Abstract
Contrast-induced acute kidney injury is a well-recognized nosocomial entity that usually arises 3 - 5 days after IV contrast administration. CI-AKI is characterized by an increase in serum creatinine, blood urea nitrogen, or a decrease in the glomerular filtration rate due to iodineinduced oxidative damage to vascular endothelial cells and renal tubular epithelium. Despite the advances in understanding the pathophysiology that has been achieved, there is still no complete and adequate prevention measure for this condition. AKI continues to be one of the most severe adverse effects related to the use of intravascular contrast agents. The condition can range from mild and asymptomatic serum creatinine elevation to acute renal failure with a hemodynamic compromise that could culminate in chronic kidney disease or patient dismissal. CI-AKI is challenging to predict and tends to be more prevalent in patients with preexisting comorbid conditions such as kidney disease, organ failure, diabetic nephropathy, and advanced age.
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