{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sagmeister MS"],"funding":["Versus Arthritis","Medical Research Council","National Institute for Health Research (NIHR)","Wellcome Trust"],"pagination":["241-249"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6334281"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["90(1)"],"pubmed_abstract":["<h4>Objective</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.<h4>Methods</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.<h4>Results</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<sup>2</sup> and median urine albumin-creatinine ratio of 3"],"journal":["Clinical endocrinology"],"pubmed_title":["Glucocorticoid activation by 11β-hydroxysteroid dehydrogenase enzymes in relation to inflammation and glycaemic control in chronic kidney disease: A cross-sectional study."],"pmcid":["PMC6334281"],"funding_grant_id":["ACF-2015-09-002","3536","CL-2018-09-002","105479/Z/14/Z","MR/P021220/1","20843"],"pubmed_authors":["Sagmeister MS","Hardy RS","Nightingale PG","Harper L","Arlt W","Cockwell P","Taylor AE","Fenton A","Chanouzas D","Wall NA","Ferro CJ"],"additional_accession":[]},"is_claimable":false,"name":"Glucocorticoid activation by 11β-hydroxysteroid dehydrogenase enzymes in relation to inflammation and glycaemic control in chronic kidney disease: A cross-sectional study.","description":"<h4>Objective</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.<h4>Methods</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.<h4>Results</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<sup>2</sup> and median urine albumin-creatinine ratio of 3","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jan","modification":"2026-06-04T09:47:05.495Z","creation":"2025-05-18T11:31:12.316Z"},"accession":"S-EPMC6334281","cross_references":{"pubmed":["30358903"],"doi":["10.1111/cen.13889"]}}