Heparin-binding protein as a novel biomarker for sepsis-related acute kidney injury

败血症 急性肾损伤 医学 肝素 生物标志物 器官功能障碍 颗粒酶A 发病机制 内科学 免疫学 胃肠病学 颗粒酶B 免疫系统 生物 CD8型 生物化学
作者
Sahra Pajenda,Andreja Figurek,Ludwig Wagner,Daniela Gerges,Alice Schmidt,Harald Herkner,Wolfgang Winnicki
出处
期刊:PeerJ [PeerJ, Inc.]
卷期号:8: e10122-e10122 被引量:5
标识
DOI:10.7717/peerj.10122
摘要

Sepsis-related acute kidney injury (AKI) is associated with high morbidity and mortality among patients. Underlying pathomechanisms include capillary leakage and fluid loss into the interstitial tissue and constant exposure to pathogens results in activation of inflammatory cascades, organ dysfunction and subsequently organ damage.To identify novel factors that trigger sepsis-related acute kidney injury, plasma levels of Granzyme A, as representative of a lymphocyte-derived protease, and heparin-binding protein as indicator for neutrophil-derived mediators, were investigated retrospectively in 60 sepsis patients.While no association was found between plasma levels of lymphocyte-derived Granzyme A and the incidence of sepsis-related AKI, sepsis patients with AKI had significantly higher plasma levels of heparin-binding protein compared to those without AKI. This applies both to heparin-binding protein peak values (43.30 ± 23.34 vs. 30.25 ± 15.63 pg/mL; p = 0.005) as well as mean values (27.93 ± 14.39 vs. 22.02 ± 7.65 pg/mL; p = 0.021). Furthermore, a heparin-binding protein cut-off value of 23.89 pg/mL was established for AKI diagnosis.This study identifies the neutrophil-derived heparin-binding protein as a valuable new biomarker for AKI in sepsis. Beyond the diagnostic perspective, this offers prospect for further research on pathogenesis of AKI and novel therapeutic approaches.
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