POLYMORPHISM OF THE FTO GENE (RS9939609) AS A RISK FACTOR FOR EARLY KIDNEY DAMAGE IN CHILDREN WITH OBESITY

Abstract

Introduction. The problem of obesity in children continues to attract the attention of pediatricians worldwide. The development of a comorbid pathology, namely kidney damage, is of particular importance. In the pathogenesis of kidney disorders in obesity, both metabolic disorders and genetically determined predisposition lie. Studying these facts will allow us to identify a high-risk group among children with obesity for early preventive and treatment measures. The aim of the study is to study the relationship between kidney functional disorders and FTO gene polymorphism in children with obesity. Material and methods. 211 children with alimentary exogenous-constitutional obesity were examined, and from the examined sample of patients, groups were formed according to the types of fat tissue distribution: a group of children with abdominal fat tissue distribution type; a group of children with a uniform fat tissue distribution type. The control group consisted of 104 children of the same age and sex with normal body weight. We investigated the features of anthropometric data, biochemical and molecular genetic studies, including determining the excretion of albumin with urine, cystatin levels, calculating glomerular filtration rate, and determining the polymorphism of the FTO gene. Results and Discussion. Our studies showed that in children with abdominal obesity, the frequency of the AA genotype was higher (28.4%) compared to the group of children with moderate obesity (16%) with a statistically significant advantage (2=4.529, p=0.034). This allowed us to classify the AA genotype as predisposing to the development of abdominal obesity. Both in children with abdominal obesity and in children with moderate obesity, the highest level of urine albumin (77.03±6.52 mg/l and 54.11±5.17 mg/l) was noted in carriers of the A/A genotype, and the lowest in children with carriers of the T/T genotype (38.83±5.03 mg/l and 21.39±3.14 mg/l; p<0.001). In children with a uniform type of obesity, carriers of the mutant A/A genotype showed a decrease in blood cystatin levels and an increase in glomerular filtration rate, which indicated hyperfiltration, which is the beginning of pathological changes in the kidneys in obesity. In children with abdominal obesity and carriage of the A/A genotype, unlike children with moderate obesity, an increase in the level of cystatin and a decrease in the glomerular filtration rate were observed, which is a manifestation of obesity glomerulopathy. Conclusion. Studies have shown that the polymorphism of the FTO gene in children with obesity is associated with functional kidney damage. Carriers of the A/A genotype with abdominal obesity are more susceptible to metabolic disorders, namely metabolic kidney damage, which is expressed in a significant increase in the level of microalbuminuria, a pathology of the level of cystatin, and a decrease in glomerular filtration rate.