Methylene tetrahydrofolate reductase (MTHFR) plays a significant role in the metabolism of methionine. MTHFR deficiency is an autosomal recessive trait that could be a significant risk factor for a number of defects, for example, vascular events, due to lower dietary folate intake among South Indians. To find the incidence of 677 C>T and 1298 A>C in MTHFR gene single nucleotide polymorphisms (SNPs) among the south Indian population, polymerase chain reaction and restriction fragment length polymorphism were employed among 152 patients with myocardial infarction and 167 controls. The MTHFR 677CT genotype was found among 35 (22.4%) cases and 08 (4.8%) controls, the MTHFR 677CC allele was found among 115 (73.7%) cases and 159 (94.6%) controls. Also, the analysis of the MTHFR 1298A>C SNP identified the MTHFR 1298CC genotype among 16 (10.3%) cases and 01 (0.6%) control, the MTHFR 1298AC genotype was found in 56 (35.9%) cases and 27 (16.2%) controls, and the MTHFR 1298AA genotype was observed in 80 (51.3%) cases and 139 (82.6%) controls. The C vs. A allele also showed significantly higher frequency among the patients in comparison with the controls (p<0.0001). The results of this study indicate that the MTHFR A1298C SNP is more prevalent among south Indians compared with the MTHFR C677T SNP, suggesting a possible role of MTHFR A1298C in the pathogenesis of heart diseases.

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Introduction: Diabetic nephropathy (DN) is a leading cause of chronic kidney disease (CKD) in diabetes patients. There is ample evidence that the inflammatory pathways are central to both diabetes and DN. Several studies that examined the link between the interleukin-10 (IL10) polymorphisms and DN risk yielded conflicting results. Objectives: The purpose of this meta-analysis is to evaluate the associations between IL10 promoter polymorphisms and DN risk. Methods: A bibliographic search was carried out on PubMed, Google scholar and Web of Science from the beginning until July 30, 2020. Association between IL10 promoter variants (-1082 A>G, -819 C>T and -592 C>A) and DN risk were assessed by considering diabetes without nephropathy (DWN) as well as healthy controls. Data were retrieved and the pooled odds ratio (OR) with 95% confidence interval (CI) was calculated. Results: For the IL10 -1082 A> G analysis, a total of 4 studies with DWN controls (682 cases and 529 controls) and 5 studies with healthy controls (1025 cases and 1625 controls) were considered. For the IL10 -819 C> T analysis, a total of three studies with DWN controls (9619 cases and 445 controls) and 5 studies with healthy controls (1005 cases and 1537 controls) were considered. For the IL10 -592 C> T analysis, a total of 5 studies with DWN controls (819 cases and 645 controls) and 5 studies with healthy controls (1005 cases and 1537 controls) were considered. In addition, there was no evidence of publication bias for IL10 promoter variants. No substantial association was observed between IL10 promoter variants and DN risk. Conclusion: Our study signifies that polymorphisms of IL10 -1082 A>G, -819 C>T and -592 C>A are not linked with DN risk.

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Introduction: Diabetic nephropathy (DN) is the leading cause of chronic kidney disease in diabetes patients. The angiotensin AGT M235T gene polymorphism, which is linked to the renin-angiotensin-aldosterone system (RAAS), has been extensively studied in DN patients, but the results are still conflicting. The current study’s goal is to conduct a meta-analysis to assess the relationship between AGT M235T gene polymorphism and DN susceptibility. Methods: Fourteen case-control studies related to AGT M235T polymorphism and DN were searched using PubMed, Web of Science and Google Scholar databases. Genotype data from the T2DM and T2DN groups were collected from all papers. The pooled odds ratio (OR) and 95 percent confidence interval (95% CI) were calculated employing a random-effects model to assess the relationship. Results: There were no statistically significant link between AGT M235T and DN risk in dominant (P=0.801, OR: 0.95; 95% CI: 0.66-1.38), allelic (P=0.933, OR: 1.01; 95% CI: 0.75-1.37) and recessive (P=0.374, OR: 1.21; 95% CI: 0.80-1.83) genetic models. Further, the stratified analysis based on ethnicity did not reveal significant link between AGT M235T and DN risk in Asian (Dom OR: 1.07; 95% CI: 0.63-1.82) and the Caucasian populations (Dom OR: 0.77; 95% CI: 0.49-1.21). In all three models, there was a high degree of heterogeneity between studies. Publication bias was not seen. Conclusion: Our findings suggest that the AGT gene M235T polymorphism does not contribute to DN risk. However, validation of this association will require multi-center and large population-based studies.