BACKGROUND: Few studies have investigated hs-CRP as a risk factor for contrast-induced nephropathy (CIN). The aim of this study was to evaluate the predictive value of high-sensitivity C-reactive protein (hs-CRP) for risk of CIN in patients with acute ST-segment elevation myocardial infarction (STEMI) who were undergoing primary percutaneous coronary intervention (PCI). METHODS: We prospectively observed 165 consenting patients with STEMI undergoing primary PCI. An increase in serum creatinine of more than 0.5 mg/dL from baseline within 48-72 hours of contrast media exposure was defined as CIN. Demographics, traditional risk factors, CIN incidence and other in-hospital clinical outcomes were compared among hs-CRP quartiles. Receiver operator characteristic curves were used to identify the optimal sensitivity for the observed range of hs-CRP. The predictive value of hs-CRP for the risk of CIN was assessed using multivariate logistic regression. RESULTS: CIN occurred in 17 patients (10%). Univariate analysis revealed CIN incidence was significantly associated with hs-CRP, with 2.4% for quartile Q1 (<6.00 mg/L), 2.3% for Q2 (6.00-13.90), 12.5% for Q3 (13.91-32.75) and 24.4% for Q4 (>32.75) (P-trend <0.001), as was in-hospital death (0% for Q1, 2.3% for Q2, 5% for Q3 and 12.2% for Q4; P-trend = 0.009). Receiver operator characteristic curve analysis showed that an hs-CRP of 16.10 mg/L was a fair discriminator for the early creatinine increase (C statistic 0.78). After adjusting for potential confounding predictors, hs-CRP >16.10 mg/L remained significantly associated with CIN (odds ratio = 6.51; 95% confidence interval, 1.26-33.61). CONCLUSION: An hs-CRP >16.10 was a significant and independent predictor of CIN after primary PCI in patients with STEMI.
BACKGROUND: Few studies have investigated hs-CRP as a risk factor for contrast-induced nephropathy (CIN). The aim of this study was to evaluate the predictive value of high-sensitivity C-reactive protein (hs-CRP) for risk of CIN in patients with acute ST-segment elevation myocardial infarction (STEMI) who were undergoing primary percutaneous coronary intervention (PCI). METHODS: We prospectively observed 165 consenting patients with STEMI undergoing primary PCI. An increase in serum creatinine of more than 0.5 mg/dL from baseline within 48-72 hours of contrast media exposure was defined as CIN. Demographics, traditional risk factors, CIN incidence and other in-hospital clinical outcomes were compared among hs-CRP quartiles. Receiver operator characteristic curves were used to identify the optimal sensitivity for the observed range of hs-CRP. The predictive value of hs-CRP for the risk of CIN was assessed using multivariate logistic regression. RESULTS:CIN occurred in 17 patients (10%). Univariate analysis revealed CIN incidence was significantly associated with hs-CRP, with 2.4% for quartile Q1 (<6.00 mg/L), 2.3% for Q2 (6.00-13.90), 12.5% for Q3 (13.91-32.75) and 24.4% for Q4 (>32.75) (P-trend <0.001), as was in-hospital death (0% for Q1, 2.3% for Q2, 5% for Q3 and 12.2% for Q4; P-trend = 0.009). Receiver operator characteristic curve analysis showed that an hs-CRP of 16.10 mg/L was a fair discriminator for the early creatinine increase (C statistic 0.78). After adjusting for potential confounding predictors, hs-CRP >16.10 mg/L remained significantly associated with CIN (odds ratio = 6.51; 95% confidence interval, 1.26-33.61). CONCLUSION: An hs-CRP >16.10 was a significant and independent predictor of CIN after primary PCI in patients with STEMI.