Abstract
Contrast-associated acute kidney injury (CA-AKI) remains a significant concern in diagnostic and invasive procedures, particularly in the context of iodinated contrast material administration. The traditional definition of CA-AKI, based on serum creatinine elevation following contrast exposure, may not accurately capture its multifactorial nature. Studies have provided new insights into the differential incidence of CA-AKI between intravenous and intraarterial contrast administration, emphasizing the importance of tailored preventative strategies for high-risk procedures. This higher risk may arise from two proposed mechanisms: one implicating free radical formation leading to cytotoxicity and apoptosis in renal cells and another suggesting that contrast media alter renal hemodynamics, particularly in the outer medulla, by constricting the vasa recta and reducing medullary flow. Advances in technology and patient care, including contemporary use of low-osmolar contrast agents and hydration protocols, mitigate CA-AKI risk. Diagnostic and invasive procedures should not be avoided solely due to concerns about renal dysfunction if the patient is likely to benefit clinically.
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