Connolly M, McEneaney D, Menown Ian, Morgan N, Harbinson M
From the *Cardiovascular Research Unit, Craigavon Cardiac Centre, Southern Trust, Northern Ireland, United Kingdom; †Department of Nephrology, Daisy Hill Hospital, Southern Trust, Northern Ireland, United Kingdom; and ‡Centre for Experimental Medicine, Queens University Belfast, Northern Ireland, United Kingdom.
Cardiol Rev. 2015 Sep-Oct;23(5):240-6. doi: 10.1097/CRD.0000000000000058.
Acute kidney injury (AKI), defined as a rise in serum creatinine of greater than 25% from baseline measured at 48 hours after renal insult, may follow iodinated contrast coronary angiography. Termed contrast-induced nephropathy, it can result in considerable morbidity and mortality. Measurement of serum creatinine as a functional biomarker of glomerular filtration rate is widely used for detection of AKI, but it lacks sensitivity for the early diagnosis of AKI (typically rising 24 hours after functional loss) and, as a solely functional marker of glomerular filtration rate, is unable to differentiate among the various causes of AKI. These intrinsic limitations to creatinine measurement and the recognition that improved clinical outcomes are linked to a more timely diagnosis of AKI, has led investigators to search for novel biomarkers of "early" kidney injury. Several studies have investigated the utility of renal injury biomarkers in a variety of clinical settings including angiography/percutaneous coronary intervention, coronary artery bypass graft surgery, sepsis in intensive care patients, and pediatric cardiac surgery. In this article, we discuss the use of iodinated contrast for coronary procedures and the risk factors for contrast-induced nephropathy, followed by a review the potential diagnostic utility of several novel biomarkers of early AKI in the clinical settings of coronary angiography/percutaneous coronary intervention. In particular, we discuss neutrophil gelatinase associated lipocalin in depth. If validated, such biomarkers would facilitate earlier AKI diagnosis and improve clinical outcomes.
急性肾损伤（AKI）定义为肾损伤后48小时测得的血清肌酐较基线水平升高超过25%，碘造影剂冠状动脉造影后可能会发生AKI。这种情况被称为造影剂肾病，可导致相当高的发病率和死亡率。血清肌酐作为肾小球滤过率的功能性生物标志物，被广泛用于检测AKI，但它对AKI的早期诊断缺乏敏感性（通常在功能丧失24小时后才升高），而且作为肾小球滤过率的单一功能性标志物，无法区分AKI的各种病因。肌酐测量存在这些内在局限性，以及认识到改善临床结局与更及时诊断AKI相关，促使研究人员寻找“早期”肾损伤的新型生物标志物。多项研究在包括血管造影/经皮冠状动脉介入治疗、冠状动脉搭桥手术、重症监护患者的脓毒症以及小儿心脏手术等多种临床环境中，对肾损伤生物标志物的效用进行了研究。在本文中，我们讨论冠状动脉造影术中碘造影剂的使用以及造影剂肾病的危险因素，随后回顾几种早期AKI新型生物标志物在冠状动脉造影/经皮冠状动脉介入治疗临床环境中的潜在诊断效用。特别是，我们将深入讨论中性粒细胞明胶酶相关脂质运载蛋白。如果得到验证，此类生物标志物将有助于更早诊断AKI并改善临床结局。
