ArticleIndian journal of clinical biochemistry : IJCB2015
Genetic Predisposition to Diabetic Nephropathy: Evidence for a Role of ACE (I/D) Gene Polymorphism in Type 2 Diabetic Population from Kutch Region.
Article in Indian journal of clinical biochemistry : IJCB, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 12 citations in OpenAlex.
- Distribution of the ACE Gene Polymorphisms in Type 2 Diabetes Mellitus Patients, Their Associations with Nephropathy Biomarkers and Metabolic Indicators at a Tertiary Hospital in Uganda.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Effect of indwelling time of double J tube on infected ureteral calculi and the distribution of pathogenic characteristics in diabetics.American journal of translational research · 2021Article
- Implications of ACE (I/D) Gene Variants to the Genetic Susceptibility of Coronary Artery Disease in Asian Indians.Indian journal of clinical biochemistry : IJCB · 2017Article
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4 authors at 1 institution in 1 country.
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Abstract
Genetic polymorphism as described with angiotensin-converting enzyme gene has been proposed as a putative mediator of diabetic nephropathy. We substantiate the hypothesis that genetic variants of the ACE have significant impacts on diabetic nephropathy. To assess the possible association between the three ACE polymorphic variants and DN in an ethnically homogeneous type 2 diabetic population from Kutch region. A 287-bp insertion/deletion polymorphism in intron 16 of the ACE gene was examined by polymerase chain reaction using a case-control approach conducted with 309 unrelated type 2 diabetic patients of Kutch origin (159 Ahir and 150 Rabari, with >10 years duration of T2DM). Of the patients, 143 had nephropathy {AER >30 mg/day (Ahir, n:73 and Rabari, n:70)} and were considered as cases; all others {n:166 (86 Ahir and 80 Rabari)} were normoalbuminuric (AER <30 mg/day) and were treated as controls. Suitable descriptive statistics was used for different variables. Genotype frequencies in all groups were all in accordance with the Hardy-Weinberg equilibrium. Genotypic distribution was significantly different between cases and controls (Ahir: x(2) :8.87, 2 d.f. p = 0.0118; Rabari: x(2) :11.01, 2 d.f. p = 0.0041). Multivariate logistic regression analysis revealed that DD genotype was a significant and strongest independent predictor of microalbuminuria (Ahir: p = 0.0362, OR = 2.65, 95 % CI 1.89-6.36; Rabari: p = 0.024, OR = 2.81, 95 % CI 1.9-6.65). However, it did not independently change the odds of having macroalbuminuria versus microalbuminuria. Analysis of the association under various genetic models revealed that ACE I/D polymorphic variant contribute to DN susceptibility under recessive mode only. Genetic variation at the ACE locus as D/D variant in intron 16, contribute to an increased risk of nephropathy in T2DM patients but not extent of DN severity, and thus this polymorphism might be considered as genetic risk factors for DN among patients with type 2 diabetes.
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