BACKGROUND: The association between contrast-induced acute kidney injury (CI-AKI) and chronic kidney disease (CKD) in patients with acute coronary syndrome (ACS) treated with percutaneous coronary intervention (PCI) has not been fully reported. We evaluated the association of CI-AKI on cardiovascular events in ACS patients with CKD. METHODS: A total of 1059 ACS patients who underwent emergent PCI in our multicenter registry were enrolled (69±12 years, 804 men, 604 STEMI patients). CKD was defined as at least stage 3 CKD, and CI-AKI was defined as an increase of at least 0.5 mg/dL and/or an increase of at least 25% of pre-PCI to post-PCI serum creatinine levels within 1 week after the procedure. Primary endpoints included cardiovascular death, myocardial infarction, and cerebrovascular disorder (stroke or transient ischemic attack). RESULTS: In our study, 368 (34.7%) patients had CKD. During follow-up periods (435±330 days), CI-AKI and primary endpoints occurred in 164 (15.5%) patients and 106 (10.0%) patients, respectively. Multivariate Cox proportional hazards model revealed that age, female gender, peak creatinine kinase>4000, IABP use, CI-AKI (hazard ratio [HR], 2.17; 95% confidential interval [CI], 1.52 to 4.00; P<0.001), and CKD (HR, 1.66; 95% CI, 1.01 to 2.72; P=0.046) were independent predictors of primary endpoints. Kaplan-Meier analysis showed that occurrence of primary endpoints increased significantly with an increase in CKD stage, and CI-AKI yielded worse long-term prognosis at every stage of CKD (P<0.001). CONCLUSIONS: CI-AKI was revealed to be a significant incremental predictor of cardiovascular events at each stage of CKD in ACS patients.
BACKGROUND: The association between contrast-induced acute kidney injury (CI-AKI) and chronic kidney disease (CKD) in patients with acute coronary syndrome (ACS) treated with percutaneous coronary intervention (PCI) has not been fully reported. We evaluated the association of CI-AKI on cardiovascular events in ACS patients with CKD. METHODS: A total of 1059 ACS patients who underwent emergent PCI in our multicenter registry were enrolled (69±12 years, 804 men, 604 STEMI patients). CKD was defined as at least stage 3 CKD, and CI-AKI was defined as an increase of at least 0.5 mg/dL and/or an increase of at least 25% of pre-PCI to post-PCI serum creatinine levels within 1 week after the procedure. Primary endpoints included cardiovascular death, myocardial infarction, and cerebrovascular disorder (stroke or transient ischemic attack). RESULTS: In our study, 368 (34.7%) patients had CKD. During follow-up periods (435±330 days), CI-AKI and primary endpoints occurred in 164 (15.5%) patients and 106 (10.0%) patients, respectively. Multivariate Cox proportional hazards model revealed that age, female gender, peak creatinine kinase>4000, IABP use, CI-AKI (hazard ratio [HR], 2.17; 95% confidential interval [CI], 1.52 to 4.00; P<0.001), and CKD (HR, 1.66; 95% CI, 1.01 to 2.72; P=0.046) were independent predictors of primary endpoints. Kaplan-Meier analysis showed that occurrence of primary endpoints increased significantly with an increase in CKD stage, and CI-AKI yielded worse long-term prognosis at every stage of CKD (P<0.001). CONCLUSIONS: CI-AKI was revealed to be a significant incremental predictor of cardiovascular events at each stage of CKD in ACS patients.