Correction of Chronic Hypoxia and Apoptosis in Nephrotic Children

Burlaka, Ievgeniia (2021) Correction of Chronic Hypoxia and Apoptosis in Nephrotic Children. In: Research Trends and Challenges in Medical Science Vol. 8. B P International, pp. 148-156. ISBN 978-93-90768-36-3

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Abstract

Objectives: The objective of this paper was to study the levels of cellular hypoxia, apoptosis and dependence of these factors on the value of kidney function impairment; to evaluate possible protective effects of the treatment with antioxidant agent tocopherol in children with nephrotic syndrome.

Background: Hypoxia-related disorders play an important role in irreversible tissue damage via activation of certain secondary processes. Nephrotic syndrome (NS) consists of peripheral edema, heavy proteinuria, and hypoalbuminemia, often with hyperlipidemia.

Methods: An examination of renal biopsies of 53 patients (aged 10 to 15 years) with nephrotic syndrome done. Conventional clinical investigations, immunochemistry, immunoblotting were used in this study.

Results: We show that children with nephrotic syndrome have high level of marker of cellular hypoxia HIF-1?. Levels of the latest depends on the level of kidney function impairment and proteinuria. The sclerosis progression which is a sign of irreversible kidney damage is accompanied by gradual increase of the proapoptotic factor Bax expression. An applied treatment composes conventional scheme and tocopherol showed an improvement in hypoxia level, proapoptotic factor Bax expression.

Conclusion: Hypoxia-induced disorders in nephrotic children presented by disturbances in apoptosis controlling system can be attenuated by the antioxidants application. Further study of the molecular mechanisms which preserve kidney in nephrotic children and non-toxic nephroprotective agents, including antioxidants are important issues in nephrology field.

Item Type: Book Section
Subjects: STM Library > Medical Science
Depositing User: Managing Editor
Date Deposited: 27 Nov 2023 03:55
Last Modified: 27 Nov 2023 03:55
URI: http://open.journal4submit.com/id/eprint/3363

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