الفهرس 
Etiology of acute kidney injuryOnly 14 pages are availabe for public view
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Abstract
Worsening renal function during AMI, even transient, is associated with adverse outcome and increased long-term mortality. The mechanism of AKI in patients with AMI is multifactorial, evidence suggests that endothelial injury of the renal vasculature play an important role in the pathogenesis of both early and chronic ischemic AKI. Thrombomodulin and Angiopoietins, were reported to be connected with endothelial injury. The aim of this study was to determine whether the serum markers of endothelial injury and activation (Thrombomodulin and Angiopoitien) could serve as predictors for acute kidney injury in patients with acute myocardial infarction before change of creatinine. In this study, 90 patients with AMI (whom were treated by PCI) were investigated and followed up for the acquiring of AKI. They were subdivided to three groups (30 patients each); the first group included patients with both AMI and AKI, the second group included patients with AMI and AKI on base of renal impairement and the last one was for those with AMI only without AKI. Renal functions were measured at admission and 48 hours later to diagnose AKI adopting KDIGO definition. TM, Ang-1 and Ang-2 were withdrawn at admission. According to the present study, significant risk factors of developing AKI in the study population were DM, HTN, Killip class ≥ 3 & EF < 45 (as an assessment of cardiac function), HB% (as assessment for anemia), TLC & hs-CRP (as indicator for inflammation) and lastly Ang-2 & TM (as biomarkers of endothelial dysfunction). Logestic regression analysis among them reveled that TM was the most independent one (p 0.007, OR: 14.37, 95% CI: 2.094-98.625). TM and Ang-2 increased significantly among the three study groups while Ang-1 didn’t. There was a strong positive correlation between late sCr & basal TM while there was a weak positive one with Ang-2. TM and Ang-2 experienced a significant elevation with advancing AKI stages but not CKD stages. TM showed a significant increase with hypertension & DM history, poor EF, Killip class ≥ 3 and with the number of diseased coronary arteries elicited by PCI, meanwhile Ang-2 increased significantly with the increasing number of diseased coronary arteries only. TM cutoff point of 4.3 ng/ml had a very high sensitivity, specificity, PPV and NPV. Ang-2 cutoff point of 345 pg/ml had a high specificity & PPV and low sensitivity & NPV.