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Abstract
Background: Studies have identified that MIF -173 G>C gene polymorphism is associated with idiopathic nephrotic syndrome (INS) susceptibility and steroid resistance, but the results remain inconclusive.Methods: We searched PubMed, Embase, and Web of Science for relevant studies published before 31 March 2021. Pooled data were reported as odds ratio (OR) with 95% confidence interval (CI). Noteworthiness of significant OR was estimated by the false positive report probability (FPRP) test. Trial sequential analysis (TSA) was used to control type I and type II errors.Results: We selected seven case-control studies that included 1,026 INS children (362 were steroid-resistant NS and 564 were steroid-sensitive NS) and 870 controls. The results showed that MIF -173 G>C polymorphism was significantly associated with INS susceptibility in allelic, heterozygous and dominant genetic models (C vs. G: OR = 1.325, 95% CI: 1.011-1.738; GC vs. GG: OR = 1.540, 95% CI: 1.249-1.899; CC + GC vs. GG: OR = 1.507, 95% CI: 1.231-1.845), and FPRP test and TSA indicated that the associations were true in heterozygous and dominant models. The pooled results also revealed that MIF -173 G>C polymorphism was significantly associated with steroid resistance in allelic, homozygous and recessive models (C vs. G: OR = 1.707, 95% CI: 1.013-2.876; CC vs. GG: OR = 4.789, 95% CI: 2.109-10.877; CC vs. GC + GG: OR = 4.188, 95% CI: 1.831-9.578), but FPRP test indicated that all these associations were not noteworthy. Furthermore, TSA revealed that the non-significant associations between MIF -173 G>C polymorphism and steroid resistance in heterozygous and dominant models were potential false negative.Conclusions: This meta-analysis could draw a firm conclusion that MIF -173 G>C polymorphism was significantly associated with increased INS risk in heterozygous and dominant genetic models. MIF -173 G>C polymorphism was not likely to affect steroid responsiveness, but more studies were needed to confirm.
Highlights
Childhood idiopathic nephrotic syndrome (INS) is characterized by severe proteinuria, hypoalbuminemia, and generalized edema
According to the literature search strategy and selection criteria, seven studies were identified as shown in Figure 1. 1,026 INS patients (564 cases diagnosed with sensitive nephrotic syndrome (SSNS) and 362 cases diagnosed with steroid-resistant nephrotic syndrome (SRNS)) and 870 control patients were enrolled in this metaanalysis
One study did not explicitly classify INS into SSNS and SRNS according to steroid responsiveness [13], so we excluded it in the meta-analysis of migration inhibitory factor (MIF) -173 G>C polymorphism and steroid responsiveness
Summary
Childhood idiopathic nephrotic syndrome (INS) is characterized by severe proteinuria, hypoalbuminemia, and generalized edema. It is one of the most common glomerular diseases with an incidence of 1·15-16·9 per 100,000 children [1]. Glucocorticoids (GCs) are the first-line treatment regimens for INS and induce complete remission (CR) in most patients, who are diagnosed with steroid-sensitive nephrotic syndrome (SSNS). Approximately 20% of patients who do not achieve CR after the initial standard course of GCs are diagnosed with steroid-resistant nephrotic syndrome (SRNS) and at high risk for progression to ESRD [1]. Studies have identified that MIF -173 G>C gene polymorphism is associated with idiopathic nephrotic syndrome (INS) susceptibility and steroid resistance, but the results remain inconclusive
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