Cruz Dinna N, Ferrer-Nadal Asunción, Piccinni Pasquale, Goldstein Stuart L, Chawla Lakhmir S, Alessandri Elisa, Belluomo Anello Clara, Bohannon Will, Bove Tiziana, Brienza Nicola, Carlini Mauro, Forfori Francesco, Garzotto Francesco, Gramaticopolo Silvia, Iannuzzi Michele, Montini Luca, Pelaia Paolo, Ronco Claudio
Due to the number of contributing authors, the affiliations are provided in the Supplemental Material.
Clin J Am Soc Nephrol. 2014 Apr;9(4):663-72. doi: 10.2215/CJN.05190513. Epub 2014 Mar 27.
Disease biomarkers require appropriate clinical context to be used effectively. Combining clinical risk factors, in addition to small changes in serum creatinine, has been proposed to improve the assessment of AKI. This notion was developed in order to identify the risk of AKI early in a patient's clinical course. We set out to assess the performance of this combination approach.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: A secondary analysis of data from a prospective multicenter intensive care unit cohort study (September 2009 to April 2010) was performed. Patients at high risk using this combination approach were defined as an early increase in serum creatinine of 0.1-0.4 mg/dl, depending on number of clinical factors predisposing to AKI. AKI was defined and staged using the Acute Kidney Injury Network criteria. The primary outcome was evolution to severe AKI (Acute Kidney Injury Network stages 2 and 3) within 7 days in the intensive care unit.
Of 506 patients, 214 (42.2%) patients had early creatinine elevation and were deemed at high risk for AKI. This group was more likely to subsequently develop the primary endpoint (16.4% versus 1.0% [not at high risk], P<0.001). The sensitivity of this grouping for severe AKI was 92%, the specificity was 62%, the positive predictive value was 16%, and the negative predictive value was 99%. After adjustment for Sequential Organ Failure Assessment score, serum creatinine, and hazard tier for AKI, early creatinine elevation remained an independent predictor for severe AKI (adjusted relative risk, 12.86; 95% confidence interval, 3.52 to 46.97). Addition of early creatinine elevation to the best clinical model improved prediction of the primary outcome (area under the receiver operating characteristic curve increased from 0.75 to 0.83, P<0.001).
Critically ill patients at high AKI risk, based on the combination of clinical factors and early creatinine elevation, are significantly more likely to develop severe AKI. As initially hypothesized, the high-risk combination group methodology can be used to identify patients at low risk for severe AKI in whom AKI biomarker testing may be expected to have low yield. The high risk combination group methodology could potentially allow clinicians to optimize biomarker use.
疾病生物标志物需要在适当的临床背景下才能有效应用。有人提出，除血清肌酐的微小变化外，结合临床风险因素可改善急性肾损伤（AKI）的评估。提出这一概念是为了在患者临床病程早期识别AKI风险。我们着手评估这种联合方法的性能。
设计、地点、参与者及测量指标：对一项前瞻性多中心重症监护病房队列研究（2009年9月至2010年4月）的数据进行二次分析。根据导致AKI的临床因素数量，使用这种联合方法被判定为高风险的患者定义为血清肌酐早期升高0.1 - 0.4mg/dl。AKI根据急性肾损伤网络标准进行定义和分期。主要结局是在重症监护病房内7天内进展为严重AKI（急性肾损伤网络2期和3期）。
506例患者中，214例（42.2%）患者血清肌酐早期升高，被认为有AKI高风险。该组随后更有可能发生主要终点事件（16.4% 对比1.0%[非高风险]，P<0.001）。这种分组对严重AKI的敏感性为92%，特异性为62%，阳性预测值为16%，阴性预测值为99%。在对序贯器官衰竭评估评分、血清肌酐和AKI风险等级进行校正后，血清肌酐早期升高仍然是严重AKI的独立预测因素（校正相对风险，12.86；95%置信区间，3.52至46.97）。将血清肌酐早期升高添加到最佳临床模型中可改善对主要结局的预测（受试者操作特征曲线下面积从0.75增加到0.83，P<0.001）。
基于临床因素和血清肌酐早期升高的组合，AKI高风险的危重症患者发生严重AKI的可能性显著更高。如最初假设的那样，高风险组合组方法可用于识别严重AKI低风险患者，在这些患者中AKI生物标志物检测可能预期产率较低。高风险组合组方法可能使临床医生优化生物标志物的使用。
