We assessed the relation between platelet-to-lymphocyte ratio (PLR) on admission and contrast-induced nephropathy (CIN) in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). A total of 488 patients with NSTE-ACS who underwent urgent coronary angiography were enrolled. Levels of PLR and creatinine were measured before angiography and at 72 hours after angiography. Patients were divided into 2 groups, namely, the CIN group, 80 patients (16.3%; age 65.3 ± 12.5years; 66.7% men) and the non-CIN group, 408 patients (83.7%; age 61.2 ± 12.3 years; 72.5% men). Patients in the CIN group had significantly higher PLR than those in the non-CIN group (152.9 ± 99.6 vs 120.4 ± 66.1, P < .001). In logistic regression analysis, PLR (odds ratio [OR] 1.004, 95% confidence interval [CI] 1.001-1.007, P = .02), diabetes mellitus (OR 1.75, 95% CI 1.02-2.98, P = .03), and ST-segment depression on admission electrocardiogram (OR 1.68, 95% CI 1.00-2.81, P = .04) were independent predictors of CIN. The PLR was an independent predictor of CIN after angiography in patients with NSTE-ACS.

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Contrast-induced acute kidney injury (CI-AKI) is associated with increased mortality, morbidity, and prolonged hospitalization. Patients with acute coronary syndrome (ACS) have a 3-fold higher risk of developing CI-AKI. The aim of our study was to evaluate the predictors of CI-AKI and long-term prognosis in patients with ACS who developed CI-AKI (1083 patients were enrolled). Contrast-induced acute kidney injury was defined as an increase of ≥0.5 mg/dL and/or an increase of ≥25% of pre-percutaneous coronary intervention (PCI) to post-PCI serum creatinine levels within 48 to 72 hours after the procedure. Primary end point was defined as all-cause mortality, myocardial infarction, and cerebrovascular event at long-term follow-up (36 ± 12 months). Contrast-induced acute kidney injury occurred in 178 (16.4%) of the 1083 patients. The primary end points were significantly high in patients with ACS who developed CI-AKI ( P < .001). The occurrence of CI-AKI was identified as an independent predictor of primary end point. Risk of CI-AKI development was more frequently seen in patients with ACS. Also, patients who developed CI-AKI have worse prognosis at long-term follow-up. Additional preventive treatment strategies need to be developed in this group of patients.

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