Beyond Proteinuria: Apoptosis and Vitamin D3 State in Children with Diabetic Nephropathy
Received Date: Feb 04, 2016 / Accepted Date: Mar 15, 2016 / Published Date: Mar 18, 2016
Abstract
Diabetic nephropathy (DN) is the leading cause of death in patients with diabetes mellitus type I (T1D). Formation of diabetic nephropathy depends on the quality of blood glucose control. The aim of the study was to investigate the level of metabolic-hypoxic disorders, condition of apoptosis controlling system and Vitamin D3 levels in children with diabetic nephropathy. The study involved 36 children with type I diabetes and diabetic nephropathy (aged 6 to 17 years). The affinity of haemoglobin to oxygen determined by spectrophotometric method. The levels of the marker of cellular hypoxia HIF-1alfa, levels of the apoptotic factor caspase-3 studied by Western Blotting, Vitamin D3 levels were analyzed using ELISA assay. In the group of children with newly diagnosed T1D an increased rate of dissociation of oxygen and haemoglobin compared to the control group was detected. Children with DN the levels of this index were significantly lower than the control group. We show stage-dependent manner in increase of the cellular hypoxia and apoptotic effector caspase-3 levels. Both markers detected at significantly higher rate in DN patients as compared to T1D. Vitamin-D3 deficiency is documented in patients with DN. Thus, the development of DN in children is associated with violation of Hb/oxygen dissociation, a sign of the high degree of the Hb glycosylation resulting to the formation of cellular hypoxia and activation of apoptosis, as one of the basic mechanisms of cell damage kidneys in DN. All mentioned above disorders accompanied by Vitamin D3 deficiency.
Keywords: Diabetes mellitus; Diabetic nephropathy; Metabolic; Cellular hypoxia; Apoptosis; Vitamin D3
Citation: Burlaka I (2016) Beyond Proteinuria: Apoptosis and Vitamin D3 State in Children with Diabetic Nephropathy. J Clin Exp Pathol 6:266. Doi: 10.4172/2161-0681.1000266
Copyright: © 2016 Burlaka I, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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