<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>28(1)</volume><submitter>Stanaway IB</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Patients with sepsis-induced AKI can be classified into two distinct sub-phenotypes (AKI-SP1, AKI-SP2) that differ in clinical outcomes and response to treatment. The biologic mechanisms underlying these sub-phenotypes remains unknown. Our objective was to understand the underlying biology that differentiates AKI sub-phenotypes and associations with kidney outcomes.&lt;h4>Methods&lt;/h4>We prospectively enrolled 173 ICU patients with sepsis from a suspected respiratory infection (87 without AKI and 86 with AKI on enrollment). Among the AKI patients, 66 were classified as AKI-SP1 and 20 as AKI-SP2 using a three-plasma biomarker classifier. Aptamer-based proteomics assessed 5,212 proteins in urine collected on ICU admission. We compared urinary protein abundances between AKI sub</pubmed_abstract><journal>Critical care (London, England)</journal><pagination>419</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11654061</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Urinary proteomics identifies distinct immunological profiles of sepsis associated AKI sub-phenotypes.</pubmed_title><pmcid>PMC11654061</pmcid><pubmed_authors>Mikacenic C</pubmed_authors><pubmed_authors>Himmelfarb J</pubmed_authors><pubmed_authors>Stanaway IB</pubmed_authors><pubmed_authors>Wurfel MM</pubmed_authors><pubmed_authors>Sathe NA</pubmed_authors><pubmed_authors>Bailey Z</pubmed_authors><pubmed_authors>Lo J</pubmed_authors><pubmed_authors>Zelnick LR</pubmed_authors><pubmed_authors>Morrell ED</pubmed_authors><pubmed_authors>Bhatraju PK</pubmed_authors><pubmed_authors>Evans L</pubmed_authors><pubmed_authors>Mabrey FL</pubmed_authors><pubmed_authors>Speckmaier S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Urinary proteomics identifies distinct immunological profiles of sepsis associated AKI sub-phenotypes.</name><description>&lt;h4>Background&lt;/h4>Patients with sepsis-induced AKI can be classified into two distinct sub-phenotypes (AKI-SP1, AKI-SP2) that differ in clinical outcomes and response to treatment. The biologic mechanisms underlying these sub-phenotypes remains unknown. Our objective was to understand the underlying biology that differentiates AKI sub-phenotypes and associations with kidney outcomes.&lt;h4>Methods&lt;/h4>We prospectively enrolled 173 ICU patients with sepsis from a suspected respiratory infection (87 without AKI and 86 with AKI on enrollment). Among the AKI patients, 66 were classified as AKI-SP1 and 20 as AKI-SP2 using a three-plasma biomarker classifier. Aptamer-based proteomics assessed 5,212 proteins in urine collected on ICU admission. We compared urinary protein abundances between AKI sub</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2025-04-19T04:24:51.703Z</modification><creation>2025-04-19T04:24:51.703Z</creation></dates><accession>S-EPMC11654061</accession><cross_references><pubmed>39695715</pubmed><doi>10.1186/s13054-024-05202-9</doi></cross_references></HashMap>