi10.1213/ANE.0000000000006839en_US
dc.type.contentTexten_US
dc.identifier.pubmedid38289858-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
crisitem.author.deptIntensive Care-
crisitem.author.deptData Analytics Research and Evaluation (DARE) Centre-
crisitem.author.deptAnaesthesia-
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