A Joint Evaluation of Neurohormone Vasopressin-Neurophysin II-Copeptin and Aortic Arch Calcification on Mortality Risks in Hemodialysis Patients
Objective: Systemic hypoperfusion is intricately involved in neurohormone secretion, vascular calcification (VC) related impaired vasodilation, and luminal stenosis. We aimed to conduct a joint evaluation of vasopressin-neurophysin II-copeptin peptide (VP) and advanced aortic arch calcification (AAC...
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Frontiers Media S.A.
2020-03-01
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Online Access: | https://www.frontiersin.org/article/10.3389/fmed.2020.00102/full |
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author | Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Yu-Shao Chou Chang-Chin Wu Chang-Chin Wu Chang-Chin Wu Chang-Chin Wu Po-Cheng Chen Wen-Chin Ko Wen-Chin Ko Jian-Chiun Liou Chih-Yu Hsieh Chih-Yu Hsieh Wei-Ning Lin Li-Li Wen Li-Li Wen Shu-Wei Chang Tao-Hsin Tung Ting-Ming Wang Ting-Ming Wang |
author_facet | Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Yu-Shao Chou Chang-Chin Wu Chang-Chin Wu Chang-Chin Wu Chang-Chin Wu Po-Cheng Chen Wen-Chin Ko Wen-Chin Ko Jian-Chiun Liou Chih-Yu Hsieh Chih-Yu Hsieh Wei-Ning Lin Li-Li Wen Li-Li Wen Shu-Wei Chang Tao-Hsin Tung Ting-Ming Wang Ting-Ming Wang |
author_sort | Jia-Feng Chang |
collection | DOAJ |
description | Objective: Systemic hypoperfusion is intricately involved in neurohormone secretion, vascular calcification (VC) related impaired vasodilation, and luminal stenosis. We aimed to conduct a joint evaluation of vasopressin-neurophysin II-copeptin peptide (VP) and advanced aortic arch calcification (AAC) on all-cause and cardiovascular (CV) mortality in maintenance hemodialysis (MHD) patients.Methods: Unadjusted and adjusted hazard ratios (aHRs) of mortality risks were analyzed for different groups of VP and AAC in 167 MHD patients. The modification effect between higher VP and advanced AAC on mortality risk was examined using an interaction product term.Results: Interactions between VP and AAC with respect to all-cause and CV mortality were statistically significant. In multivariable analysis, higher VP predicted all-cause and CV mortality [aHR: 2.2 (95% confidence interval (CI): 1.1–4.5)] and 2.6 (95% CI: 1.1–4.6), respectively. Advanced AAC was associated with incremental risks of all-cause and CV mortality [aHR: 2.1 (95% CI: 1.1–4.0)and 2.5 (95% CI: 1.0–4.3), respectively]. Patients with combined higher VP (>101.5 ng/mL) and advanced AAC were at the greatest risk of all-cause and CV mortality [aHR: 4.7 (95% CI: 1.2–16.2)and 4.9 (95% CI: 1.1–18.9), respectively].Conclusion: Combined VP and advanced AAC predict not only all-cause but also CV death in MHD patients, and a joint evaluation is more comprehensive than single marker. In light of hypoperfusion and ischemic events in vital organs, VP and AAC could act as more robust dual marker for prognostic assessment. |
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spelling | doaj.art-c73ff097583f4b17a66b2e98caf9906d2022-12-22T03:01:29ZengFrontiers Media S.A.Frontiers in Medicine2296-858X2020-03-01710.3389/fmed.2020.00102511951A Joint Evaluation of Neurohormone Vasopressin-Neurophysin II-Copeptin and Aortic Arch Calcification on Mortality Risks in Hemodialysis PatientsJia-Feng Chang0Jia-Feng Chang1Jia-Feng Chang2Jia-Feng Chang3Jia-Feng Chang4Jia-Feng Chang5Yu-Shao Chou6Chang-Chin Wu7Chang-Chin Wu8Chang-Chin Wu9Chang-Chin Wu10Po-Cheng Chen11Wen-Chin Ko12Wen-Chin Ko13Jian-Chiun Liou14Chih-Yu Hsieh15Chih-Yu Hsieh16Wei-Ning Lin17Li-Li Wen18Li-Li Wen19Shu-Wei Chang20Tao-Hsin Tung21Ting-Ming Wang22Ting-Ming Wang23Division of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, TaiwanGraduate Institute of Aerospace and Undersea Medicine, Academy of Medicine, National Defense Medical Center, Taipei, TaiwanDepartment of Nursing, Yuanpei University of Medical Technology, Hsinchu, TaiwanDivision of Nephrology, Department of Internal Medicine, En Chu Kong Hospital, New Taipei City, TaiwanRenal Care Joint Foundation, New Taipei City, TaiwanCollege of Medicine, Fu Jen Catholic University, New Taipei City, TaiwanDepartment of Emergency Medicine, En Chu Kong Hospital, New Taipei City, TaiwanDepartment of Orthopaedic Surgery, School of Medicine, National Taiwan University, Taipei, TaiwanDepartment of Orthopaedic Surgery, National Taiwan University Hospital, Taipei, Taiwan0Department of Orthopedics, En Chu Kong Hospital, New Taipei City, Taiwan1Department of Biomedical Engineering, Yuanpei University of Medical Technology, Hsinchu, Taiwan2Department of Urology, En Chu Kong Hospital, New Taipei City, TaiwanCollege of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan3Division of Cardiology, Department of Internal Medicine, Cathay General Hospital, Taipei, Taiwan4School of Biomedical Engineering, Taipei Medical University, Taipei, Taiwan4School of Biomedical Engineering, Taipei Medical University, Taipei, Taiwan5Department of Pathology, National Defense Medical Center, Tri-Service General Hospital, Taipei, Taiwan6Graduate Institution of Biomedical and Pharmaceutical Science, College of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan7Department of Medical Laboratory Science and Biotechnology, Yuanpei University, Hsinchu, Taiwan8Department of Clinical Laboratory, En Chu Kong Hospital, New Taipei City, Taiwan9Department of Civil Engineering, National Taiwan University, Taipei, Taiwan0Department of Medical Research and Education, Cheng Hsin General Hospital, Taipei, TaiwanDepartment of Orthopaedic Surgery, School of Medicine, National Taiwan University, Taipei, TaiwanDepartment of Orthopaedic Surgery, National Taiwan University Hospital, Taipei, TaiwanObjective: Systemic hypoperfusion is intricately involved in neurohormone secretion, vascular calcification (VC) related impaired vasodilation, and luminal stenosis. We aimed to conduct a joint evaluation of vasopressin-neurophysin II-copeptin peptide (VP) and advanced aortic arch calcification (AAC) on all-cause and cardiovascular (CV) mortality in maintenance hemodialysis (MHD) patients.Methods: Unadjusted and adjusted hazard ratios (aHRs) of mortality risks were analyzed for different groups of VP and AAC in 167 MHD patients. The modification effect between higher VP and advanced AAC on mortality risk was examined using an interaction product term.Results: Interactions between VP and AAC with respect to all-cause and CV mortality were statistically significant. In multivariable analysis, higher VP predicted all-cause and CV mortality [aHR: 2.2 (95% confidence interval (CI): 1.1–4.5)] and 2.6 (95% CI: 1.1–4.6), respectively. Advanced AAC was associated with incremental risks of all-cause and CV mortality [aHR: 2.1 (95% CI: 1.1–4.0)and 2.5 (95% CI: 1.0–4.3), respectively]. Patients with combined higher VP (>101.5 ng/mL) and advanced AAC were at the greatest risk of all-cause and CV mortality [aHR: 4.7 (95% CI: 1.2–16.2)and 4.9 (95% CI: 1.1–18.9), respectively].Conclusion: Combined VP and advanced AAC predict not only all-cause but also CV death in MHD patients, and a joint evaluation is more comprehensive than single marker. In light of hypoperfusion and ischemic events in vital organs, VP and AAC could act as more robust dual marker for prognostic assessment.https://www.frontiersin.org/article/10.3389/fmed.2020.00102/fullvasopressinneurophysin IIcopeptinvascular calcificationmortalitydialysis |
spellingShingle | Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Jia-Feng Chang Yu-Shao Chou Chang-Chin Wu Chang-Chin Wu Chang-Chin Wu Chang-Chin Wu Po-Cheng Chen Wen-Chin Ko Wen-Chin Ko Jian-Chiun Liou Chih-Yu Hsieh Chih-Yu Hsieh Wei-Ning Lin Li-Li Wen Li-Li Wen Shu-Wei Chang Tao-Hsin Tung Ting-Ming Wang Ting-Ming Wang A Joint Evaluation of Neurohormone Vasopressin-Neurophysin II-Copeptin and Aortic Arch Calcification on Mortality Risks in Hemodialysis Patients Frontiers in Medicine vasopressin neurophysin II copeptin vascular calcification mortality dialysis |
title | A Joint Evaluation of Neurohormone Vasopressin-Neurophysin II-Copeptin and Aortic Arch Calcification on Mortality Risks in Hemodialysis Patients |
title_full | A Joint Evaluation of Neurohormone Vasopressin-Neurophysin II-Copeptin and Aortic Arch Calcification on Mortality Risks in Hemodialysis Patients |
title_fullStr | A Joint Evaluation of Neurohormone Vasopressin-Neurophysin II-Copeptin and Aortic Arch Calcification on Mortality Risks in Hemodialysis Patients |
title_full_unstemmed | A Joint Evaluation of Neurohormone Vasopressin-Neurophysin II-Copeptin and Aortic Arch Calcification on Mortality Risks in Hemodialysis Patients |
title_short | A Joint Evaluation of Neurohormone Vasopressin-Neurophysin II-Copeptin and Aortic Arch Calcification on Mortality Risks in Hemodialysis Patients |
title_sort | joint evaluation of neurohormone vasopressin neurophysin ii copeptin and aortic arch calcification on mortality risks in hemodialysis patients |
topic | vasopressin neurophysin II copeptin vascular calcification mortality dialysis |
url | https://www.frontiersin.org/article/10.3389/fmed.2020.00102/full |
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