<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jo E</submitter><funding>National Research Foundation of Korea</funding><funding>Pusan National University</funding><funding>Korea Disease Control and Prevention Agency</funding><pagination>785-796</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11615453</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(6)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Transferrin saturation (TSAT) has been used as an indicator of iron deficiency. However, there is no consensus regarding its optimal range for patient with chronic kidney disease (CKD). We aimed to analyze the effect of TSAT on the prognosis of patients with non-dialysis CKD (NDCKD).&lt;h4>Methods&lt;/h4>From 2011 to 2016, 2157 NDCKD patients with baseline TSAT measurements were followed for 10 years. Patients were divided into three groups based on baseline TSAT values: &lt;25%, ≥25% and &lt;45%, and ≥45%. All-cause mortality and 4-point major adverse cardiovascular events (MACE) were analyzed using multivariable Cox regression analysis. Other iron biomarkers and mortality were also analyzed.&lt;h4>Results&lt;/h4>During a mean follow-up of 7.1 ± 2.9 years, 182 of a total of 2,157 patient</pubmed_abstract><journal>Kidney research and clinical practice</journal><pubmed_title>The association between transferrin saturation and all-cause mortality in chronic kidney disease: findings from Korean Cohort Study for Outcome in Patients with Chronic Kidney Disease.</pubmed_title><pmcid>PMC11615453</pmcid><funding_grant_id>2011E3300300</funding_grant_id><funding_grant_id>2011E3300300, 2012E3301100, 2013E3301600, 2013E 3301601, 2013E3301602, 2016E3300200, 2016E3300201, 2016E3300202,2019E320100, 2019E320101, 2019E320102, 2022-11-007</funding_grant_id><funding_grant_id>2013E3301602</funding_grant_id><funding_grant_id>RS-2023-00223764</funding_grant_id><funding_grant_id>2013E3301600</funding_grant_id><funding_grant_id>2016E3300200</funding_grant_id><funding_grant_id>2016E3300201</funding_grant_id><funding_grant_id>2016E3300202,2019E320100</funding_grant_id><funding_grant_id>202310510001</funding_grant_id><funding_grant_id>2019E320101</funding_grant_id><funding_grant_id>2019E320102</funding_grant_id><funding_grant_id>2012E3301100</funding_grant_id><funding_grant_id>2013E 3301601</funding_grant_id><funding_grant_id>2022-11-007</funding_grant_id><pubmed_authors>Kim SW</pubmed_authors><pubmed_authors>Seong EY</pubmed_authors><pubmed_authors>Yoo TH</pubmed_authors><pubmed_authors>Kim HJ</pubmed_authors><pubmed_authors>Jo E</pubmed_authors><pubmed_authors>Kim Y</pubmed_authors><pubmed_authors>Kim J</pubmed_authors><pubmed_authors>Song SH</pubmed_authors><pubmed_authors>Oh KH</pubmed_authors></additional><is_claimable>false</is_claimable><name>The association between transferrin saturation and all-cause mortality in chronic kidney disease: findings from Korean Cohort Study for Outcome in Patients with Chronic Kidney Disease.</name><description>&lt;h4>Background&lt;/h4>Transferrin saturation (TSAT) has been used as an indicator of iron deficiency. However, there is no consensus regarding its optimal range for patient with chronic kidney disease (CKD). We aimed to analyze the effect of TSAT on the prognosis of patients with non-dialysis CKD (NDCKD).&lt;h4>Methods&lt;/h4>From 2011 to 2016, 2157 NDCKD patients with baseline TSAT measurements were followed for 10 years. Patients were divided into three groups based on baseline TSAT values: &lt;25%, ≥25% and &lt;45%, and ≥45%. All-cause mortality and 4-point major adverse cardiovascular events (MACE) were analyzed using multivariable Cox regression analysis. Other iron biomarkers and mortality were also analyzed.&lt;h4>Results&lt;/h4>During a mean follow-up of 7.1 ± 2.9 years, 182 of a total of 2,157 patient</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2025-04-04T01:15:08.444Z</modification><creation>2025-04-04T01:15:08.444Z</creation></dates><accession>S-EPMC11615453</accession><cross_references><pubmed>38934042</pubmed><doi>10.23876/j.krcp.23.278</doi></cross_references></HashMap>