Features of diabetic nephropathy in individuals with various polymorphic variants of the Interleukin-6 (C174G) gene
Type 1 diabetes mellitus is a polygenic multifactorial disease based on immune mediated or idiopathic destruction of beta cells of the pancreas, leading to absolute insulin deficiency. Diseases related to multifactorial diseases are based on genetic predisposition and environmental factors. The most severe complication is diabetic nephropathy, which may remain undiagnosed for a long time. In addition, there are still many unresolved problems regarding nephropathy. To identify predictors that will help predict the severity of this complication is an important task of modern diabetology and nephrology. The aim of the work was to study the role of polymorphic variants of the interleukin-6 gene (IL-6 gene (C174G)) and the activity of antioxidant protection enzymes and lipid peroxidation in the development of diabetic nephropathy in patients with type 1 diabetes mellitus. The study included patients with type 1 diabetes mellitus (50 people) and healthy individuals (20 people). Molecular-genetic, clinical-laboratory and biochemical research methods were used. As a result of the work done, we came to the conclusion that the activity of the processes of free radical oxidation and lipid peroxidation increases many times in type 1 diabetes mellitus, which is confirmed in our study by an increase in the content of malondialdehyde products against the background of an increase in the activity of enzymes of the antioxidant defense system. This is especially evident in individuals who carry homozygotes for the allele 1 (+/0) of the IL-6 (C174G) gene. This also correlates with a more severe course of diabetic nephropathy in this subgroup (the level of glomerular filtration rate is lower, and the level of microalbuminuria is higher than in individuals with other genotypes of the main group). It can be assumed that this polymorphic variant of the IL-6 gene, combined with deviations in oxidative stress indicators, makes a negative contribution to the course of diabetic nephropathy, making it heavier by increasing the activity of free radical oxidation processes.