期刊文献+

ANCA相关性血管炎伴血清补体C3降低的临床分析 被引量:8

Clinical analysis of anti-neutrophil cytoplasmic antibody-associated vasculitis with low serum complement C3 levels
下载PDF
导出
摘要 目的探讨血清补体C3(serum complement C3,sC3)降低的抗中性粒细胞胞浆抗体相关性血管炎(AAV)患者的临床病理特征及预后。方法回顾性分析2011年1月至2016年3月我院肾内科穿刺活检确诊的54例AAV患者的临床及病理资料。采用免疫比浊法检测sC3,以我院sC3测值的正常范围下线值为截点将AAV患者分成低sC3组(sC3<0.9 g/L)与正常sC3组(sC3≥0.9 g/L),比较2组患者流行病学、实验室检查、肾脏病理、临床症状、治疗及预后的差异。结果低sC3组,血肌酐基线值明显高于正常sC3组(P=0.008);C反应蛋白、eGFR值明显低于正常sC3组(P值分别<0.001、0.012);快速肾功能衰竭以及即时透析的发生率明显高于正常sC3组(P值分别为0.035、0.014);缓解率显著低于正常sC3组(P<0.001)。Kaplan-Meier生存分析显示低sC3组的肾脏累积生存率明显低于正常sC3组(log-rank=10.197,P=0.001)。结论血清补体C3降低的AAV患者病情严重,进展较快,预后差。 To investigate the clinicopathological features and outcomes of anti-neutrophil cytoplasmicantibody(ANCA)-associated vasculitis(AAV) with low serum complement C3(sC3) levels, total of 54 patients withAAV underwent renal biopsy were analyzed by retrospective observational study in our department from January2011 to March 2016. The sC3 levels of AAV patients were determined by immunoturbidimetric method, then thepatients were divided into two groups of the low sC3 group(sC3〈0.9 g/L) and the normal sC3 group(sC3≥0.9 g/L)based on the lower limit of sC3 normal range. The patients were compared in baseline variables, laboratory data,clinical symptoms, histological features and therapeutic outcomes after treatments. Data showed that patients with lowersC3 presented a higher level of initial serum creatinine than patients with normal sC3(P=0.008). The levels of c-reactiveprotein and eGFR were significant lower in low sC3 group than those in normal sC3 group(P〈0.001, 0.012, respectively).Furthermore, the incidences of rapid progressive renal failure and renal replacement therapy at diagnosis were highersignificantly in the low sC3 group than those in normal sC3 level group(P=0.035, 0.014, respectively). However, theincidence of remission was lower in the low sC3 level group than that in normal sC3 level group(P〈0.001). The low sC3 group showed worse renal survival than normal sC3 level group(log-rank=10.197, P=0.001) confirmed by patients with low sC3 levels tend to have severe renalimpairment with a rapid progression and poor prognosis.
出处 《免疫学杂志》 CAS CSCD 北大核心 2017年第5期410-414,421,共6页 Immunological Journal
基金 第三军医大学新桥医院临床科研基金(2014YLC06) 重庆市社会民生科技创新专项(cstc2015shmszx120029)
关键词 ANCA相关性血管炎 血清补体C3 预后 ANCA-associated vasculitis Serum complement C3 Prognosis
  • 相关文献

参考文献2

二级参考文献42

  • 1Chen M, Kallenberg CG. New advances in the pathogenesis of ANCA-associated vasculitides[J]. Clin Exp rheumatol, 2009, 27(1 Suppl 52): S108-Sl14.
  • 2van Paassen P, Tervaert JWC, Heeringa P. Mechanisms of vasculitig How pauci-immune is ANCA-associated renal vasculitis? [J]. Nephron Exp Nephrol, 2007, 105(1):E10-E16.
  • 3Kain R, Exner M, Brandes R, et al. Molecular mimicry in pauci-immune focal necrotizing glomerulonephritis[J]. Nat Med, 2008, 14(10): 1088-1096.
  • 4Willcocks LC, Lyons PA, Rees AJ, et al. The contribution of genetic variation and infection to the pathogenesis of ANCA-associated systemic vasculitis[J]. Arthritis Res Ther, 2010, 12(1): 202.
  • 5Zhou XJ, Cheng FJ, Lv JC, et al. Higher DEFB4 genomic copy number in SLE and ANCA-associated small vasculitis[J]. Rheumatology (Oxford), 2012, 51(6): 992-995.
  • 6Gatenby PA. ANCA-associated systemic vasculitis: Nature or Nurture?[J]. Int Med J, 2012, 42(4): 351-359.
  • 7Csernok E, Lamprecht P, Gross WL. Clinical and immunological features of drug-induced and infection- induced proteinase 3-antineutrophil cytoplasmic antibodies and myeloperoxidase-antineutrophil cytoplasmic antibodies and vasculitis[J]. Curr Opin Rheumatol, 2010, 22(1): 43-48.
  • 8Laudien M, Gadola SD, Podsehun R, et al. Nasal carriage of Staphylococcus aureus and endonasal activity in Wegener's granulomatosis as compared to rheumatoid arthritis and chronic rhinosinusitis with nasal polyps[J]. Clin Exp Rheumatol, 2010, 28(1): S51-S55.
  • 9Delogu LG, Deidda S, Delitala G, et al. Infectious diseases and autoimmunity[J]. J Infect Dev Ctries, 2011, 5(10): 679- 687.
  • 10Pendergraft WF, Preston GA, Shah RR, et al. Autoimmunity is triggered by ePR-3 (105-201), a protein complementary to human autoantigen proteinase-3[J]. Nat Med, 2004, 10(1): 72-79.

共引文献25

同被引文献56

引证文献8

二级引证文献21

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部