Koyner Jay L, Coca Steven G, Thiessen-Philbrook Heather, Patel Uptal D, Shlipak Michael G, Garg Amit X, Parikh Chirag R
Section of Nephrology, Department of Medicine, University of Chicago, Pritzker School of Medicine, Chicago, IL.
Department of Internal Medicine, Clinical Epidemiology Research Center, Yale University School of Medicine, New Haven, CT.
Am J Kidney Dis. 2015 Dec;66(6):1006-14. doi: 10.1053/j.ajkd.2015.07.027. Epub 2015 Sep 16.
The interaction between baseline kidney function and the performance of biomarkers of acute kidney injury (AKI) on the development of AKI is unclear.
Post hoc analysis of prospective cohort study.
SETTING & PARTICIPANTS: The 1,219 TRIBE-AKI Consortium adult cardiac surgery cohort participants.
Unadjusted postoperative urinary biomarkers of AKI measured within 6 hours of surgery.
AKI was defined as AKI Network stage 1 (any AKI) or higher, as well as a doubling of serum creatinine level from the preoperative value or the need for post-operative dialysis (severe AKI).
Stratified analyses by preoperative estimated glomerular filtration rate (eGFR) ≤ 60 versus > 60mL/min/1.73m(2).
180 (42%) patients with preoperative eGFRs≤60mL/min/1.73m(2) developed clinical AKI compared with 246 (31%) of those with eGFRs>60mL/min/1.73m(2) (P<0.001). For log2-transformed biomarker concentrations, there was a significant interaction between any AKI and baseline eGFR for interleukin 18 (P=0.007) and borderline significance for liver-type fatty acid binding protein (P=0.06). For all biomarkers, the adjusted relative risk (RR) point estimates for the risk for any AKI were higher in those with elevated baseline eGFRs compared with those with eGFRs≤60mL/min/1.73m(2). However, the difference in magnitude of these risks was low (adjusted RRs were 1.04 [95% CI, 0.99-1.09] and 1.11 [95% CI, 1.07-1.15] for those with preoperative eGFRs≤60mL/min/1.73m(2) and those with higher eGFRs, respectively). Although no biomarker displayed an interaction for baseline eGFR and severe AKI, log2-transformed interleukin 18 and kidney injury molecule 1 had significant adjusted RRs for severe AKI in those with and without baseline eGFRs≤60mL/min/1.73m(2).
Limited numbers of patients with severe AKI and post-operative dialysis.
The association between early postoperative AKI urinary biomarkers and AKI is modified by preoperative eGFR. The degree of this modification and its impact on the biomarker-AKI association is small across biomarkers. Our findings suggest that distinct biomarker cutoffs for those with and without a preoperative eGFR≤60mL/min/1.73m(2) is not necessary.
急性肾损伤(AKI)生物标志物的性能与基线肾功能之间的相互作用对AKI发生发展的影响尚不清楚。
前瞻性队列研究的事后分析。
1219名TRIBE-AKI联盟成人心脏手术队列参与者。
术后6小时内测量的未经调整的AKI术后尿生物标志物。
AKI定义为AKI网络分期1期(任何AKI)或更高,以及血清肌酐水平较术前值翻倍或术后需要透析(严重AKI)。
根据术前估计肾小球滤过率(eGFR)≤60与>60mL/min/1.73m²进行分层分析。
术前eGFR≤60mL/min/1.73m²的患者中有180例(42%)发生临床AKI,而eGFR>60mL/min/1.73m²的患者中有246例(31%)发生临床AKI(P<0.001)。对于经log2转换的生物标志物浓度,白细胞介素18在任何AKI与基线eGFR之间存在显著交互作用(P=0.007),肝型脂肪酸结合蛋白存在临界显著性(P=0.06)。对于所有生物标志物,与eGFR≤60mL/min/1.73m²的患者相比,基线eGFR升高的患者中任何AKI风险的调整后相对风险(RR)点估计值更高。然而,这些风险的大小差异较小(术前eGFR≤60mL/min/1.73m²和eGFR较高的患者的调整后RR分别为1.04[95%CI,0.99-1.09]和1.11[95%CI,1.07-1.15])。虽然没有生物标志物显示出基线eGFR与严重AKI之间的交互作用,但经log2转换的白细胞介素18和肾损伤分子1在基线eGFR≤60mL/min/1.73m²和未≤60mL/min/1.73m²的患者中对严重AKI有显著的调整后RR。
严重AKI和术后透析的患者数量有限。
术前eGFR可改变术后早期AKI尿生物标志物与AKI之间的关联。这种改变的程度及其对生物标志物与AKI关联的影响在各生物标志物中较小。我们的研究结果表明,对于术前eGFR≤60mL/min/1.73m²和未≤60mL/min/1.73m²的患者,无需设置不同的生物标志物临界值。