摘要目的 比较肾病综合征患者与正常人的血清肽谱,寻找差异表达的血清肽谱.方法 将研究对象分成试验组和对照组.试验组为49例肾病综合征患者,包括17例系膜增生患者、12例微小病变患者、10例膜性肾病患者和10例局灶硬化患者;对照组为10例健康志愿者.采用ClinProt磁珠浓缩和基质辅助激光解吸电离法分析两组研究对象血清肽谱的差异.结果 系膜增生组vs对照组筛选出5个差异表达的多肽(15.28±7.61,P＜0.01).微小病变组vs对照组筛选出7个差异表达的多肽(2.16±1.59,P＜0.01).膜性肾病组vs对照组筛选出6个差异表达的多肽(35.48±13.71,P＜0.01).局灶硬化组vs对照组筛选出5个差异表达的多肽(18.06±8.07,P＜0.05).以P＜0.05为差异有统计学意义.采用遗传算法对样本进行分类并建立诊断预测模型,对区分系膜增生组、微小病变组、膜性肾病组、局灶硬化组与对照组的交叉验证能力分别为96.18%、100%、98.53%、94.12%,而识别率均为100%.结论 应用蛋白质组学建立了肾病综合征患者的血清肽谱模型,为人们更好地了解肾病综合征的发病机制提供了新的思路.

abstractsObjective To compare the serum peptidome spectrum between nephrotic syndrome patients and normal controls, and to search for their variations. Methods The serum peptide profiling was determined by ClinProt magnetic bead enrichment and matrix assisted laser desorption ionisation time-of-flight mass spectrometry (MALDI-TOF MS) in 17 mesangial proliferative glomerulonephritis (MsPGN) patients, 12 minimal change nephrotic syndrome (MCNS) patients, 10 membranous nephropathy (MN) patients, 10 focal segmental glomerulosclerosis (FSGS) patients, and 10 healthy volunteers. Results 5 differentially expressed polypeptides were screened out between MsPGN and normal controls (15.28±7.61, P＜0.01). 7 differentially expressed polypeptides were screened out between MCNS and normal controls (2.16±1.59, P＜0.01). 6 differential expressed polypeptides were screened out between MN and normal controls (35.48±13.71, P＜0.01). 5 differential expressed polypeptides were screened out between FSGS and normal controls (18.06±8.07, P＜0.05). The statistical significance was set at P＜0.05. A Genetic Algorithm was used to set up the classification model between patients and normal controls. The model separated MsPGN, MCNS, MN and FSGS group from normal controls with a cross validation of 96.18%, 100%, 98.53% and 94.12%, respectively. The recognition capabilities were 100%. Conclusions The study established the serum peptidome spectrum for nephrotic syndrome by proteomic technology, and provided a new viewpoint to better understand the pathogenesis of nephrotic syndrome.