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Antithrombin III Protects Against Contrast-Induced Nephropathy.

Zeyuan Lu1, Dongsheng Cheng2, Jianyong Yin2

  • 1Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China; Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA; Center of Systems Molecular Medicine, Medical College of Wisconsin, Milwaukee, WI, USA.

Ebiomedicine
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PubMed
Summary
This summary is machine-generated.

Antithrombin III (ATIII) deficiency worsens kidney injury after contrast procedures. ATIII administration protected against contrast-induced nephropathy in rats by reducing inflammation and improving blood flow.

Keywords:
Acute kidney injuryAntithrombin IIIContrast induced nephropathyInflammation

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Area of Science:

  • Nephrology
  • Cardiology
  • Hematology

Background:

  • Antithrombin III (ATIII) is a key anticoagulant.
  • ATIII insufficiency has been linked to exacerbated renal ischemia-reperfusion injury.
  • Contrast-induced nephropathy (CIN) is a significant clinical concern following angiography.

Purpose of the Study:

  • To investigate the correlation between ATIII levels and CIN in patients.
  • To evaluate the therapeutic potential of ATIII in a rat model of CIN.

Main Methods:

  • Retrospective analysis of patients undergoing coronary angiography to assess the relationship between baseline ATIII activity and acute kidney injury (AKI).
  • Administration of ATIII (500 μg/kg) intravenously before or after AKI induction in Sprague-Dawley rats.
  • Assessment of renal function markers (serum creatinine, blood urea nitrogen), histological damage, inflammation, oxidative stress, apoptosis, and renal blood flow.

Main Results:

  • Patients with lower ATIII activity exhibited a higher incidence of AKI post-coronary angiography.
  • ATIII treatment in rats significantly attenuated increases in serum creatinine and blood urea nitrogen.
  • ATIII administration reduced renal histological injury, inflammation, oxidative stress, and apoptosis, while improving renal blood flow.

Conclusions:

  • ATIII deficiency is associated with increased risk of CIN.
  • ATIII demonstrates protective effects against CIN in a preclinical model.
  • ATIII attenuates CIN by mitigating inflammation, oxidative stress, and apoptosis, and enhancing renal perfusion.