<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sagmeister MS</submitter><funding>Versus Arthritis</funding><funding>Medical Research Council</funding><funding>National Institute for Health Research (NIHR)</funding><funding>Wellcome Trust</funding><pagination>241-249</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6334281</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>90(1)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>Patients with chronic kidney disease (CKD) have dysregulated cortisol metabolism secondary to changes in 11β-hydroxysteroid dehydrogenase (11β-HSD) enzymes. The determinants of this and its clinical implications are poorly defined.&lt;h4>Methods&lt;/h4>We performed a cross-sectional study to characterize shifts in cortisol metabolism in relation to renal function, inflammation and glycaemic control. Systemic activation of cortisol by 11β-HSD was measured as the metabolite ratio (tetrahydrocortisol [THF]+5α-tetrahydrocortisol [5αTHF])/tetrahydrocortisone (THE) in urine.&lt;h4>Results&lt;/h4>The cohort included 342 participants with a median age of 63 years, median estimated glomerular filtration rate (eGFR) of 28 mL/min/1.73 m&lt;sup>2&lt;/sup> and median urine albumin-creatinine ratio of 3</pubmed_abstract><journal>Clinical endocrinology</journal><pubmed_title>Glucocorticoid activation by 11β-hydroxysteroid dehydrogenase enzymes in relation to inflammation and glycaemic control in chronic kidney disease: A cross-sectional study.</pubmed_title><pmcid>PMC6334281</pmcid><funding_grant_id>ACF-2015-09-002</funding_grant_id><funding_grant_id>3536</funding_grant_id><funding_grant_id>CL-2018-09-002</funding_grant_id><funding_grant_id>105479/Z/14/Z</funding_grant_id><funding_grant_id>MR/P021220/1</funding_grant_id><funding_grant_id>20843</funding_grant_id><pubmed_authors>Sagmeister MS</pubmed_authors><pubmed_authors>Hardy RS</pubmed_authors><pubmed_authors>Nightingale PG</pubmed_authors><pubmed_authors>Harper L</pubmed_authors><pubmed_authors>Arlt W</pubmed_authors><pubmed_authors>Cockwell P</pubmed_authors><pubmed_authors>Taylor AE</pubmed_authors><pubmed_authors>Fenton A</pubmed_authors><pubmed_authors>Chanouzas D</pubmed_authors><pubmed_authors>Wall NA</pubmed_authors><pubmed_authors>Ferro CJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Glucocorticoid activation by 11β-hydroxysteroid dehydrogenase enzymes in relation to inflammation and glycaemic control in chronic kidney disease: A cross-sectional study.</name><description>&lt;h4>Objective&lt;/h4>Patients with chronic kidney disease (CKD) have dysregulated cortisol metabolism secondary to changes in 11β-hydroxysteroid dehydrogenase (11β-HSD) enzymes. The determinants of this and its clinical implications are poorly defined.&lt;h4>Methods&lt;/h4>We performed a cross-sectional study to characterize shifts in cortisol metabolism in relation to renal function, inflammation and glycaemic control. Systemic activation of cortisol by 11β-HSD was measured as the metabolite ratio (tetrahydrocortisol [THF]+5α-tetrahydrocortisol [5αTHF])/tetrahydrocortisone (THE) in urine.&lt;h4>Results&lt;/h4>The cohort included 342 participants with a median age of 63 years, median estimated glomerular filtration rate (eGFR) of 28 mL/min/1.73 m&lt;sup>2&lt;/sup> and median urine albumin-creatinine ratio of 3</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Jan</publication><modification>2026-06-04T09:47:05.495Z</modification><creation>2025-05-18T11:31:12.316Z</creation></dates><accession>S-EPMC6334281</accession><cross_references><pubmed>30358903</pubmed><doi>10.1111/cen.13889</doi></cross_references></HashMap>