Abstract
IntroductionAcute kidney injury (AKI) following acute myocardial infarction (AMI) is associated with unfavorable prognosis. Endothelial activation and injury were found to play a critical role in the development of both AKI and AMI. This pilot study aimed to determine whether the plasma markers of endothelial injury and activation could serve as independent predictors for AKI in patients with AMI.MethodsThis prospective study was conducted from March 2010 to July 2012 and enrolled consecutive 132 patients with AMI receiving percutaneous coronary intervention (PCI). Plasma levels of thrombomodulin (TM), von Willebrand factor (vWF), angiopoietin (Ang)-1, Ang-2, Tie-2, and vascular endothelial growth factor (VEGF) were measured on day 1 of AMI. AKI was defined as elevation of serum creatinine of more than 0.3 mg/dL within 48 hours.ResultsIn total, 13 out of 132 (9.8%) patients with AMI developed AKI within 48 hours. Compared with patients without AKI, patients with AKI had increased plasma levels of Ang-2 (6338.28 ± 5862.77 versus 2412.03 ± 1256.58 pg/mL, P = 0.033) and sTM (7.6 ± 2.26 versus 5.34 ± 2.0 ng/mL, P < 0.001), and lower estimated glomerular filtration rate (eGFR) (46.5 ± 20.2 versus 92.5 ± 25.5 mL/min/1.73 m2, P < 0.001). Furthermore, the areas under the receiver operating curves demonstrated that plasma thrombomodulin (TM) and Ang-2 levels on day 1 of AMI had modest discriminative powers for predicting AKI development following AMI (0.796, P <0.001; 0.833, P <0.001; respectively).ConclusionsEndothelial activation, quantified by plasma levels of TM and Ang-2 may play an important role in development of AKI in patients with AMI.
Highlights
Acute kidney injury (AKI) following acute myocardial infarction (AMI) is associated with unfavorable prognosis
Study population This prospective study was conducted from March 2010 to July 2012 and enrolled consecutive patients with AMI receiving percutaneous coronary intervention (PCI)
One hundred and thirty-two patients who were diagnosed with AMI from March 2010 to July 2012 were consecutively recruited for this study
Summary
Acute kidney injury (AKI) following acute myocardial infarction (AMI) is associated with unfavorable prognosis. Endothelial activation and injury were found to play a critical role in the development of both AKI and AMI. Alterations in peritubular capillary blood flow during reperfusion have been documented to associate with loss of normal endothelial cell function [7]. Several molecules, such as thrombomodulin (TM) and angiopoietins, were reported to be connected with endothelial injury [8,9]. Increased levels of plasma sTM can serve as a marker of endothelial injury, and have been found to be associated with worse outcomes in patients with acute coronary syndrome [13]. Increased plasma levels of sTM have been reported to be associated with kidney injury induced by sepsis [14] and diabetes [15]
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