Gleeson Patrick James, Crippa Ilaria Alice, Sannier Aurélie, Koopmansch Caroline, Bienfait Lucie, Allard Justine, Sexton Donal J, Fontana Vito, Rorive Sandrine, Vincent Jean-Louis, Creteur Jacques, Taccone Fabio Silvio
Department of Intensive Care Medicine, Hôpital Erasme, Université Libre de Bruxelles, Brussels, Belgium.
Université de Paris Cité, INSERM UMR1149 & CNRS EMR8252, Centre de Recherche sur l'Inflammation, Inflamex Laboratory of Excellence, Paris, France.
Clin Kidney J. 2023 May 22;16(10):1664-1673. doi: 10.1093/ckj/sfad113. eCollection 2023 Oct.
Acute kidney injury (AKI) requiring renal replacement therapy (RRT) in the intensive care unit (ICU) portends a poor prognosis. We aimed to better characterize predictors of survival and the mechanism of kidney failure in these patients.
This was a retrospective observational study using clinical and radiological electronic health records, analysed by univariable and multivariable binary logistic regression. Histopathological examination of post-mortem renal tissue was performed.
Among 157 patients with AKI requiring RRT, higher serum creatinine at RRT initiation associated with increased ICU survival [odds ratio (OR) 0.33, 95% confidence interval (CI) 0.17-0.62, = .001]; however, muscle mass (a marker of frailty) interacted with creatinine ( = .02) and superseded creatinine as a predictor of survival (OR 0.26, 95% CI 0.08-0.82; = .02). Achieving lower cumulative fluid balance (mL/kg) predicted ICU survival (OR 1.01, 95% CI 1.00-1.01, < .001), as supported by sensitivity analyses showing improved ICU survival with the use of furosemide (OR 0.40, 95% CI 0.18-0.87, = .02) and increasing net ultrafiltration (OR 0.97, 95% CI 0.95-0.99, = .02). A urine output of >500 mL/24 h strongly predicted successful liberation from RRT (OR 0.125, 95% CI 0.05-0.35, < .001). Post-mortem reports were available for 32 patients; clinically unrecognized renal findings were described in 6 patients, 1 of whom had interstitial nephritis. Experimental staining of renal tissue from patients with sepsis-associated AKI (S-AKI) showed glomerular loss of synaptopodin ( = .02).
Confounding of creatinine by muscle mass undermines its use as a marker of AKI severity in clinical studies. Volume management and urine output are key determinants of outcome. Loss of synaptopodin implicates glomerular injury in the pathogenesis of S-AKI.
在重症监护病房（ICU）中，需要肾脏替代治疗（RRT）的急性肾损伤（AKI）预示着预后不良。我们旨在更好地描述这些患者生存的预测因素及肾衰竭的机制。
这是一项回顾性观察性研究，使用临床和放射学电子健康记录，通过单变量和多变量二元逻辑回归进行分析。对尸检肾组织进行组织病理学检查。
在157例需要RRT的AKI患者中，RRT开始时较高的血清肌酐水平与ICU生存率增加相关[比值比（OR）0.33，95%置信区间（CI）0.17 - 0.62，P = 0.001]；然而，肌肉量（衰弱的一个标志物）与肌酐存在相互作用（P = 0.02），并取代肌酐成为生存的预测因素（OR 0.26，95%CI 0.08 - 0.82；P = 0.02）。实现更低的累积液体平衡（mL/kg）可预测ICU生存（OR 1.01，95%CI 1.00 - 1.01，P < 0.001），敏感性分析支持这一点，该分析显示使用呋塞米可改善ICU生存（OR 0.40，95%CI 0.18 - 0.87，P = 0.02）以及增加净超滤量（OR 0.97，95%CI 0.95 - 0.99，P = 0.02）。尿量>500 mL/24 h强烈预测RRT成功脱机（OR 0.125，95%CI 0.05 - 0.35，P < 0.001）。32例患者有尸检报告；6例患者描述了临床上未识别的肾脏发现，其中1例患有间质性肾炎。脓毒症相关AKI（S - AKI）患者肾组织的实验性染色显示突触素在肾小球丢失（P = 0.02）。
肌肉量对肌酐的混淆作用削弱了其在临床研究中作为AKI严重程度标志物的用途。容量管理和尿量是结局的关键决定因素。突触素的丢失提示肾小球损伤在S - AKI发病机制中起作用。
