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KCNJ5 Somatic Mutation Is Associated With Higher Aortic Wall Thickness and Less Calcification in Patients With Aldosterone-Producing Adenoma
Primary aldosteronism (PA) is the most common type of secondary hypertension, and it is associated with a higher rate of cardiovascular complications. KCNJ5 somatic mutations have recently been identified in aldosterone-producing adenoma (APA), however their influence on vascular remodeling and inju...
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Published in: | Frontiers in endocrinology (Lausanne) 2022-03, Vol.13, p.830130-830130 |
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creator | Lee, Bo-Ching Kang, Victor Jing-Wei Pan, Chien-Ting Huang, Jia-Zheng Lin, Yu-Li Chang, Yi-Yao Tsai, Cheng-Hsuan Chou, Chia-Hung Chen, Zheng-Wei Liao, Che-Wei Chiu, Yu-Wei Wu, Vin-Cent Hung, Chi-Sheng Chang, Chin-Chen Lin, Yen-Hung |
description | Primary aldosteronism (PA) is the most common type of secondary hypertension, and it is associated with a higher rate of cardiovascular complications. KCNJ5 somatic mutations have recently been identified in aldosterone-producing adenoma (APA), however their influence on vascular remodeling and injury is still unclear. The aim of this study was to investigate the association between KCNJ5 somatic mutation status and vascular status.
We enrolled 179 APA patients who had undergone adrenalectomy from a prospectively maintained database, of whom 99 had KCNJ5 somatic mutations. Preoperative clinical, biochemical and imaging data of abdominal CT, including abdominal aortic calcification (AAC) score, aortic diameter and wall thickness at levels of superior (SMA) and inferior (IMA) mesenteric arteries were analyzed.
After propensity score matching for age, sex, body mass index, triglycerides and low-density lipoprotein, there were 48 patients in each KCNJ5 (+) and KCNJ5 (-) group. Mutation carriers had a lower AAC score (217.3 ± 562.2 vs. 605.6 ± 1359.1, P=0.018), higher aortic wall thickness (SMA level: 2.2 ± 0.6 mm vs. 1.8 ± 0.6 mm, P=0.006; IMA level: 2.4 ± 0.6 mm vs. 1.8 ± 0.7 mm, P |
doi_str_mv | 10.3389/fendo.2022.830130 |
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We enrolled 179 APA patients who had undergone adrenalectomy from a prospectively maintained database, of whom 99 had KCNJ5 somatic mutations. Preoperative clinical, biochemical and imaging data of abdominal CT, including abdominal aortic calcification (AAC) score, aortic diameter and wall thickness at levels of superior (SMA) and inferior (IMA) mesenteric arteries were analyzed.
After propensity score matching for age, sex, body mass index, triglycerides and low-density lipoprotein, there were 48 patients in each KCNJ5 (+) and KCNJ5 (-) group. Mutation carriers had a lower AAC score (217.3 ± 562.2 vs. 605.6 ± 1359.1, P=0.018), higher aortic wall thickness (SMA level: 2.2 ± 0.6 mm vs. 1.8 ± 0.6 mm, P=0.006; IMA level: 2.4 ± 0.6 mm vs. 1.8 ± 0.7 mm, P<0.001) than non-carriers. In multivariate analysis, KCNJ5 mutations were independently associated with AAC score (P=0.014) and aortic wall thickness (SMA level: P<0.001; IMA level: P=0.004). After adrenalectomy, mutation carriers had less aortic wall thickness progression than non-carriers (Δthickness SMA: -0.1 ± 0.8 mm vs. 0.9 ± 0.6 mm, P=0.024; IMA: -0.1 ± 0.6 mm vs. 0.8 ± 0.7 mm, P=0.04).
KCNJ5 mutation carriers had less calcification burden of the aorta, thickened aortic wall, and less wall thickness progression than non-carriers.</description><identifier>ISSN: 1664-2392</identifier><identifier>EISSN: 1664-2392</identifier><identifier>DOI: 10.3389/fendo.2022.830130</identifier><identifier>PMID: 35311227</identifier><language>eng</language><publisher>Switzerland: Frontiers Media S.A</publisher><subject>Adenoma - genetics ; Adrenal Cortex Neoplasms - complications ; Adrenal Cortex Neoplasms - genetics ; Adrenal Cortex Neoplasms - surgery ; Adrenocortical Adenoma - complications ; Adrenocortical Adenoma - genetics ; Adrenocortical Adenoma - surgery ; Aldosterone ; Aorta ; aortic calcification ; Calcinosis - genetics ; Endocrinology ; G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics ; Humans ; Hyperaldosteronism - complications ; Hyperaldosteronism - genetics ; hypertension ; KCNJ5 somatic mutation ; Mutation ; primary aldosteronism</subject><ispartof>Frontiers in endocrinology (Lausanne), 2022-03, Vol.13, p.830130-830130</ispartof><rights>Copyright © 2022 Lee, Kang, Pan, Huang, Lin, Chang, Tsai, Chou, Chen, Liao, Chiu, Wu, Hung, Chang and Lin.</rights><rights>Copyright © 2022 Lee, Kang, Pan, Huang, Lin, Chang, Tsai, Chou, Chen, Liao, Chiu, Wu, Hung, Chang and Lin 2022 Lee, Kang, Pan, Huang, Lin, Chang, Tsai, Chou, Chen, Liao, Chiu, Wu, Hung, Chang and Lin</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c465t-2240ac02293d5eb114c75e39def3700f55579ac0d53c063a46185735ad611a83</citedby><cites>FETCH-LOGICAL-c465t-2240ac02293d5eb114c75e39def3700f55579ac0d53c063a46185735ad611a83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8924484/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8924484/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35311227$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Bo-Ching</creatorcontrib><creatorcontrib>Kang, Victor Jing-Wei</creatorcontrib><creatorcontrib>Pan, Chien-Ting</creatorcontrib><creatorcontrib>Huang, Jia-Zheng</creatorcontrib><creatorcontrib>Lin, Yu-Li</creatorcontrib><creatorcontrib>Chang, Yi-Yao</creatorcontrib><creatorcontrib>Tsai, Cheng-Hsuan</creatorcontrib><creatorcontrib>Chou, Chia-Hung</creatorcontrib><creatorcontrib>Chen, Zheng-Wei</creatorcontrib><creatorcontrib>Liao, Che-Wei</creatorcontrib><creatorcontrib>Chiu, Yu-Wei</creatorcontrib><creatorcontrib>Wu, Vin-Cent</creatorcontrib><creatorcontrib>Hung, Chi-Sheng</creatorcontrib><creatorcontrib>Chang, Chin-Chen</creatorcontrib><creatorcontrib>Lin, Yen-Hung</creatorcontrib><title>KCNJ5 Somatic Mutation Is Associated With Higher Aortic Wall Thickness and Less Calcification in Patients With Aldosterone-Producing Adenoma</title><title>Frontiers in endocrinology (Lausanne)</title><addtitle>Front Endocrinol (Lausanne)</addtitle><description>Primary aldosteronism (PA) is the most common type of secondary hypertension, and it is associated with a higher rate of cardiovascular complications. KCNJ5 somatic mutations have recently been identified in aldosterone-producing adenoma (APA), however their influence on vascular remodeling and injury is still unclear. The aim of this study was to investigate the association between KCNJ5 somatic mutation status and vascular status.
We enrolled 179 APA patients who had undergone adrenalectomy from a prospectively maintained database, of whom 99 had KCNJ5 somatic mutations. Preoperative clinical, biochemical and imaging data of abdominal CT, including abdominal aortic calcification (AAC) score, aortic diameter and wall thickness at levels of superior (SMA) and inferior (IMA) mesenteric arteries were analyzed.
After propensity score matching for age, sex, body mass index, triglycerides and low-density lipoprotein, there were 48 patients in each KCNJ5 (+) and KCNJ5 (-) group. Mutation carriers had a lower AAC score (217.3 ± 562.2 vs. 605.6 ± 1359.1, P=0.018), higher aortic wall thickness (SMA level: 2.2 ± 0.6 mm vs. 1.8 ± 0.6 mm, P=0.006; IMA level: 2.4 ± 0.6 mm vs. 1.8 ± 0.7 mm, P<0.001) than non-carriers. In multivariate analysis, KCNJ5 mutations were independently associated with AAC score (P=0.014) and aortic wall thickness (SMA level: P<0.001; IMA level: P=0.004). After adrenalectomy, mutation carriers had less aortic wall thickness progression than non-carriers (Δthickness SMA: -0.1 ± 0.8 mm vs. 0.9 ± 0.6 mm, P=0.024; IMA: -0.1 ± 0.6 mm vs. 0.8 ± 0.7 mm, P=0.04).
KCNJ5 mutation carriers had less calcification burden of the aorta, thickened aortic wall, and less wall thickness progression than non-carriers.</description><subject>Adenoma - genetics</subject><subject>Adrenal Cortex Neoplasms - complications</subject><subject>Adrenal Cortex Neoplasms - genetics</subject><subject>Adrenal Cortex Neoplasms - surgery</subject><subject>Adrenocortical Adenoma - complications</subject><subject>Adrenocortical Adenoma - genetics</subject><subject>Adrenocortical Adenoma - surgery</subject><subject>Aldosterone</subject><subject>Aorta</subject><subject>aortic calcification</subject><subject>Calcinosis - genetics</subject><subject>Endocrinology</subject><subject>G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics</subject><subject>Humans</subject><subject>Hyperaldosteronism - complications</subject><subject>Hyperaldosteronism - genetics</subject><subject>hypertension</subject><subject>KCNJ5 somatic mutation</subject><subject>Mutation</subject><subject>primary aldosteronism</subject><issn>1664-2392</issn><issn>1664-2392</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVks9u1DAQxiMEolXpA3BBPnLJ4v9xLkirFdCFBSqxUo-W157sumTtYidIvEMfuk5TqtaXGY2_-XnG-qrqLcELxlT7oYPg4oJiSheKYcLwi-qUSMlrylr68kl-Up3nfI3L4Zi0rXpdnTDBCKG0Oa1uv61-fBXoVzyawVv0fRxKjAGtM1rmHK03Azh05YcDuvD7AyS0jGlSXpm-R9uDt78D5IxMcGgzJSvTW995O2N8QJclgzDkGbLsXcwDpBigvkzRjdaHPVo6CGWCN9WrzvQZzh_iWbX9_Gm7uqg3P7-sV8tNbbkUQ00px8aWxVvmBOwI4bYRwFoHHWsw7oQQTVsETjCLJTNcEiUaJoyThBjFzqr1jHXRXOub5I8m_dPReH1fiGmvzbRjD3rXKSeVa4HzjrPye84BJuAsb3cKGCusjzPrZtwdS71smkz_DPr8JviD3se_WrWUc8UL4P0DIMU_I-RBH3220PcmQByzppITQaSSokjJLLUp5pyge3yGYD15Qt97Qk-e0LMnSs-7p_M9dvx3ALsDd060dA</recordid><startdate>20220302</startdate><enddate>20220302</enddate><creator>Lee, Bo-Ching</creator><creator>Kang, Victor Jing-Wei</creator><creator>Pan, Chien-Ting</creator><creator>Huang, Jia-Zheng</creator><creator>Lin, Yu-Li</creator><creator>Chang, Yi-Yao</creator><creator>Tsai, Cheng-Hsuan</creator><creator>Chou, Chia-Hung</creator><creator>Chen, Zheng-Wei</creator><creator>Liao, Che-Wei</creator><creator>Chiu, Yu-Wei</creator><creator>Wu, Vin-Cent</creator><creator>Hung, Chi-Sheng</creator><creator>Chang, Chin-Chen</creator><creator>Lin, Yen-Hung</creator><general>Frontiers Media S.A</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20220302</creationdate><title>KCNJ5 Somatic Mutation Is Associated With Higher Aortic Wall Thickness and Less Calcification in Patients With Aldosterone-Producing Adenoma</title><author>Lee, Bo-Ching ; Kang, Victor Jing-Wei ; Pan, Chien-Ting ; Huang, Jia-Zheng ; Lin, Yu-Li ; Chang, Yi-Yao ; Tsai, Cheng-Hsuan ; Chou, Chia-Hung ; Chen, Zheng-Wei ; Liao, Che-Wei ; Chiu, Yu-Wei ; Wu, Vin-Cent ; Hung, Chi-Sheng ; Chang, Chin-Chen ; Lin, Yen-Hung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c465t-2240ac02293d5eb114c75e39def3700f55579ac0d53c063a46185735ad611a83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenoma - genetics</topic><topic>Adrenal Cortex Neoplasms - complications</topic><topic>Adrenal Cortex Neoplasms - genetics</topic><topic>Adrenal Cortex Neoplasms - surgery</topic><topic>Adrenocortical Adenoma - complications</topic><topic>Adrenocortical Adenoma - genetics</topic><topic>Adrenocortical Adenoma - surgery</topic><topic>Aldosterone</topic><topic>Aorta</topic><topic>aortic calcification</topic><topic>Calcinosis - genetics</topic><topic>Endocrinology</topic><topic>G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics</topic><topic>Humans</topic><topic>Hyperaldosteronism - complications</topic><topic>Hyperaldosteronism - genetics</topic><topic>hypertension</topic><topic>KCNJ5 somatic mutation</topic><topic>Mutation</topic><topic>primary aldosteronism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Bo-Ching</creatorcontrib><creatorcontrib>Kang, Victor Jing-Wei</creatorcontrib><creatorcontrib>Pan, Chien-Ting</creatorcontrib><creatorcontrib>Huang, Jia-Zheng</creatorcontrib><creatorcontrib>Lin, Yu-Li</creatorcontrib><creatorcontrib>Chang, Yi-Yao</creatorcontrib><creatorcontrib>Tsai, Cheng-Hsuan</creatorcontrib><creatorcontrib>Chou, Chia-Hung</creatorcontrib><creatorcontrib>Chen, Zheng-Wei</creatorcontrib><creatorcontrib>Liao, Che-Wei</creatorcontrib><creatorcontrib>Chiu, Yu-Wei</creatorcontrib><creatorcontrib>Wu, Vin-Cent</creatorcontrib><creatorcontrib>Hung, Chi-Sheng</creatorcontrib><creatorcontrib>Chang, Chin-Chen</creatorcontrib><creatorcontrib>Lin, Yen-Hung</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Frontiers in endocrinology (Lausanne)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Bo-Ching</au><au>Kang, Victor Jing-Wei</au><au>Pan, Chien-Ting</au><au>Huang, Jia-Zheng</au><au>Lin, Yu-Li</au><au>Chang, Yi-Yao</au><au>Tsai, Cheng-Hsuan</au><au>Chou, Chia-Hung</au><au>Chen, Zheng-Wei</au><au>Liao, Che-Wei</au><au>Chiu, Yu-Wei</au><au>Wu, Vin-Cent</au><au>Hung, Chi-Sheng</au><au>Chang, Chin-Chen</au><au>Lin, Yen-Hung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>KCNJ5 Somatic Mutation Is Associated With Higher Aortic Wall Thickness and Less Calcification in Patients With Aldosterone-Producing Adenoma</atitle><jtitle>Frontiers in endocrinology (Lausanne)</jtitle><addtitle>Front Endocrinol (Lausanne)</addtitle><date>2022-03-02</date><risdate>2022</risdate><volume>13</volume><spage>830130</spage><epage>830130</epage><pages>830130-830130</pages><issn>1664-2392</issn><eissn>1664-2392</eissn><abstract>Primary aldosteronism (PA) is the most common type of secondary hypertension, and it is associated with a higher rate of cardiovascular complications. KCNJ5 somatic mutations have recently been identified in aldosterone-producing adenoma (APA), however their influence on vascular remodeling and injury is still unclear. The aim of this study was to investigate the association between KCNJ5 somatic mutation status and vascular status.
We enrolled 179 APA patients who had undergone adrenalectomy from a prospectively maintained database, of whom 99 had KCNJ5 somatic mutations. Preoperative clinical, biochemical and imaging data of abdominal CT, including abdominal aortic calcification (AAC) score, aortic diameter and wall thickness at levels of superior (SMA) and inferior (IMA) mesenteric arteries were analyzed.
After propensity score matching for age, sex, body mass index, triglycerides and low-density lipoprotein, there were 48 patients in each KCNJ5 (+) and KCNJ5 (-) group. Mutation carriers had a lower AAC score (217.3 ± 562.2 vs. 605.6 ± 1359.1, P=0.018), higher aortic wall thickness (SMA level: 2.2 ± 0.6 mm vs. 1.8 ± 0.6 mm, P=0.006; IMA level: 2.4 ± 0.6 mm vs. 1.8 ± 0.7 mm, P<0.001) than non-carriers. In multivariate analysis, KCNJ5 mutations were independently associated with AAC score (P=0.014) and aortic wall thickness (SMA level: P<0.001; IMA level: P=0.004). After adrenalectomy, mutation carriers had less aortic wall thickness progression than non-carriers (Δthickness SMA: -0.1 ± 0.8 mm vs. 0.9 ± 0.6 mm, P=0.024; IMA: -0.1 ± 0.6 mm vs. 0.8 ± 0.7 mm, P=0.04).
KCNJ5 mutation carriers had less calcification burden of the aorta, thickened aortic wall, and less wall thickness progression than non-carriers.</abstract><cop>Switzerland</cop><pub>Frontiers Media S.A</pub><pmid>35311227</pmid><doi>10.3389/fendo.2022.830130</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adenoma - genetics Adrenal Cortex Neoplasms - complications Adrenal Cortex Neoplasms - genetics Adrenal Cortex Neoplasms - surgery Adrenocortical Adenoma - complications Adrenocortical Adenoma - genetics Adrenocortical Adenoma - surgery Aldosterone Aorta aortic calcification Calcinosis - genetics Endocrinology G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics Humans Hyperaldosteronism - complications Hyperaldosteronism - genetics hypertension KCNJ5 somatic mutation Mutation primary aldosteronism |
title | KCNJ5 Somatic Mutation Is Associated With Higher Aortic Wall Thickness and Less Calcification in Patients With Aldosterone-Producing Adenoma |
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