Acute Kidney Injury after Primary Angioplasty: Is Contrast Induced Nephropathy the Culprit?

Background: Acute kidney injury (AKI) following primary PCI is frequently interpreted as contrast-induced AKI (CI-AKI). However, in the setting of ST-elevation myocardial infarction (STEMI), AKI may be the result of other contributing factors.

Methods and Results: We studied 960 STEMI patients who underwent primary PCI and 1025 patients receiving fibrinolysis or no reperfusion (control group). The incidence of AKI (defined as serum creatinine of ≥0.5 mg/dL or a >25% rise within 72h after contrast exposure) was not significantly different between the primary PCI and control group (10.8% vs. 12.1%, respectively; P=0.38). In the PPCI cohort, independent predictors of AKI included age≥70, hypertension, anterior infarction, baseline eGFR, higher Killip class and cardiogenic shock, but not to contrast-media dose. A risk score based on the PPCI cohort had similar discriminatory capacity for AKI in the control group (c-statistic 0.79±0.03 and 0.78±0.02, respectively; P=0.80). A linear mixed model demonstrated that the increase in serum creatinine with primary PCI was 0.042 mg/dL (95% confidence interval [CI] 0.027–0.057) with each day and 0.027 mg/dL (95% CI 0.015–0.039) in the non-PCI group (P = 0.44). AKI was associated with similar risk for death, reinfarction and readmission for heart failure with (adjusted HR 1.77; 95% CI 1.40–2.26; P<0.0001) and without (HR 2.15; 95% CI 1.39–3.40; P=0.001) PPCI (P for interaction = 0.45).

Conclusions: The development of AKI in STEMI undergoing primary PCI is independent of contrast material exposure. AKI risk in STEMI patients is mainly related to baseline eGFR, heart failure and hemodynamic instability.