Research Journal of Clinical Pediatrics

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Microvascular and hypoxic disorders in children with diabetic nephropathy

Background: In diabetes mellitus type I (T1D) progression of cardio-renal disorders, i.e. arterial hypertension and its complications, diabetic nephropathy (DN), is still the most important side-effect. Search of the mechanisms underlying these damages is on priority list. Vitamin D deficiency identified as a common metabolic/endocrine disorder worldwide in health and diseases.  There are data about the role of Vitamin D in T1D in adults. However, this issue remains to be open in pediatric practice. 

Aim: To study the levels of Vitamin D, Endothelin-1 and primary cellular hypoxia markers in children with T1D and DN and to find out the network of these markers inter-relation.

Material and Methods: Thirty six (36) children T1D aged 6 to 17 years hospitalized in Endocrinology unit in Children Clinical Hospital â„–6 (Kyiv, Ukraine) studied. Vitamin D3 levels measured using ELISA assay and commercially available kit (Vitamin D3 (human) ELISA kit (BioVision, USA). Endothelin-1 levels measured using ELISA assay and commercially available Endothelin-1 ELISA kit (Abcam, USA). The O2-Hb dissociation rate studied spectrophotometrically. Results processed using STATISTICA 6.0 and non-parametric statistical method (Mann-Whitney test).

Results: In our study normal level, insufficiency and deficiency of the Vitamin D defined as - ≥30ng/mL, 21-29ng/mL and ≤20ng/mL, respectively. All patients included into the study during the period September-May. We show that the most prominent Vitamin D3 deficiency detected in the group of patients with diabetic nephropathy (DN). In control group Vitamin D3 was detected at level 35.68±1.56ng/mL, in patients with T1D – 32.37±5.1ng/mL, in patients with DN – 19.39±1.76ng/mL (Ñ€<0.01 as compared to control group). Analysis of the Vitamin D3 levels and the disease course show negative correlation (R=-0.79, Ñ€<0.001). In all children the hemoglobin affinity to O2 molecule studied based on Sore peak analysis. Control group show this index at level 3.05±0.23 a.u., children with T1D – 3.61±0.25 a.u. (p<0.05), patients with DN 1.76±0.27 a.u. (p<0.01, compared to control group value). In all children with T1D and DN increased level of ET-1 measured.

Conclusion: Our data show the prominent deficiency of Vitamin D in T1D patients and patients with DN, increased ET-1 level (a potent vasoconstrictor peptide), and reduction of the O2-Hb dissociation rate. We hypothesize that Vitamin D deficiency is a result of toxic effect of glucose. Increased ET-1 in all patients is a sign of early microvascular changes and resistant vessels damage leading to DN progression and arterial hypertension. All mentioned above changes accompanied by reduced O2-Hb dissociation as a result of increased level of HbA1C and may be a reason of cellular hypoxia.

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