Background: Among patients with rhabdomyolysis, the leakage of intracellular skeletal muscle content such as creatine phosphokinase (CPK) into the bloodstream has been associated with an increased risk of acute kidney injury (AKI). We evaluated the possible relationship between serum CPK levels and AKI occurrence among patients with myocyte injury secondary to ST-elevation myocardial infarction (STEMI).
Methods: We retrospectively included 2794 patients with STEMI. Patients were stratified according to peak serum CPK levels into mild (<1000 U/L, n = 1603), moderate (1000-5000 U/L, n = 1111), and severe (>5000 U/L, n = 80) categories. The occurrence of AKI was defined by the KDIGO criteria as an increase in serum creatinine (sCR) ≥0.3 mg/dL within 48 h following PCI. The predictive value of CPK for the risk of AKI occurrence was assessed using multivariate logistic regression models.
Results: The overall occurrence of AKI was 10.4%. Incidence of AKI showed a gradual increase between patients with mild, moderate, and severe serum CPK level elevations (7.8% vs. 11% vs. 26% respectively; p < 0.001). In multivariate logistic regression models, both moderate or higher (OR 1.6, 95% CI 1.1-2.2; p = 0.01) and severe (OR 2.8 95% CI 1.4-5.6; p = 0.004) serum CPK level elevations were independently associated with AKI.
Conclusions: Among STEMI patients, elevated CPK levels were associated with AKI. This association is presumably independent; however, it remains unclear whether it is due to direct toxic (myoglobin-related) or hemodynamic effects (poor left ventricular function). Further studies are required to reveal the underlying mechanism.
Keywords: ST-segment elevation myocardial infarction; acute kidney injury; acute myocardial infarction; creatine phosphokinase.