ROLE OF HYPOXIA–INDUCED APOPTOSIS IN CHRONIC GLOMERULONEPHRITIS PROGRESSION IN CHILDREN

Aim of the study: to study the indicators of cellular hypoxia and apoptosis in pediatric patients with nephritic type of chronic glomerulonephritis. Material and methods: 52patients with active stage of nephrotic type ofChronic glomerulonephritis were inspected. All patients were divided into groups of Chronic Kidney Disease (CKD) by the level of glomerular filtration rate (GFR). Detection of the hypoxia–induced factor (HIF) and antiapoptotic factor Bcl–xL in serum performed using Western Blotting assay and immunohistochemically on material of kidney biopsies. Imaging was done using confocal laser microscopy. Results: it has been found that the disease course is accompanied by increased levels of hypoxia–induced factor HIF–1a and decreased expression of antiapoptotic factor Bcl–xL (in plasma and on biopsies). Detected changes significantly depended on the degree of proteinuria and declining of glomerular filtration rate. Dependence between the levels of hypoxia–induced damages and level of kidney function impairment was documented. In children with Chronic Kidney Disease (SKDIst.) HIF–1a was at level 128.6±2.3% (P<0.01, compared to Control group), in children with CKD II–III st. – 141.3±1.9% (P<0.01, compared to Control group and CKD I st.). Level of antiapoptotic defense in children with nephrotic type of Chronic glomerulonephritis was related to the level of kidney function impairment as well. In group of patient with CKDIst. Bcl–xL expression was down–regulated to 75.1±2.2%, in group with CKDII–IIIst. — to 60.1+1.8% (P<0.01 and P<0.001, compared to Control group, respectively). The level of evaluated changes has a dependence on levels ofproteinuria and kidney function impairment. Conclusion. Studied parameters might be used as predictors of unfavorable disease course.