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目的探讨原发性肾病综合征(PNS)患儿肾组织核因子κB(NFκB)活化水平及其与肾组织病理类型、24h尿蛋白定量的关系。方法2002年2月至2004年9月,收集山东大学齐鲁医院小儿内科51例PNS患儿活检肾组织及5例肾脏手术切除的正常肾组织。采用免疫组织化学染色法及多媒体彩色病理图文分析系统MPIAS500,观察PNS患儿各病理类型肾组织及正常肾组织NFκB的活化水平,同期收集PNS患儿24h尿蛋白定量。结果微小病变型(MCD)、非微小病变型(NMCD)PNS患儿肾小球及肾小管中NFκB活化水平均较对照组显著增强;NMCD患儿肾小球及肾小管中NFκB的表达水平显著高于MCD患儿;20例系膜增殖性肾小球肾炎(MsPGN)患儿肾组织NFκB活化水平随系膜增殖程度加重而增高;PNS患儿肾小球及肾小管NFκB表达水平与24h尿蛋白定量呈显著正相关。结论PNS患儿肾小球及肾小管中NFκB活化水平上调,且与组织病理类型、尿蛋白量相关,NFκB的异常活化在PNS发病中起重要作用。
Objective To investigate the activation of nuclear factor kappa B (NFκB) in renal tissues of children with primary nephrotic syndrome (PNS) and its relationship with the pathological type of kidney and the quantitative urinary protein in 24 hours. Methods From February 2002 to September 2004, 51 cases of PNS children with renal biopsies and 5 cases of normal renal tissue resected by kidney surgery were collected from Department of Pediatrics, Qilu Hospital of Shandong University. Immunohistochemistry and MPIAS500 system were used to observe the activation of NFκB in renal tissues and normal renal tissues of children with PNS. The urinary protein excretion of 24-hour urine samples was collected in the same period. Results The levels of NFκB activation in glomeruli and tubules of patients with minimal change type (MCD) and non-minimal change type (NMCD) were significantly higher than those in control group. The expression of NFκB in glomeruli and tubules of NMCD children was significantly Higher than that in MCD. The level of NFκB activation in renal tissue of 20 patients with mesangial proliferative glomerulonephritis (MsPGN) increased with the increase of mesangial proliferation. The expression of NFκB in renal glomerulus and renal tubules in children with PNS was significantly higher than that in 24- Protein quantitation was positively correlated. Conclusions The level of NFκB activation in glomeruli and tubules of PNS children is upregulated, which is correlated with histopathological types and urinary protein levels. Abnormal activation of NFκB plays an important role in the pathogenesis of PNS.