Soto-Fajardo Juan M, Castillo-Avalos Valeria J, Hernandez-Paredes Elisa Naomi, Santillán-Cerón Airy, Gaytan-Arocha Jorge E, Vega-Vega Olynka, Uribe Norma, Correa-Rotter Ricardo, Ramirez-Sandoval Juan C
Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Department of Pathology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Int J Nephrol. 2022 Apr 26;2022:8556793. doi: 10.1155/2022/8556793. eCollection 2022.
Acute kidney injury (AKI) is a common complication of COVID-19. Several etiologies have been identified, including pigment deposition likely associated with myopathic damage. Nevertheless, the relationship between longitudinal creatine-kinase trends and renal outcomes is uncertain.
To correlate longitudinal changes in serum creatine-kinase levels with hospital-acquired AKI (beyond 48 h of hospital admission) in severe COVID-19 patients.
This is a retrospective cohort study, and creatine-kinase levels were assessed over time in 1551 hospitalized patients with normal renal function at the time of hospital admission.
In subjects who developed hospital-acquired AKI ( = 126, 8.1%), the serum creatine-kinase concentration before AKI onset was not different when compared to patients without AKI (slope of log creatine-kinase/day = -0.09 [95% CI -0.17 to +0.19] vs. +0.03 [95% CI -0.1 to +0.1]). After AKI diagnosis, serum creatine-kinase levels showed a significantly ascendent slope (slope of log creatine-kinase/day after AKI diagnosis = +0.14; 95% CI + 0.05 to +0.3). The AKI evolution was the main factor associated with the creatine-kinase trend. Subjects with persistent AKI ( = 40, 32%) had rising creatine-kinase levels during hospitalization (slope of log creatine-kinase/day = +0.30 95% CI + 0.19 to +0.51). A rising creatine-kinase trend ( = 114, 8%) was associated with a 1.89-fold higher risk of in-hospital death (95% CI 1.14 to 3.16). Nevertheless, this association disappeared after adjusting AKI evolution and LDH baseline levels.
In severe COVID-19 patients, a slight increase in creatine-kinase levels was observed after AKI occurrence but not before. Our results show that, at least for the appearance of hospital-acquired AKI, the CK rise does not meet the temporality criterion of causality regarding the occurrence of AKI. Rising creatine-kinase trends were associated with a higher risk of mortality, but this association was modified by AKI evolution and inflammation. There is a limited efficiency for AKI prognosis in the serial follow-up of CK levels in severe COVID-19 patients with normal renal function.
急性肾损伤(AKI)是新型冠状病毒肺炎(COVID-19)的常见并发症。已确定多种病因,包括可能与肌病损伤相关的色素沉着。然而,肌酸激酶纵向变化趋势与肾脏结局之间的关系尚不确定。
将重症COVID-19患者血清肌酸激酶水平的纵向变化与医院获得性AKI(入院48小时后)相关联。
这是一项回顾性队列研究,对1551例入院时肾功能正常的住院患者的肌酸激酶水平进行了随时间评估。
在发生医院获得性AKI的患者(n = 126,8.1%)中,与未发生AKI的患者相比,AKI发作前的血清肌酸激酶浓度无差异(肌酸激酶对数/天斜率=-0.09 [95%CI -0.17至+0.19] 对比 +0.03 [95%CI -0.1至+0.1])。AKI诊断后,血清肌酸激酶水平呈现显著上升斜率(AKI诊断后肌酸激酶对数/天斜率=+0.14;95%CI +0.05至+0.3)。AKI的进展是与肌酸激酶趋势相关的主要因素。持续性AKI患者(n = 40,32%)在住院期间肌酸激酶水平升高(肌酸激酶对数/天斜率=+0.30,95%CI +0.19至+0.51)。肌酸激酶趋势上升(n = 114,8%)与院内死亡风险高1.89倍相关(95%CI 1.14至3.16)。然而,在调整AKI进展和乳酸脱氢酶基线水平后,这种关联消失。
在重症COVID-19患者中,AKI发生后观察到肌酸激酶水平略有升高,但发生前未观察到。我们的结果表明,至少对于医院获得性AKI的出现,肌酸激酶升高不符合AKI发生因果关系的时间标准。肌酸激酶趋势上升与较高的死亡风险相关,但这种关联因AKI进展和炎症而改变。对肾功能正常的重症COVID-19患者进行肌酸激酶水平的系列随访,对AKI预后的预测效率有限。