TY - JOUR
T1 - Relation between Serum Creatine Phosphokinase Levels and Acute Kidney Injury among ST-Segment Elevation Myocardial Infarction Patients
AU - Zahler, David
AU - Rozenfeld, Keren Lee
AU - Merdler, Ilan
AU - Itach, Tamar
AU - Morgan, Samuel
AU - Levit, Dana
AU - Banai, Shmuel
AU - Shacham, Yacov
N1 - Publisher Copyright:
© 2022 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2022/2/21
Y1 - 2022/2/21
N2 - 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.
AB - 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.
KW - Acute kidney injury
KW - Acute myocardial infarction
KW - Creatine phos-phokinase
KW - ST-segment elevation myocardial infarction
UR - http://www.scopus.com/inward/record.url?scp=85124960726&partnerID=8YFLogxK
U2 - 10.3390/jcm11041137
DO - 10.3390/jcm11041137
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C2 - 35207410
AN - SCOPUS:85124960726
SN - 2077-0383
VL - 11
JO - Journal of Clinical Medicine
JF - Journal of Clinical Medicine
IS - 4
M1 - 1137
ER -