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New terms and definitions New terms and definitions
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Consensus on contrast-induced acute kidney injury Consensus on contrast-induced acute kidney injury
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Pathophysiology Pathophysiology
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Classification of iodinated contrast agents Classification of iodinated contrast agents
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Intravascular volume expansion to improve renal blood flow Intravascular volume expansion to improve renal blood flow
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Dialysis and haemofiltration Dialysis and haemofiltration
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Prophylactic agents Prophylactic agents
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After care After care
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Novel biomarkers for contrast-induced AKI Novel biomarkers for contrast-induced AKI
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Future approaches Future approaches
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Conclusion Conclusion
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References References
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27 Contrast-induced acute kidney injury
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Published:June 2010
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Abstract
Contrast-induced acute kidney injury (AKI), previously known as contrast-induced nephropathy (CIN) is an important complication in the catheterization laboratory. The most commonly used definition in clinical trials was a rise in serum creatinine (Cr) of 44.2mmol/L (0.5mg/dL) or a 25% increase from the baseline value, assessed at 48h after the procedure. In 2007, the Acute Kidney Injury Network proposed the definition to a rise in serum Cr ≥26.5mmol/L (0.3mg/dL) or a 50% rise in Cr with oliguria which is compatible with previous definitions and is a new standard to follow. If there is a sustained reduction in estimated glomerular function (eGFR) from a baseline above 60 to a new baseline below 60mL/min/1.73m2 at 90 days after the procedure, then a definition of chronic kidney disease (CKD) (Stage 3) would be met as a late outcome of this complication.
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