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  • Title: Macrophage migration inhibitory factor -173G/C gene polymorphism increases the risk of renal disease: a meta-analysis.
    Author: Tong X, He J, Liu S, Peng S, Yan Z, Zhang Y, Fan H.
    Journal: Nephrology (Carlton); 2015 Feb; 20(2):68-76. PubMed ID: 25329590.
    Abstract:
    AIM: Macrophage migration inhibitory factor (MIF) -173G/C (rs755622) gene polymorphism has been associated with renal disease risk. However, lots of studies have reported inconclusive results. Therefore, we performed a meta-analysis to investigate the relationship between MIF -173G/C gene polymorphism and renal disease susceptibility. METHODS: We conducted a search in PubMed, Embase (OvidSP), Wanfang databases and China National Knowledge Internet (CNKI) up to 20 June 2014. Odds ratio (OR) and 95% confidence interval (95% CI) were used to test the association. Statistical analyses were performed with STATA version 11.0 software. RESULTS: In total, 2755 participants from eight case-control studies were included in this meta-analysis. The pooled results indicated the significant association between MIF -173G/C polymorphism and renal disease risk (CC + CG vs GG, OR = 1.77, P < 0.01; C vs G, OR = 3.94, P < 0.01). In the subgroup analysis, a significant relationship of MIF -173G/C gene polymorphism and renal disease risk in Asians and Caucasians were observed. Additionally, we found that the heterozygote (CG) may strongly increase renal disease risk in children, while the homozygote (CC) may increase the renal disease susceptibility more significantly in adults. Surprisingly, the results found a significant association between MIF -173G/C polymorphism and glucocorticoid resistance in child patients with idiopathic nephrotic syndrome (INS) (C vs G, OR: 3.83, P < 0.01). CONCLUSION: This study suggested that MIF -173G/C gene polymorphism may increase risk of renal disease, especially in children. Furthermore, the meta-analysis also indicated that this gene polymorphism may increase risk of glucocorticoid resistance in child patients with INS.
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