الفهرس 
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Abstract
Diabetes mellitus (DM) is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, or loss of its action. Insulin is an anabolic hormone produced by the beta cells of the islets of Langerhans located in the pancreas, and the absence, destruction, or loss of these cells results in type 1diabetes (insulin-dependent diabetes mellitus (IDDM). Most children with diabetes have type 1 diabetes mellitus (T1DM) and a life time dependence on exogenous insulinto prevent acute complications and to reduce the risk of long-term complications.
The two most common forms of diabetes are type 1 diabetes (T1DM, previously known as insulin-dependent diabetes or IDDM) and type 2 diabetes (T2DM, previously known as non-insulin-dependent diabetes or NIDDM). Both are caused by a combination of genetic and environmental risk factors.
VDBP, a multifunction and highly polymorphic plasma protein synthesized primarily in the liver, was identified about ahalf a century ago and characterize to be able to bind various form of vitamin D.
DBP (also referred to as Gc-globulin) is a member of the albumin gene family.
Vitamin D circulate bound to vitamin D –binding protein (85%to90%) and albumin (10%to 15%), with less than 1% of circulating hormone in its free from.
Vitamin D-binding protein (DBP) prolongs the serum half-life of 25(OH) D and protects against vitamin D deficiency by serving as a vitamin D reservoir.
Vitamin DBP complexes filtered by the glomerulus are reabsorbed via megalin/cubilin-mediated endocytosis in the proximal tubule, tubular injury (which aggrevated by diabetes) would be expected to result in urinary VDBP loss.
So, aim of our study was to evaluate urinary level of vitamin D –binding protein as anew biomarker for diabetic nephropathy and its correlation to other study parameteres
Patient and method:-
The present study was carried out on forty childern:(group 1) twenty of Type 1 diabetic childern selected according to WHO criteria attended to our pediatric genetic and endocrinology unit in Menoufia University Hospital.
And (group 2) Twenty of apparently healthy children matched with the diabetic patients in the same age and sex from our pediatric general clinic in Menoufia University Hospital as acontrol group.
The diabetic children and adolescent:-
Included 9males and 11 females, their ages ranged from 7 to 15 years with duration of illness not less than 5 years and variable degree of diabetic control. Children with (Urinary tract infection, collagen diseases, Decompansated heart failure, Liver diseases, renal diseases other than diabetic nephropathy, malignancy and congintal anomalies) were excluded.
After taking informed consent, all patients and control were subjected to the following:
1. Detailed history taking.
2. Complete general examination including anthropometric measurements (Weight, Height, BMI).
3. Laboratory investigation including:
Estimation of fasting blood glucose levels.
Estimation of post prandial blood glucose levels
Estimation of glycosylated hemoglobin (HbA1c).
Renal and liver function tests.
Complete blood count.
4. Specific investigation including:
Detection of macro and micro albumin ineurine .
Assessment of urinary vitamin D binding protein in urine.
5. Genetic counseling of the diabetic group and their families.
This study revealed that:
Consanguinity in diabetic patients was75%versus 25% with unconsanguineous marriage with (p<0.001) considered highly significant in diabetic group compared to control group.
Anthropometric data of diabetic group showed their heights and weights mean were increasedversus cotrol group was found to be significant statistically (p<0.001).
Body mass index(BMI) is (mean= 22.8+3.99) in diabetic group which is increased versus control group with( mean =14.1 ± 5.3)this was found to be significant statiscally(p<0.001)
The percentage of diabetic pateints with DKA and addmited to ICU was 60%while,the percentage of the diabetic patients who presented with classic symptoms was 40 %.
Laboratory data of the diabetic group showed higher levels of fasting blood suger which ranging from (287.085 ±83.20)and post prandial blood suger ranges from(342.40±86.86) which is statiscally significant in concordance withWHO cariteria.
Glycosylated hemoglobin (HbA1c) in our study ranged from (11.32±1.45) in diabetic pateints in relation to average ranges (controled<7.5 and uncontrolled>7.5) which was statiscally significant associations (p<0.001).
In the present study, Urinary VDBP level showed significant increases in type 1 diabetic patients with microalbuminuria and macroalbuminuria (mean=562.990+194.771) when compared to Control group (mean=172. 480+41.856)with(p<0.001), there is positive correlation between UVDBP as a marker of diabetic nephropathy and fasting blood glucose, 2hr PP, HbA1c, Duration of the disease, ACR,and microalbumin and no significant correlation between Urinary VDBP as a marker of diabetic nephropathy and other laboratory data, this is in agreement with the idea that VDBP only reflects tubular damage in early stages of renal disease.