<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Natov PS</submitter><funding>NIDDK NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>e009776</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10150783</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(3)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Improvement in renal function (IRF) in acute decompensated heart failure is associated with adverse outcomes. The mechanisms driving this paradox remain undefined.&lt;h4>Methods&lt;/h4>Using the ROSE-AHF study (Renal Optimization Strategies Evaluation-Acute Heart Failure), 277 patients were grouped according to renal function, with IRF defined by a ≥20% increase (N=75), worsening renal function by a ≥20% decline (N=53), and stable renal function (SRF) by a &lt;20% change (N=149) in estimated glomerular filtration rate between baseline and 72 hours. Three well-validated renal tubular injury markers, NGAL (neutrophil gelatinase-associated lipocalin), NAG (N-acetyl-β-d-glucosaminidase), and KIM-1 (kidney injury molecule 1), were evaluated at baseline and 72 hours. Patients were also</pubmed_abstract><journal>Circulation. Heart failure</journal><pubmed_title>Improvement in Renal Function During the Treatment of Acute Decompensated Heart Failure: Relationship With Markers of Renal Tubular Injury and Prognostic Importance.</pubmed_title><pmcid>PMC10150783</pmcid><funding_grant_id>R01 HL128973</funding_grant_id><funding_grant_id>R01 DK130997</funding_grant_id><funding_grant_id>R01 HL128526</funding_grant_id><funding_grant_id>R01 HL148354</funding_grant_id><funding_grant_id>U01 HL160226</funding_grant_id><funding_grant_id>R01 DK130870</funding_grant_id><funding_grant_id>R01 HL139629</funding_grant_id><pubmed_authors>Cox ZL</pubmed_authors><pubmed_authors>Estrella MM</pubmed_authors><pubmed_authors>Ivey-Miranda JB</pubmed_authors><pubmed_authors>Shlipak MG</pubmed_authors><pubmed_authors>Moreno-Villagomez J</pubmed_authors><pubmed_authors>Bellumkonda L</pubmed_authors><pubmed_authors>Natov PS</pubmed_authors><pubmed_authors>Maulion C</pubmed_authors><pubmed_authors>Rao VS</pubmed_authors><pubmed_authors>Borlaug BA</pubmed_authors><pubmed_authors>Testani JM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Improvement in Renal Function During the Treatment of Acute Decompensated Heart Failure: Relationship With Markers of Renal Tubular Injury and Prognostic Importance.</name><description>&lt;h4>Background&lt;/h4>Improvement in renal function (IRF) in acute decompensated heart failure is associated with adverse outcomes. The mechanisms driving this paradox remain undefined.&lt;h4>Methods&lt;/h4>Using the ROSE-AHF study (Renal Optimization Strategies Evaluation-Acute Heart Failure), 277 patients were grouped according to renal function, with IRF defined by a ≥20% increase (N=75), worsening renal function by a ≥20% decline (N=53), and stable renal function (SRF) by a &lt;20% change (N=149) in estimated glomerular filtration rate between baseline and 72 hours. Three well-validated renal tubular injury markers, NGAL (neutrophil gelatinase-associated lipocalin), NAG (N-acetyl-β-d-glucosaminidase), and KIM-1 (kidney injury molecule 1), were evaluated at baseline and 72 hours. Patients were also</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Mar</publication><modification>2025-04-03T23:49:50.919Z</modification><creation>2025-04-03T23:49:50.919Z</creation></dates><accession>S-EPMC10150783</accession><cross_references><pubmed>36700431</pubmed><doi>10.1161/CIRCHEARTFAILURE.122.009776</doi><doi>10.1161/circheartfailure.122.009776</doi></cross_references></HashMap>