败血症相关急性肾损伤的基于生物标志物的诊断和风险分层：从分子机制到多标志物面板
Biomarker-Based Diagnosis and Risk Stratification in Sepsis-Associated Acute Kidney Injury: From Molecular Mechanisms to Multimarker Panels.
摘要(中文译文)
脓毒症相关急性肾损伤（SA-AKI）在危重症患者中仍是一项重大诊断挑战，因为传统的功能性标准——血清肌酐和尿量——往往在临床相关的病理生理紊乱已经发生后才能检出AKI。越来越多的证据表明，SA-AKI反映的是一个异质性过程，其特征为在明显的功能下降之前已出现早期细胞应激、微循环功能障碍、炎症相关损伤以及适应不良性修复。在此背景下，基于生物标志物的方法已被研究用于改善脓毒症患者的早期风险分层、表型特征描述和预后评估。本叙述性综述综合了与SA-AKI相关的已确立和新兴生物标志物的当前证据，涵盖应激标志物（[TIMP-2]•[IGFBP7]）、肾小管损伤标志物（如NGAL、KIM-1、IL-18）、功能标志物（如脑啡肽原/penKid、胱抑素C），以及探索性分子特征如循环microRNA（miRNA）。我们审视了它们在脓毒症中的时间动态、性能估计和情境依赖性适用性，并讨论了与异质性、检测变异性和阈值标准化相关的局限性。特别关注了将生物标志物与KDIGO标准及临床表型相结合的多模态和纵向策略。最后，我们勾勒了一个锚定于病理生理窗口和临床决策点的SA-AKI生物标志物分层解读框架。尽管现有证据支持所选生物标志物在短期风险分层和轨迹评估方面的潜力，但其临床应用需要前瞻性验证，以证明其超越现有模型的增量价值以及对以患者为中心结局的可测量影响。
Abstract
Sepsis-associated acute kidney injury (SA-AKI) remains a major diagnostic challenge in critically ill patients, as conventional functional criteria-serum creatinine and urine output-often detect AKI after clinically relevant pathophysiological derangement has already evolved. Increasing evidence suggests that SA-AKI reflects a heterogeneous process characterized by early cellular stress, microcirculatory dysfunction, inflammation-associated injury, and maladaptive repair preceding overt functional decline. In this context, biomarker-based approaches have been investigated to improve early risk stratification, phenotypic characterization, and prognostic assessment in septic patients. This narrative review synthesizes current evidence on established and emerging biomarkers relevant to SA-AKI, encompassing stress markers ([TIMP-2]•[IGFBP7]), tubular injury markers (e.g., NGAL, KIM-1, IL-18), functional markers (e.g., proenkephalin/penKid, cystatin C), and exploratory molecular signatures such as circulating microRNAs (miRNAs). We examine their temporal dynamics, performance estimates, and context-dependent applicability in sepsis, and discuss limitations related to heterogeneity, assay variability, and threshold standardization. Particular attention is given to multimodal and longitudinal strategies integrating biomarkers with KDIGO criteria and clinical phenotyping. Finally, we outline a stratified framework for biomarker interpretation in SA-AKI anchored to pathophysiological windows and clinical decision points. While available evidence supports the potential of selected biomarkers for short-term risk stratification and trajectory assessment, implementation requires prospective validation demonstrating incremental value beyond established models and measurable impact on patient-centered outcomes.
如何引用
AMA
Breallan De Jesús Romero Pajaro, Diana Carolina Caicedo Sánchez, Michael Mario Vélez Lora, John Freddy Mina Gasca, Damián Alberto Ochoa Guette, Geraldine Romero Martínez, et al. Biomarker-Based Diagnosis and Risk Stratification in Sepsis-Associated Acute Kidney Injury: From Molecular Mechanisms to Multimarker Panels.. Diagnostics (Basel, Switzerland). 2026; doi:10.3390/diagnostics16091262.
APA
Breallan De Jesús Romero Pajaro, Diana Carolina Caicedo Sánchez, Michael Mario Vélez Lora, John Freddy Mina Gasca, Damián Alberto Ochoa Guette, Geraldine Romero Martínez, et al (2026). Biomarker-Based Diagnosis and Risk Stratification in Sepsis-Associated Acute Kidney Injury: From Molecular Mechanisms to Multimarker Panels.. Diagnostics (Basel, Switzerland). https://doi.org/10.3390/diagnostics16091262
GB/T 7714
Breallan De Jesús Romero Pajaro, Diana Carolina Caicedo Sánchez, Michael Mario Vélez Lora, John Freddy Mina Gasca, Damián Alberto Ochoa Guette, Geraldine Romero Martínez, et al. Biomarker-Based Diagnosis and Risk Stratification in Sepsis-Associated Acute Kidney Injury: From Molecular Mechanisms to Multimarker Panels.[J]. Diagnostics (Basel, Switzerland), 2026 doi:10.3390/diagnostics16091262.
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