Antithrombin III Protects Against Contrast-Induced Nephropathy

We previously reported that insufficiency of antithrombin III (ATIII), the major anti-coagulation molecule in vivo, exacerbated renal ischemia-reperfusion injury in animal models and possibly humans. In the present study, we investigated the relationship between ATIII level and contrast induced neph...

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Main Authors: Zeyuan Lu, Dongsheng Cheng, Jianyong Yin, Rui Wu, Guangyuan Zhang, Qing Zhao, Niansong Wang, Feng Wang, Mingyu Liang
Format: Article
Language:English
Published: Elsevier 2017-03-01
Series:EBioMedicine
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2352396417300683
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author Zeyuan Lu
Dongsheng Cheng
Jianyong Yin
Rui Wu
Guangyuan Zhang
Qing Zhao
Niansong Wang
Feng Wang
Mingyu Liang
author_facet Zeyuan Lu
Dongsheng Cheng
Jianyong Yin
Rui Wu
Guangyuan Zhang
Qing Zhao
Niansong Wang
Feng Wang
Mingyu Liang
author_sort Zeyuan Lu
collection DOAJ
description We previously reported that insufficiency of antithrombin III (ATIII), the major anti-coagulation molecule in vivo, exacerbated renal ischemia-reperfusion injury in animal models and possibly humans. In the present study, we investigated the relationship between ATIII level and contrast induced nephropathy (CIN) in patients and examined therapeutic effect of ATIII on CIN in Sprague-Dawley rats. Patients with low ATIII activity presented a higher incidence of acute kidney injury (AKI) following coronary angiography. ATIII (500 μg/kg) was intravenously injected before or after the induction of AKI in rats. Our data demonstrated ATIII significantly attenuated the elevation of serum creatinine, blood urea nitrogen, and renal histological injury. The beneficial effects of ATIII were accompanied by diminished renal inflammatory response, oxidative stress, cell apoptosis and improved renal blood flow in rats. In conclusion, ATIII appears to attenuate CIN through inhibiting inflammation, oxidative stress, apoptosis and improving renal blood flow. ATIII administration may represent a promising strategy for the prevention and treatment of contrast-induced AKI.
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spelling doaj.art-0a319878d9ec4eb59c283dee0f1fdf502022-12-22T00:54:04ZengElsevierEBioMedicine2352-39642017-03-0117C10110710.1016/j.ebiom.2017.02.009Antithrombin III Protects Against Contrast-Induced NephropathyZeyuan Lu0Dongsheng Cheng1Jianyong Yin2Rui Wu3Guangyuan Zhang4Qing Zhao5Niansong Wang6Feng Wang7Mingyu Liang8Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, ChinaDepartment of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, ChinaDepartment of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, ChinaDepartment of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, ChinaDepartment of Urology, Zhongda Hospital, Southeast University, Nanjing, ChinaDepartment of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, ChinaDepartment of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, ChinaDepartment of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, ChinaDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI, USAWe previously reported that insufficiency of antithrombin III (ATIII), the major anti-coagulation molecule in vivo, exacerbated renal ischemia-reperfusion injury in animal models and possibly humans. In the present study, we investigated the relationship between ATIII level and contrast induced nephropathy (CIN) in patients and examined therapeutic effect of ATIII on CIN in Sprague-Dawley rats. Patients with low ATIII activity presented a higher incidence of acute kidney injury (AKI) following coronary angiography. ATIII (500 μg/kg) was intravenously injected before or after the induction of AKI in rats. Our data demonstrated ATIII significantly attenuated the elevation of serum creatinine, blood urea nitrogen, and renal histological injury. The beneficial effects of ATIII were accompanied by diminished renal inflammatory response, oxidative stress, cell apoptosis and improved renal blood flow in rats. In conclusion, ATIII appears to attenuate CIN through inhibiting inflammation, oxidative stress, apoptosis and improving renal blood flow. ATIII administration may represent a promising strategy for the prevention and treatment of contrast-induced AKI.http://www.sciencedirect.com/science/article/pii/S2352396417300683Antithrombin IIIAcute kidney injuryContrast induced nephropathyInflammation
spellingShingle Zeyuan Lu
Dongsheng Cheng
Jianyong Yin
Rui Wu
Guangyuan Zhang
Qing Zhao
Niansong Wang
Feng Wang
Mingyu Liang
Antithrombin III Protects Against Contrast-Induced Nephropathy
EBioMedicine
Antithrombin III
Acute kidney injury
Contrast induced nephropathy
Inflammation
title Antithrombin III Protects Against Contrast-Induced Nephropathy
title_full Antithrombin III Protects Against Contrast-Induced Nephropathy
title_fullStr Antithrombin III Protects Against Contrast-Induced Nephropathy
title_full_unstemmed Antithrombin III Protects Against Contrast-Induced Nephropathy
title_short Antithrombin III Protects Against Contrast-Induced Nephropathy
title_sort antithrombin iii protects against contrast induced nephropathy
topic Antithrombin III
Acute kidney injury
Contrast induced nephropathy
Inflammation
url http://www.sciencedirect.com/science/article/pii/S2352396417300683
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AT ruiwu antithrombiniiiprotectsagainstcontrastinducednephropathy
AT guangyuanzhang antithrombiniiiprotectsagainstcontrastinducednephropathy
AT qingzhao antithrombiniiiprotectsagainstcontrastinducednephropathy
AT niansongwang antithrombiniiiprotectsagainstcontrastinducednephropathy
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