[Relationship of the I/D-polymorphism of the ACE gene and the T174M-polymorphism of the AGT gene to diabetic microangiopathies in children and adolescents].

2006 
: The purpose of the study was to examine a role of candidate genes of the renin-angiotensin system in the development of microangiopathies in children and adolescents with type 1 diabetes mellitus (DM) and to systematize the risk factors of development of diabetic microangiopathies in order to substantiate the optimal approaches to prevention and therapeutic correction. A hundred and thirty-eight children (73 boys and 65 girls) with type 1 DM were examined. Their mean age was 13.2±0.3 years. Based on the findings, it may be assumed that patients with type DM who are the carriers of the D allele are genetically predisposed to the development of diabetic nephropathy. An association of the ID polymorphism of the ACE gene with the development of diabetic nephropathy was established in children with type 1 DM in the Siberian population. Allele I of the ACE gene ACE less frequently occurs in DM patients with nephropathy (p > 0.05) and a factor that reduces the risk of its development. The association of the D allele with the development of diabetic nephropathy suggests that the polymorphism of the ACE gene contributes to the regulation of generation of angiotensin-converting enzyme that plays an important role in the pathogenesis of this complication. There was no association of the polymorphism in question with the concomitance of diabetic nephro- and retinopathy in the patient. Analysis of the associations of the T174M polymorphism of the AGT gene with diabetic microangiopathies revealed no statistically significant differences when the distribution of the AGT gene was compared in the groups of patients with and without microangiopathies. There was an association of the T allele of the AGT gene with Type 1 DM, as evidenced by a negative TDT test in with healthy sibs. An association of the T allele with diabetic nephropathy was also ascertained.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    0
    Citations
    NaN
    KQI
    []