PURPOSE: The aim is to report the incidence and risk factors of contrast-induced nephropathy after the use of iodine-based contrast for the endovascular treatment of acute ischemic stroke. METHODS: Data from patients who underwent neuroendovascular procedures in a center over a period of 22 months were analysed retrospectively. Contrast-induced nephropathy was determined by an increase in serum creatinine level of >25% of baseline or an absolute increase in serum creatinine level of at least 44 µmol/L (0.50 mg/dL) occurring after intravascular administration of contrast media without alternative explanation. The primary outcome measure of this study was the presence of contrast-induced nephropathy in these treated patients. Continuous data were presented as mean ± standard deviation, and categorical data as frequencies or percentages. The comparison was made using Student's t-test or Fisher's test. Logistic regression was performed to find independent contrast-induced nephropathy predictors. All statistical analyses were performed using Microsoft Excel. A p value of less than 0.05 was considered statistically significant. RESULTS: One hundred and eighty-nine patients undergoing endovascular treatment for acute ischemic stroke. Twenty cases of the total cohort (n = 189) presented contrast-induced nephropathy (10.58%). Only diabetes and creatinine levels between 1.3 and 2.5 mg/dL were associated with contrast-induced nephropathy. No patient was treated with dialysis. CONCLUSION: Contrast-induced nephropathy is a relatively common complication after endovascular treatment of acute ischemic stroke and is associated with worse outcome in patients with this condition. However, there is no increase in the frequency of hemodialysis after the use of iodinated contrast medium.
PURPOSE: The aim is to report the incidence and risk factors of contrast-induced nephropathy after the use of iodine-based contrast for the endovascular treatment of acute ischemic stroke. METHODS: Data from patients who underwent neuroendovascular procedures in a center over a period of 22 months were analysed retrospectively. Contrast-induced nephropathy was determined by an increase in serum creatinine level of >25% of baseline or an absolute increase in serum creatinine level of at least 44 µmol/L (0.50 mg/dL) occurring after intravascular administration of contrast media without alternative explanation. The primary outcome measure of this study was the presence of contrast-induced nephropathy in these treated patients. Continuous data were presented as mean ± standard deviation, and categorical data as frequencies or percentages. The comparison was made using Student's t-test or Fisher's test. Logistic regression was performed to find independent contrast-induced nephropathy predictors. All statistical analyses were performed using Microsoft Excel. A p value of less than 0.05 was considered statistically significant. RESULTS: One hundred and eighty-nine patients undergoing endovascular treatment for acute ischemic stroke. Twenty cases of the total cohort (n = 189) presented contrast-induced nephropathy (10.58%). Only diabetes and creatinine levels between 1.3 and 2.5 mg/dL were associated with contrast-induced nephropathy. No patient was treated with dialysis. CONCLUSION: Contrast-induced nephropathy is a relatively common complication after endovascular treatment of acute ischemic stroke and is associated with worse outcome in patients with this condition. However, there is no increase in the frequency of hemodialysis after the use of iodinated contrast medium.
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