Why the study?
Does the contrast medium dose-to-eGFR ratio predict the risk of contrast-induced nephropathy in patients undergoing primary PCI for STEMI?
Does the contrast medium dose-to-eGFR ratio predict the risk of contrast-induced nephropathy in patients undergoing primary PCI for STEMI?
Limiting the contrast medium dose (in grams of iodine) to numerically less than or equal to the patient's eGFR (ml/min) may be relatively safe to prevent contrast-induced nephropathy during primary PCI.
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Supports g-I/eGFR ratio for CIN risk stratification in primary PCI; leaves open prospective validation of dose limitation.
BACKGROUND: The contrast medium (CM) dose-to-eGFR (estimated glomerular filtration rate) ratio has recently been advocated to express systemic exposure to CM in assessing the risk of contrast medium-induced nephropathy (CIN). PURPOSE: To evaluate how CIN risk might vary with decreasing eGFR at fixed CM-dose/eGFR ratios and other CIN risk factors, and to find a relatively safe CM-dose/eGFR ratio. MATERIAL AND METHODS: 391 patients underwent primary coronary angioplasty for ST-segment elevation acute myocardial infarction. CM dose (grams iodine; g I), eGFR (ml/min), and preprocedural CIN risk factors were entered into a multiple logistic regression model. From the established statistical model, the probability of CIN (>or=44.2 micromol/l serum creatinine rise or oliguria/anuria) was calculated at various eGFR levels based on g-I/eGFR ratios of 1:2, 1:1, 2:1, and 3:1. RESULTS: At a g-I/eGFR ratio <1 the risk of CIN was 3%, while it was 25% at a g-I/eGFR ratio >or=1. Independent predictors of CIN were CM dose, eGFR, left ventricular ejection fraction (LVEF) and cardiogenic shock (ROC area =0.87). An estimated CIN risk of 10% would for example occur at a g-I/eGFR ratio of 1.5:1 in patients with 50% LVEF without shock. At a 1:2, 1:1, 2:1, and 3:1 g-I/eGFR ratio with 50% LVEF without shock, the CIN risk was about 2, 6, 18, and 30%, respectively, over a wide range of eGFR values (30-90 ml/min). At a 1:1 g-I/eGFR ratio with 50% LVEF+shock, 25% LVEF without shock, or 25% LVEF+shock, the CIN risk was 20, 55, and 80%, respectively. CONCLUSION: Relating CM dose to eGFR appears to be an attractive pharmacotoxic model to assess CIN risk. At fixed CM-dose/eGFR ratios, CIN risk increased marginally with decreasing eGFR. Limiting the CM dose in g I numerically to the eGFR value in ml/min or less may be relatively safe with regard to CIN, unless multiple risk factors are present.
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Nyman et al. (2008) studied this question.
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