Background Fluctuation of Kidney Function Versus Contrast-Induced Nephrotoxicity

Abstract

OBJECTIVE: The reported incidence of contrast-induced acute kidney injury varies widely. Almost no studies have been conducted to quantify the background fluctuation of kidney function of patients receiving iodinated contrast medium. The purpose of this study was a retrospective comparison of the incidence of acute kidney injury among patients undergoing CT with low-osmolar (iohexol) or isoosmolar (iodixanol) contrast medium with the incidence among patients undergoing CT without contrast administration. MATERIALS AND METHODS: Creatinine concentration and estimated glomerular filtration rate were evaluated for 11,588 patients. Rates of acute kidney injury (defined as a 0.5 mg/dL increase in serum creatinine concentration or a 25% or greater decrease in estimated glomerular filtration rate within 3 days after CT) were compared among groups and stratified according to creatinine concentration and estimated glomerular filtration rate before the imaging examination. RESULTS: In all groups, the incidence of acute kidney injury increased with increasing baseline creatinine concentration. No significant difference in incidence of presumed contrast-induced kidney injury was identified between the isoosmolar contrast medium and the control groups. The incidence of acute kidney injury in the low-osmolar contrast medium cohort paralleled that of the control cohort up to a creatinine level of 1.8 mg/dL, but increases above this level were associated with a higher incidence of acute kidney injury. CONCLUSION: We identified a high incidence of acute kidney injury among control subjects undergoing unenhanced CT. The incidence of creatinine elevation in this group was statistically similar to that in the isoosmolar contrast medium group for all baseline creatinine values and all stages of chronic kidney disease. These findings suggest that the additional risk of acute kidney injury accompanying administration of contrast medium (contrast-induced nephrotoxicity) may be overstated and that much of the creatinine elevation in these patients is attributable to background fluctuation, underlying disease, or treatment.