Zahler David, Rozenfeld Keren-Lee, Merdler Ilan, Itach Tamar, Morgan Samuel, Levit Dana, Banai Shmuel, Shacham Yacov
Department of Cardiology, Tel-Aviv Sourasky Medical Center Affiliated to the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv 64239, Israel.
Internal Medicine Department H, Tel-Aviv Sourasky Medical Center Affiliated to the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv 64239, Israel.
J Clin Med. 2022 Feb 21;11(4):1137. doi: 10.3390/jcm11041137.
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).
We retrospectively included 2794 patients with STEMI. Patients were stratified according to peak serum CPK levels into mild (<1000 U/L, = 1603), moderate (1000-5000 U/L, = 1111), and severe (>5000 U/L, = 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.
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; < 0.001). In multivariate logistic regression models, both moderate or higher (OR 1.6, 95% CI 1.1-2.2; = 0.01) and severe (OR 2.8 95% CI 1.4-5.6; = 0.004) serum CPK level elevations were independently associated with AKI.
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.
在横纹肌溶解症患者中,细胞内骨骼肌成分如肌酸磷酸激酶(CPK)泄漏到血液中与急性肾损伤(AKI)风险增加有关。我们评估了ST段抬高型心肌梗死(STEMI)继发心肌细胞损伤患者血清CPK水平与AKI发生之间的可能关系。
我们回顾性纳入了2794例STEMI患者。根据血清CPK峰值水平将患者分为轻度(<1000 U/L,n = 1603)、中度(1000 - 5000 U/L,n = 1111)和重度(>5000 U/L,n = 80)三类。AKI的发生根据KDIGO标准定义为PCI后48小时内血清肌酐(sCR)升高≥0.3 mg/dL。使用多因素逻辑回归模型评估CPK对AKI发生风险的预测价值。
AKI的总体发生率为10.4%。AKI的发生率在血清CPK水平轻度、中度和重度升高的患者中呈逐渐上升趋势(分别为7.8%、11%和26%;P < 0.001)。在多因素逻辑回归模型中,中度或更高水平(OR 1.6,95% CI 1.1 - 2.2;P = 0.01)和重度(OR 2.8,95% CI 1.4 - 5.6;P = 0.004)的血清CPK水平升高均与AKI独立相关。
在STEMI患者中,CPK水平升高与AKI相关。这种关联可能是独立的;然而,尚不清楚这是由于直接毒性(与肌红蛋白相关)还是血流动力学效应(左心室功能不良)。需要进一步研究以揭示潜在机制。