الفهرس 
Aim of The WorkOnly 14 pages are availabe for public view
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Abstract
CIN has been generally defined as an absolute rise in serum creatinine of >0.5 mg/dl or an increase of >25% from the patient’s prior baseline 48–72 h after contrast administration.
Many comorbidities and risk factors have been suggested as contributors to develop CIN as diabetes mellitus, chronic kidney diseases, advanced age, anemia, heart failure and high contrast volume.
Serum uric acid is a degradation metabolite of purines and a risk factor for cardiovascular disease. Hyperuricemia is characterized by inhibited nitric oxide system, activation of the local rennin-angiotensin system, pro- inflammatory and proliferative actions and enhanced synthesis of reactive oxygen species with increased oxidative stress.
This study included 70 patients presented with STEMI who have undergone primary PCI. The Patients were divided into three groups according to their baseline serum uric acid levels. group A included patients with serum uric acid less than or equal 5.5 mg/dl (30 patients), group B included patients with serum uric acid ranges from 5.6 to 7 mg/dl (12 patients) and group C included patients with serum uric acid more than 7 mg/dl (28 patients). Nine (12.9%) cases from 70 patients developed CIN. The main finding in this study was the association between increasing serum uric acid level and development of CIN. In addition, patients who developed CIN were older, had lower LVEF, higher prevalence of diabetes and lower serum hemoglobin level. Serum uric acid cutoff point 8.7 mg/dl has sensitivity of 66.67% and specificity of 81.97 % to predict CIN.
Serum uric acid levels were recognized as independent predictors of CIN based on the multivariate logistic regression analysis.