血清肝素结合蛋白在脓毒血症患者急性肾衰竭过程中的表达与意义
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摘要
目的探讨血清肝素结合蛋白(HBP)在脓毒血症患者急性肾衰竭过程中的表达与意义,了解其临床价值。方法选取2014年9月～2017年9月于首都医科大学附属北京潞河医院急诊就诊的124例脓毒血症患者,根据是否发生急性肾衰竭分为脓毒血症急性肾衰竭组42例(A组),脓毒血症无急性肾衰竭组82例(B组),另选取非脓毒血症急性肾衰竭患者60例(C组),以及60名健康志愿者(D组)作为健康对照组。每组分别在入院24 h内及在相应治疗后采集静脉血,测定血清中HBP和血肌酐浓度水平。结果治疗前,脓毒血症患者与健康对照组比较,A组和B组HBP水平明显高于C组和D组(P <0.05),而发生急性肾衰竭的A组血清中HBP浓度较B组明显升高(P <0.05)。治疗后,只有A组HBP水平有明显下降(P <0.05)。结论 HBP可作为评估脓毒血症患者急性肾衰竭的发生指标,也可作为评价其治疗效果的一种方法。
Objective To investigate the purpose of this study was to investigate the expression and significance of serum heparin binding protein(HBP) in the process of acute renal failure in patients with sepsis and to understand its clinical value. Methods From September 2014 to September 2015, 124 patients with sepsis admitted to the emergency Department of Beijing Luhe Hospital Affiliated to Capital Medical University were selected. According to the occurrence of acute renal failure, 42 patients in the acute renal failure group with sepsis(group A), 82 patients in the group without acute renal failure group with sepsis(group B), 60 patients with acute renal failure without sepsis(group C),and 60 healthy volunteers(group D) were selected as the healthy control group. Venous blood was collected in each group within 24 h after admission and after corresponding treatment, and serum HBP and serum creatinine concentrations were measured. Results Before treatment, compared with the healthy control group, the HBP level of group A and group B was significantly higher than that of group C and group D(P < 0.05), while the serum HBP level of group A with acute renal failure was significantly higher than that of group B(P < 0.05). After treatment, only group A showed A significant decrease in HBP level(P < 0.05). Conclusion HBP can be used as a method to evaluate the occurrence of acute renal failure in patients with sepsis and to evaluate its therapeutic effect.
Objective To investigate the purpose of this study was to investigate the expression and significance of serum heparin binding protein(HBP) in the process of acute renal failure in patients with sepsis and to understand its clinical value. Methods From September 2014 to September 2015, 124 patients with sepsis admitted to the emergency Department of Beijing Luhe Hospital Affiliated to Capital Medical University were selected. According to the occurrence of acute renal failure, 42 patients in the acute renal failure group with sepsis(group A), 82 patients in the group without acute renal failure group with sepsis(group B), 60 patients with acute renal failure without sepsis(group C),and 60 healthy volunteers(group D) were selected as the healthy control group. Venous blood was collected in each group within 24 h after admission and after corresponding treatment, and serum HBP and serum creatinine concentrations were measured. Results Before treatment, compared with the healthy control group, the HBP level of group A and group B was significantly higher than that of group C and group D(P < 0.05), while the serum HBP level of group A with acute renal failure was significantly higher than that of group B(P < 0.05). After treatment, only group A showed A significant decrease in HBP level(P < 0.05). Conclusion HBP can be used as a method to evaluate the occurrence of acute renal failure in patients with sepsis and to evaluate its therapeutic effect.
引文
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[17]Linder A,Akesson P,Inghammar M,et al.Elevated plasma levels of heparin-binding protein in intensive care unit patients with severe sepsis and septic shock[J].Crit Care,2012,16(3):R90.
[18]Olofsson AM,Vestberg M,Herwald H,et al.Heparinbinding protein targeted to mitochondrial compartments protects endothelial cells from apoptosis[J].J Clin Invest,1999,104(7):885-894.
[19]Fjell CD,Thair S,Hsu JL,et al.Cytokines and signaling molecules predict clinical outcomes in sepsis[J].PLo SOne,2013,8(11):e79207.
[20]Lee TD,Gonzalez m L,Kumar P,et al.CAP37,a nertrophilderived inflammatory mediator,augments leukocyte adhesion to endothelial monolayers[J].Microcasc Res,2003,66(1):38-48.
[2]Cornet AD,Smit EG,Beishuizen A,et al.The role of heparin and allied compounds in the treatment of sepsis[J].Thromb Haemost,2007,98(3):579-586.
[3]Ostergaard E,Flodgaard H.A neutrophil-derived proteolytic inactive elastase homologue(h HBP)mediates reversible contraction of fibroblasts and endothelial cell monolayers and stimulates monocyte survival and thrombospondin secretion[J].J Leukoc Biol,1992,51(4):316-323.
[4]Zarychanski R,Doucette S,Fergusson D,et al.Early intravenous unfractionated heparin and mortality inseptic shock[J].Crit Care Med,2008,36(11):2973-2979.
[5]Slofstra SH,van fstra SHi,Buurman WA,et al.Low molecular weight heparin attenuates multiple organ failure in a murine model of disseminated intravascular coagulation[J].Crit Care Med,2005,33(6):1365-1370.
[6]许程,徐元宏.脓毒症早期预警生物标志物的研究进展[J].检验医学,2015,30(5):533-536.
[7]Kellum JA,Lameire N.Diagnosis,evaluation,and management of acute kidney injury:a KDIGO summary(Part 1)[J]Crit Care,2013,17(1):204.
[8]Hotchkiss RS,Karl IE.The pathophysiology and treatment of sepsis[J].N Engl J Med,2003,348(2):138-150.
[9]Gomez H,Ince C,De Backer D,et al.A unified theory of sepsis-induced acute kidney injury:inflammation,microcirculatory dysfunction,bioenergetics,and the tubular cell adaptation to injury[J].Shock,2014,41(1):3-11.
[10]Soehnlein O,Lindbom L.Neutrophil-derived azurocidin alarms the immune system[J].J Leukoc Biol,2009,85(3):344-351.
[11]Soehnlein O,Xie X,Ulbrich H,et al.Neutrophil-derived heparin-binding protein(HBP/CAP37)deposited on endothelium enhances monocyte arrest under flow conditions[J].J Immunol,2005,174(10):6399-6405.
[12]Herwald H,Cramer H,Moamer HH,et al.Mprotein,a classical bacterial virulence determinant,forms complexes with fibrinogen that induce vascular leakage[J].Cell,2004,116(3):367-379.
[13]Gautam N,Olofsson AM,Herwald H,et al.Heparin-binding protein(HBP/CAP37):a missing link in neutrophilevoked alteration of vascular permeability[J].Nat Med,2001,7(10):1123-1127.
[14]Bentzer P,Fisher J,Kong HJ,et al.Heparin-binding protein is important for vascular leak in sepsis[J].Intensive Care Med Exp,2016,4(1):33.
[15]Linder A,Christensson B,Herwald H,et al.Heparinbinding protein:an early marker of circulatory failure in sepsis[J].Clin Infect Dis,2009,49(7):1044-1050.
[16]Linder A,Arnold R,Boyd JH,et al.Heparin-binding protein measurement improves the prediction of severe infection with organ dysfunction in the emergency department[J].Crit Care Med,2015,43(11):2378-2386.
[17]Linder A,Akesson P,Inghammar M,et al.Elevated plasma levels of heparin-binding protein in intensive care unit patients with severe sepsis and septic shock[J].Crit Care,2012,16(3):R90.
[18]Olofsson AM,Vestberg M,Herwald H,et al.Heparinbinding protein targeted to mitochondrial compartments protects endothelial cells from apoptosis[J].J Clin Invest,1999,104(7):885-894.
[19]Fjell CD,Thair S,Hsu JL,et al.Cytokines and signaling molecules predict clinical outcomes in sepsis[J].PLo SOne,2013,8(11):e79207.
[20]Lee TD,Gonzalez m L,Kumar P,et al.CAP37,a nertrophilderived inflammatory mediator,augments leukocyte adhesion to endothelial monolayers[J].Microcasc Res,2003,66(1):38-48.