2 Association of ACE I/D gene polym

2 Association of ACE I/D gene polymorphism with treatment response to steroid

2.1 Association of ACE I/D gene polymorphism with SRNS risk

In this meta-analysis, five investigations [4], [8], [26], [27], [28] were included into our study to explore the association of ACE I/D gene polymorphism with SRNS susceptibility in Asian children. Pooled OR were computed twice, by using the fixed effects method and the random effects method (Table 4). Random effects model were more appropriate when marked heterogeneity was present among the studies. When the fixed effects method was used to analysis those associations, the pooled OR of the ACE I/D gene polymorphism associated with SRNS risk were 1.38(95%CI: 1.04–1.83) for comparison of D allele vs I allele, 1.26(95%CI: 0.84–1.90) for comparison of combined wild homozygous and variant homozygous and heterozygous DD vs DI+II respectively. In the results of fixed effects method, D allele was associated with the onset of SRNS, but DD wasn't. However, in this study, significant heterogeneity among the included studies was observed for the analysis of D vs I or DD vs DI+II (P = 0.003, P = 0.0008; respectively; Table 4). The results coming from the random effects method might be more stable compared with those in the fixed effects method. In the analysis using the random effects method, we found that D allele and DD genotype were not associated with SRNS risk (D: OR = 1.60, P = 0.26; DD: OR = 1.90, P = 0.38; Figure 1-A for D, Figure 2-A for DD; Table 4). Furthermore, the fixed effects method was performed and we documented that there was significant association between II genotype and risk of SRNS relative to both other genotypes combined when the fixed effects method was used (OR = 0.51, P = 0.02; Table 4). Interestingly, II homozygous seemed not to play a protective role against the onset of SRNS when the random effects method was conducted (OR = 0.55, P = 0.23; Table 4). There was no significant heterogeneity for the comparison of II vs DD+DI, and the result from the fixed effects method might be more suitable for our investigation. The result for the comparison of II vs DD+DI was not stable and more investigations were needed to be performed to study this association.

Hasil (Bahasa Indonesia) 1:

2 Asosiasi Ace saya / D Polimorfisme gen dengan menanggapi pengobatan steroid2.1 Asosiasi Ace saya / D Polimorfisme gen dengan risiko SRNSIn this meta-analysis, five investigations [4], [8], [26], [27], [28] were included into our study to explore the association of ACE I/D gene polymorphism with SRNS susceptibility in Asian children. Pooled OR were computed twice, by using the fixed effects method and the random effects method (Table 4). Random effects model were more appropriate when marked heterogeneity was present among the studies. When the fixed effects method was used to analysis those associations, the pooled OR of the ACE I/D gene polymorphism associated with SRNS risk were 1.38(95%CI: 1.04–1.83) for comparison of D allele vs I allele, 1.26(95%CI: 0.84–1.90) for comparison of combined wild homozygous and variant homozygous and heterozygous DD vs DI+II respectively. In the results of fixed effects method, D allele was associated with the onset of SRNS, but DD wasn't. However, in this study, significant heterogeneity among the included studies was observed for the analysis of D vs I or DD vs DI+II (P = 0.003, P = 0.0008; respectively; Table 4). The results coming from the random effects method might be more stable compared with those in the fixed effects method. In the analysis using the random effects method, we found that D allele and DD genotype were not associated with SRNS risk (D: OR = 1.60, P = 0.26; DD: OR = 1.90, P = 0.38; Figure 1-A for D, Figure 2-A for DD; Table 4). Furthermore, the fixed effects method was performed and we documented that there was significant association between II genotype and risk of SRNS relative to both other genotypes combined when the fixed effects method was used (OR = 0.51, P = 0.02; Table 4). Interestingly, II homozygous seemed not to play a protective role against the onset of SRNS when the random effects method was conducted (OR = 0.55, P = 0.23; Table 4). There was no significant heterogeneity for the comparison of II vs DD+DI, and the result from the fixed effects method might be more suitable for our investigation. The result for the comparison of II vs DD+DI was not stable and more investigations were needed to be performed to study this association.