The ratio of contrast volume to estimated glomerular filtration rate is predictor of contrast-induced acute kidney injury after primary PCI

Aims: We have previously demonstrated that age, baseline renal function and ejection fraction are pre-procedural predictors of Contrast-Induced Acute Kidney Injury (CI-AKI) in the setting of primary PCI, whereas the potential impact of renal function-adjusted contrast dose remains not fully explored. To date, Maximum Accepted Contrast Dose (MACD) based on the Cigarroa formula and Contrast Volume to eGFR ratio (CV/eGFR) have been proposed to calculate a maximum CV not to be overcome, although a universally accepted cutoff for CV/eGFR has not been endorsed. The CV/eGFR has the advantage to be a pharmaco-kinetically derived measure of the risk of CI-AKI. We investigated the association between CV/eGFR and the occurrence of CI-AKI in a consecutive population of patients undergoing primary PCI. Methods and results: CI-AKI was defined as an absolute increase in serum creatinine ≥0.5 mg/dL or an increase ≥25% from baseline within 72 hours after the administration of contrast medium. A multivariate logistic regression analysis was carried out to assess independent predictors of CI-AKI. Receiver-operating characteristic (ROC) curve analysis was performed to assess accuracy of CV/eGFR as predictor of CI-AKI, as expressed by the AUC. The cutoff value was identified at the point where the sum of sensitivity and specificity was the highest according to the Youden index [(sensitivity+specificity)−1]. 470 consecutive patients were prospectively enrolled. We observed 25 (5.3%) cases of CI-AKI. These patients were older (73±10 vs. 61±12 years, p<0.001), had more severe impairment of haemodynamic status (Killip score 1.4±0.8 vs. 1.1±0.5, p=0.01) and worse basal renal function (eGFR 53±19 vs. 94±32 mL/min per 1.73 m, p<0.001) than patients without CI-AKI. In addition, patients with CI-AKI had a higher prevalence of hypertension and diabetes and a higher troponin at admission (22±68 vs. 8±39, p=0.01). Mean procedural CV was 164±63 ml; the incidence of CI-AKI was not higher across different quartiles of CV and, notably, no patient exceeded the MACD. Despite patients developing CI-AKI had not received an absolutely higher total contrast volume (165±79 vs. 163±62 mL, p=NS) nor a higher number of stents, they had received a much higher renal function-adjusted CV (CV/eGFR 3.62 vs. 1.96, p<0.001). Conversely, the difference in CV/MACD, as calculated by the Cigarroa formula, was not significant (0.52 vs. 0.40, p=0.07). By using ROC curve analysis for CIN risk according to CV/eGFR ratio, the AUC was 0.77, with the best cutoff value set at 2.5 (72% sensitivity and 78% specificity). Of note, CIN incidence was much higher (15%, p<0.001) in patients in the highest quartile of CV/eGFR ratio, corresponding to the cutoff indicated by the ROC curve (>2,5). At univariate analysis, several variables were associated with the occurrence of CIN. At multivariable analysis, however, only age (OR 1.08, p=0.023), ejection fraction (OR 0.95, p=0.026), troponin at admission (OR 1.01, p=0.038) and CV/eGFR above the threshold or in the highest quartile (OR 5.13, p=0.004) remained independent predictors of CIN. Conclusions: Contrast volume remains a key risk factor for CI-AKI and our study supports the need for minimising contrast dose in patients with STEMI undergoing primary PCI. A CV restricted to no more than twice and a half the baseline eGFR might be valuable in reducing the risk of CI-AKI.