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Intensive Care"],"published-print":{"date-parts":[[2021,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Acute kidney injury (AKI) is a frequent form of organ injury in cardiogenic shock. However, data on AKI markers such as plasma proenkephalin (P-PENK) and neutrophil gelatinase-associated lipocalin (P-NGAL) in cardiogenic shock populations are lacking. The objective of this study was to assess the ability of P-PENK and P-NGAL to predict acute kidney injury and mortality in cardiogenic shock.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      P-PENK and P-NGAL were measured at different time points between baseline and 48\u00a0h in 154 patients from the prospective CardShock study. The outcomes assessed were AKI defined by an increase in creatinine within 48\u00a0h and all-cause 90-day mortality. Mean age was 66\u00a0years and 26% were women. Baseline levels of P-PENK and P-NGAL (median [interquartile range]) were 99 (71\u2013150) pmol\/mL and 138 (84\u2013214) ng\/mL. P-PENK\u2009&gt;\u200984.8\u00a0pmol\/mL and P-NGAL\u2009&gt;\u2009104\u00a0ng\/mL at baseline were identified as optimal cut-offs for AKI prediction and independently associated with AKI (adjusted HRs 2.2 [95% CI 1.1\u20134.4,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.03] and 2.8 [95% CI 1.2\u20136.5,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.01], respectively). P-PENK and P-NGAL levels at baseline were also associated with 90-day mortality. For patients with oliguria\u2009&lt;\u20090.5\u00a0mL\/kg\/h for\u2009&gt;\u20096\u00a0h before study enrollment, 90-day mortality differed significantly between patients with low and high P-PENK\/P-NGAL at baseline (5% vs. 68%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). However, the biomarkers provided best discrimination for mortality when measured at 24\u00a0h. Identified cut-offs of P-PENK\n                      <jats:sub>24h<\/jats:sub>\n                      \u2009&gt;\u2009105.7\u00a0pmol\/L and P-NGAL\n                      <jats:sub>24h<\/jats:sub>\n                      \u2009&gt;\u2009151\u00a0ng\/mL had unadjusted hazard ratios of 5.6 (95% CI 3.1\u201310.7,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) and 5.2 (95% CI 2.8\u20139.8,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) for 90-day mortality. The association remained significant despite adjustments with AKI and two risk scores for mortality in cardiogenic shock.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>High levels of P-PENK and P-NGAL at baseline were independently associated with AKI in cardiogenic shock patients. Furthermore, oliguria before study inclusion was associated with worse outcomes only if combined with high baseline levels of P-PENK or P-NGAL. High levels of both P-PENK and P-NGAL at 24\u00a0h were found to be strong and independent predictors of 90-day mortality.<\/jats:p>\n                    <jats:p>\n                      <jats:italic>Trial registration<\/jats:italic>\n                      : NCT01374867 at\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"http:\/\/www.clinicaltrials.gov\">www.clinicaltrials.gov<\/jats:ext-link>\n                      , registered 16 Jun 2011\u2014retrospectively registered\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s13613-021-00814-8","type":"journal-article","created":{"date-parts":[[2021,2,7]],"date-time":"2021-02-07T22:58:51Z","timestamp":1612738731000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Predictive value of plasma proenkephalin and neutrophil gelatinase-associated lipocalin in acute kidney injury and mortality in cardiogenic shock"],"prefix":"10.1016","volume":"11","author":[{"name":"for the CardShock investigators","sequence":"first","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8348-0844","authenticated-orcid":false,"given":"Toni","family":"J\u00e4ntti","sequence":"first","affiliation":[]},{"given":"Tuukka","family":"Tarvasm\u00e4ki","sequence":"additional","affiliation":[]},{"given":"Veli-Pekka","family":"Harjola","sequence":"additional","affiliation":[]},{"given":"Kari","family":"Pulkki","sequence":"additional","affiliation":[]},{"given":"Heidi","family":"Turkia","sequence":"additional","affiliation":[]},{"given":"Tuija","family":"Sabell","sequence":"additional","affiliation":[]},{"given":"Heli","family":"Tolppanen","sequence":"additional","affiliation":[]},{"given":"Raija","family":"Jurkko","sequence":"additional","affiliation":[]},{"given":"Mari","family":"Hongisto","sequence":"additional","affiliation":[]},{"given":"Anu","family":"Kataja","sequence":"additional","affiliation":[]},{"given":"Alessandro","family":"Sionis","sequence":"additional","affiliation":[]},{"given":"Jose","family":"Silva-Cardoso","sequence":"additional","affiliation":[]},{"given":"Marek","family":"Banaszewski","sequence":"additional","affiliation":[]},{"given":"Salvatore","family":"DiSomma","sequence":"additional","affiliation":[]},{"given":"Alexandre","family":"Mebazaa","sequence":"additional","affiliation":[]},{"given":"Mikko","family":"Haapio","sequence":"additional","affiliation":[]},{"given":"Johan","family":"Lassus","sequence":"additional","affiliation":[]}],"member":"78","published-online":{"date-parts":[[2021,2,5]]},"reference":[{"key":"814_CR1","doi-asserted-by":"publisher","first-page":"e232","DOI":"10.1161\/CIRCULATIONAHA.117.029532","volume":"136","author":"S van Diepen","year":"2017","unstructured":"van Diepen S, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, et al. 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Written informed consent was obtained from the patient or next of kin if the patients were unable to give the consent on admission.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"Not applicable.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"VPH: advisory board fees from Roche Diagnostics, research grant from Abbott, speaker fees from Orion. KP: advisory board fees from Roche Diagnostics. JSC has consulted and received speaker fees, or advisory boards\u2019 participation fees, or investigational grants for Abbott, Astra-Zeneca Pharmaceuticals, Bial, Boehringer Ingelheim, Menarini, Merck Serono, Merck Sharp & Dohme, Novartis, Orion, Pfizer, Sanofi, Servier and Vifor. AM: lecture fees from Novartis, Orion, and Abbott, research grants from Roche, consultant fees from Servier and Sanofi and fees as a member of the advisory board and\/or steering committee from Cardiorentis, Adrenomed, Sphingotec, Sanofi, Roche, Abbott, and Bristol-Myers Squibb. JL: Speakers bureau and consultancy fees: Astra-Zeneca, Bayer, Boehringer-Ingelheim, Novartis, Orion, Pfizer, Roche Diagnostics, and ViforPharma. All other authors report that they have no relationships with industry to disclose.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"25"}}