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  • Editorial: Sodium Bicarbonate, Contrast-Associated Acute Kidney Injury, and Long-Term Outcomes: The End of an Era?

    Contrast-associated acute kidney injury (CA-AKI) is defined by a rapid and often reversible decline in kidney function following contrast media administration in the absence of any alternative etiology [  ,  ]. The first observations of CA-AKI were reported in the mid-fifties among patients undergoing X-ray imaging of the urinary tract. Since then, there has been a progressive understanding of the pathophysiology underlying this clinical manifestation. Multiple mechanisms have been implicated in the development of CA-AKI, the most relevant being a direct injury of the contrast material on the tubular cells and a vasoconstrictive effect leading to renal ischemia, especially in the outer medulla [  ]. Different risk factors relating to both the patient and the procedure impact on the occurrence and severity of CA-AKI. Elderly patients, and those with chronic kidney disease, diabetes, and congestive heart failure, have been shown to be more vulnerable. Procedures involving large amounts of contrast media, and characterized by hemodynamic instability (e.g., bleeding, cardiogenic shock) leading to renal hypoperfusion, also play a pivotal role [  ].

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