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目的 探讨血管紧张素Ⅰ转换酶 (ACE)基因多态性在不同激素效应和病理改变的原发性肾病综合征 (NS)患儿中的分布及意义。方法 用聚合酶链反应 (PCR)分别检测 10 7例健康儿童和42例NS患儿的ACE基因 ,并同时用紫外法分别测定血清ACE的活性。结果 (1)NS患儿激素部分效应及无效应组的DD型基因频率为 6 0 % ,与激素完全效应组 (5 % )比较差异有显著意义 (P <0 .0 1)。(2 )肾活检 15例中局灶节段性硬化 (FSGS)的病理改变者 6例 ,其中ID基因型 1例 ,DD基因型 5例 ,无II基因型 ;non FSGS病理改变者 9例 ,其中II基因 5例 ,ID基因 3例 ,DD基因 1例。两组各基因型分布比较显示 :FSGS组以DD型为主 (与non FSGS组比较P =0 .0 0 19) ,non FSGS组以II型为主 (与FSGS组比较P =0 .0 419)。 (3)正常儿童ACE的活性为 (2 5± 17)U/L ,NS患儿血清ACE的活性为 (2 8± 18)U/L ,两组比较差异无显著意义 (t=1.0 7,P >0 .0 5 ) ;但每组不同基因型之间血清ACE活性差异均有显著意义 (正常组F =2 9.0 1,NS组F =6 5 .5 6 ;P均 <0 .0 1)。 (4)激素完全效应者的血清ACE活性为 (13± 3)U/L ,激素无效应及部分效应者血清ACE活性为 (18± 4)U/L ,两组比较差异有显著性意义 (t=3.0 9,P <0 .0 1)。 (5 )FSGS患儿血清的ACE活性为 (38± 10 )
Objective To investigate the distribution and significance of angiotensin Ⅰ converting enzyme (ACE) gene polymorphism in children with primary nephrotic syndrome (NS) with different hormonal effects and pathological changes. Methods Polymerase chain reaction (PCR) was used to detect the ACE gene in 107 healthy children and 42 NS children, respectively. Meanwhile, the serum ACE activity was measured by UV. Results (1) The frequency of DD genotypes in hormone-bearing and non-effector NS patients was 60%, which was significantly different from that in hormone-complete effect group (5%) (P <0.01). (2) pathological changes of focal segmental sclerosis (FSGS) in renal biopsy in 6 cases, including ID genotype in 1 case, DD genotype in 5 cases, no genotype II; non-FSGS pathological changes in 9 cases, Including II gene in 5 cases, ID gene in 3 cases, DD gene in 1 case. The distribution of genotypes between the two groups showed that DD genotype was the main component of FSGS group (P = 0.019 vs non-FSGS group), and type II genotype in non-FSGS group (P = 0.041 409 ). (2) The activity of ACE in normal children was (2 5 ± 17) U / L, the serum ACE activity in children with NS was (2 8 ± 18) U / L, there was no significant difference between the two groups (t = 1.07, P> 0.05), but there was significant difference in serum ACE activity between different genotypes (F = 2 9.01 in normal group and F = 65.55 in NS group; all P <0.01 ). (4) Serum ACE activity was (13 ± 3) U / L in hormone-complete effect group, and serum ACE activity was (18 ± 4) U / L in hormone-ineffective and partial effect group, with significant difference between the two groups t = 3.09, P <0.01). (5) The serum ACE activity of FSGS children was (38 ± 10)