Griffin Benjamin R, Gist Katja M, Faubel Sarah
Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Department of Pediatrics, The Heart Institute, University of Colorado, Aurora, CO, USA.
J Intensive Care Med. 2020 May;35(5):415-424. doi: 10.1177/0885066618824531. Epub 2019 Jan 17.
Acute kidney injury (AKI) is a common and serious medical condition associated with significant increases in morbidity, mortality, and cost of care. Because of the high incidence and poor outcomes associated with AKI, there has been significant interest in the development of new therapies for the prevention and treatment of the disease. A lack of efficacy in drug trials led to the concern that AKI was not being diagnosed early enough for an effective intervention and that a rise in serum creatinine itself is not a sensitive-enough marker. Researchers have been searching for novel biomarkers that can not only assess a decline in kidney function but also demonstrate structural damage to the kidney and at time points earlier than increases in serum creatinine measurements allow. Over the past 10 years, there have been 3300 new publications and hundreds of new biomarkers investigated, yet concern still remains regarding AKI biomarker performance. The AKI biomarkers are yet to be widely utilized in clinical practice, leading some to question whether AKI biomarkers will ever reach their initial promise. However, we believe that biomarkers are an important part of current and future AKI research and clinical management. In this review, we compare the historical contexts of acute myocardial ischemia and AKI biomarker development to illustrate the progress that has been made within AKI biomarker research in a relatively short period of time and also to point out key differences between the disease processes that have been barriers to widespread AKI biomarker adoption. Finally, we discuss potential paths by which biomarkers can lead to appropriate AKI treatment responses that lower morbidity and mortality.
急性肾损伤(AKI)是一种常见且严重的病症,与发病率、死亡率及护理成本的显著增加相关。由于AKI的高发病率和不良预后,人们对开发预防和治疗该疾病的新疗法有着浓厚兴趣。药物试验缺乏疗效引发了人们的担忧,即AKI未得到足够早的诊断以进行有效干预,且血清肌酐升高本身并非足够敏感的标志物。研究人员一直在寻找新型生物标志物,这些标志物不仅可以评估肾功能下降,还能在血清肌酐测量值升高之前的时间点显示肾脏的结构损伤。在过去10年中,已有3300篇新出版物,研究了数百种新生物标志物,但对于AKI生物标志物的性能仍存在担忧。AKI生物标志物尚未在临床实践中广泛应用,这使得一些人质疑AKI生物标志物是否能实现其最初的承诺。然而,我们认为生物标志物是当前和未来AKI研究及临床管理的重要组成部分。在本综述中,我们比较了急性心肌缺血和AKI生物标志物开发的历史背景,以说明在相对较短的时间内AKI生物标志物研究取得的进展,并指出疾病过程之间的关键差异,这些差异一直是AKI生物标志物广泛应用的障碍。最后,我们讨论了生物标志物可导致适当的AKI治疗反应从而降低发病率和死亡率的潜在途径。