Predictive Value of Point-of-Care Proenkephalin for Worsening Renal Function and Mortality in Patients Presenting to Emergency Department with Acute Heart Failure

床旁检测前脑啡肽对因急性心力衰竭就诊于急诊科的患者肾功能恶化和死亡率的预测价值

阅读:1

Abstract

Background: Enkephalins are endogenous opioid peptides that modulate cardiovascular and renal function and are overexpressed in patients with acute heart failure (AHF). Although biologically active enkephalins lack a favorable biomarker profile, their stable surrogate proenkephalin 119-159 (PENK) appears to display prognostic value in AHF settings. The aim of the present study was to evaluate the role of point-of-care (POC) PENK in predicting mortality and worsening renal function (WRF) in patients presenting to the emergency department (ED) with AHF. Methods: In this single-center observational study, 107 patients presenting to the ED with AHF were prospectively enrolled. We measured PENK levels upon ED presentation with a commercially available POC immunoassay and investigated their association with WRF within 48 h and all-cause mortality during a 1-year follow-up. Results: The patients had a mean age of 72 ± 13 years, and 58% were men. Moreover, 62% had acutely decompensated chronic heart failure (HF), 24% had pulmonary edema, 9% had cardiogenic shock, and 5% had right HF. The median PENK levels were 111 [60-193] pmol/L. PENK was independently associated with WRF (adjusted OR, 95% CI: 15.4 [2.0-120.2]; p = 0.009), with levels of ≥90.5 pmol/L identified as the optimal cut-off for predicting WRF (AUC: 0.690; p < 0.001). PENK was also an independent predictor of short- and long-term all-cause mortality, with an optimal cut-off of ≥95.8 pmol/L (AUC for 30-day, 90-day, and 1-year mortality: 0.717, 0.723, and 0.724, respectively; all p < 0.001). Conclusions: In patients presenting to the ED with AHF, POC PENK may serve as an early prognostic marker of WRF and short- and long-term mortality.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。