<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Flannery AH</submitter><funding>National Center for Advancing Translational Sciences</funding><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>University of Kentucky Center for Clinical and Translational Science</funding><pagination>153986</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9727727</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>69</volume><pubmed_abstract>&lt;h4>Purpose&lt;/h4>To evaluate the effect of renin-angiotensin system (RAS) inhibiting medications prior to admission on the severity of kidney injury in patients presenting with sepsis-associated acute kidney injury (SA-AKI).&lt;h4>Materials and methods&lt;/h4>A single center, retrospective cohort study of critically ill adult patients admitted with diagnoses of both sepsis and AKI. RAS inhibition was defined as angiotensin converting enzyme inhibitors or angiotensin receptor blockers. The primary outcome was Kidney Disease: Improving Global Outcomes stage AKI upon hospital admission.&lt;h4>Results&lt;/h4>Of 707 individuals studied, patients receiving RAS inhibition prior to admission (vs. those not) had more stage 3 AKI (40.1% vs. 28.7%; p = 0.008) and more frequently reached stage 3 AKI during the first week (49.8% vs. 41.1%; p = 0.047). In an adjusted multinomial regression model, patients receiving RAS inhibition (vs. those not) had an increased relative risk of presenting with stage 3 AKI on admission (vs. stage 1 AKI reference): RRR 2.32 (95% CI 1.50-3.59). Similar findings were observed in a propensity score matched analysis.&lt;h4>Conclusion&lt;/h4>Patients receiving RAS inhibition (vs. those not) prior to an admission with SA-AKI presented with more severe AKI on admission and during the first week. Hospital mortality and kidney function at discharge were similar between groups.</pubmed_abstract><journal>Journal of critical care</journal><pubmed_title>RAS inhibition and sepsis-associated acute kidney injury.</pubmed_title><pmcid>PMC9727727</pmcid><funding_grant_id>UL1TR001998</funding_grant_id><funding_grant_id>K23 DK128562</funding_grant_id><funding_grant_id>UL1 TR001998</funding_grant_id><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Kiser AS</pubmed_authors><pubmed_authors>Neyra JA</pubmed_authors><pubmed_authors>Behal ML</pubmed_authors><pubmed_authors>Flannery AH</pubmed_authors></additional><is_claimable>false</is_claimable><name>RAS inhibition and sepsis-associated acute kidney injury.</name><description>&lt;h4>Purpose&lt;/h4>To evaluate the effect of renin-angiotensin system (RAS) inhibiting medications prior to admission on the severity of kidney injury in patients presenting with sepsis-associated acute kidney injury (SA-AKI).&lt;h4>Materials and methods&lt;/h4>A single center, retrospective cohort study of critically ill adult patients admitted with diagnoses of both sepsis and AKI. RAS inhibition was defined as angiotensin converting enzyme inhibitors or angiotensin receptor blockers. The primary outcome was Kidney Disease: Improving Global Outcomes stage AKI upon hospital admission.&lt;h4>Results&lt;/h4>Of 707 individuals studied, patients receiving RAS inhibition prior to admission (vs. those not) had more stage 3 AKI (40.1% vs. 28.7%; p = 0.008) and more frequently reached stage 3 AKI during the first week (49.8% vs. 41.1%; p = 0.047). In an adjusted multinomial regression model, patients receiving RAS inhibition (vs. those not) had an increased relative risk of presenting with stage 3 AKI on admission (vs. stage 1 AKI reference): RRR 2.32 (95% CI 1.50-3.59). Similar findings were observed in a propensity score matched analysis.&lt;h4>Conclusion&lt;/h4>Patients receiving RAS inhibition (vs. those not) prior to an admission with SA-AKI presented with more severe AKI on admission and during the first week. Hospital mortality and kidney function at discharge were similar between groups.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2025-04-26T22:55:42.475Z</modification><creation>2025-04-06T17:25:28.239Z</creation></dates><accession>S-EPMC9727727</accession><cross_references><pubmed>35085853</pubmed><doi>10.1016/j.jcrc.2022.153986</doi></cross_references></HashMap>