الفهرس 
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Abstract
Obesity is nowadays, one of the most frequently encountered medical problems. Among the complications of this pathologic entity, renal disease is an important issue and its pathophysiologic mechanisms are a challenge for the physician, since a variety of etiologic factors are implicated in its genesis. For example, hypertension, hyperlipidemia and insulin resistance affect renal function, each one in a different way. However, obesity predisposes toward renal disease independently of diabetes and hypertension.
Studies of renal structure in obese patients have indicated either normal findings or obesity related glomerulopathy, which includes focal segmental glomerulosclerosis, glomerulomegaly, mesangial hyperplasia and minimal foot process fusion. The functional changes that occur in the kidneys of obese patients include increase in glomerular filtration rate (GFR), renal plasma flow (RBF), nephritic range proteinuria or sub-nephrotic proteinuria. The first sign of renal injury is microalbuminuria or frank proteinuria, in particular in the presence of hypertension.
Fat tissue is increasingly viewed as an active endocrine organ with a high metabolic activity. Adipocytes produce and secrete several proteins (adipokines) that act as veritable hormones responsible for the regulation of energy intake and expenditure
One of these adipokines is adiponectin, which is a 30-kDa circulating plasma protein primarily secreted by adipocytes, and has been recently recognized to have anti-atherogenic, anti-inflammatory and insulin-sensetizing properties.
Higher adiponectin gene expression and protein content was found in adipocytes localized in the subcutaneous than in visceral adipose tissue.
Oxidative stress is defined as an imbalance between prooxidant and antioxidant factors in favor of prooxidants, thereby potentiating oxidative damage. Oxidative stress has been reported to contribute to the development and progression of atherosclerosis. In the diabetic condition, oxidative stress impairs glucose uptake in muscle and fat, and decreases insulin secretion from pancreatic β cells.
This study aimed at assessing serum adiponectin level and oxidative stress in obese subjects and its relationship to renal glomerular and tubular dysfunction.
This study was conducted on 60 subjects divided into 3 groups:
Group I: 20 normal healthy subjects with body mass index (BMI) less than 25 and of comparable age and sex as control group
Group II: 20 obese subjects with BMI greater than 30 and normal albumin excretion rate (AER).
Group III: 20 obese subjects with BMI greater than 30 and increased AER. .
Patients with diabetes, chronic liver disease, connective tissue diseases, infections, any kind of malignancy, cardiac, respiratory or renal disease were excluded.
The study was conducted in accordance with the ethical guidelines of the 1975 Declaration of Helsinki and an informed consent was obtained from each patient.
All subjects were evaluated as regards:
I- Thorough history taking and full clinical examination
II- Anthropometric measurements (triceps skin fold (TSF), mid-arm circumference (MAC), mid-arm muscle circumference (MAMC), waist circumference (WC) and calculation of body mass index (BMI) were done.
III- 12 leads electrocardiogram.
IV- Ultrasonographic assessment of the kidneys.
V- Laboratory Investigations:
1- preliminary investigations including: Serum fasting, postprandial blood glucose.
Serum cholesterol (C): total, high and low density lipoprotein fractions (HDL-C and LDL-C respectively), triglycerides (TG), Liver function tests: serum alanine aminotransferase (ALT), aspartate aminotransaminase (AST), and gamma glutamyl transferase (GGT) activities.
2- Renal function tests including: serum urea, creatinine (S.Cr), uric acid, complete urine analysis and calculation of estimated glomerular filtration rate (e-GFR) using the Cockcroft-Gault equation.
3- Estimation of albumin to creatinine ratio in urine to assess AER.
4- Estimation of urinary gamma glutamyl transferase (GGT) enzyme: by enzyme linked immunosorbant assay (ELISA) technique; as a marker of tubular function.
5- Estimation of serum thiobarbituric acid-reactive substances (TBARs) as a marker of the oxidative stress.
6- Estimation of serum adiponectin level by enzyme linked immunosorbant assay (ELIZA).
Clinical evaluation of the blood pressure revealed that 5 obese with normal AER and 7 obese with abnormal AER were hypertensive (BP≥140/90). None of the patients had lower limb oedema. The systolic blood pressure was significantly increased in obese subjects than control group.
In the present study the anthropometric measurements (body mass index, mid arm circumference, mid arm muscle circumference, triceps skin fold thickness, and waist circumference) were significantly increased in obese with normal and abnormal AER than the control group. They strongly correlated with each others
There was insignificant difference between the studied groups as regards the serum ALT, AST, GGT, urea and creatinine.
The e-GFR was significantly lower in obese with abnormal AER than both the obese with normal AER and the control subjects.
There were significant increase in serum FSG, PPSG, total cholesterol, LDL-C, TG, uric acid, urinary GGT and serum TBARs in obese with normal and abnormal AER than control group with insignificant difference between obese with normal and abnormal AER except with serum uric acid where it was higher in obese with abnormal AER than obese with normal AER.
Serum HDL-C was significantly decreased in both obese subject groups than the controls, while serum adiponectin was significantly decreased in obese with abnormal AER than the control group. In obese with normal AER it was also decreased but statistically insignificant.
Serum adiponectin showed a statistically significant negative correlation with TBARS, U.GGT and BMI in both groups of obese subjects and with AER in obese with abnormal AER, while it showed a positive correlation with HDL-C in obese subjects with abnormal AER.
The serum TBARS showed a statistically significant positive correlation with U.GGT, BMI and a negative correlation with HDL-C in both obese groups and with AER in obese with abnormal AER.
A statistically significant positive correlation was found between UGGT and BMI in both obese groups and between BMI and AER in obese with abnormal AER. A negative correlation was found between U GGT and HDL-C in obese with normal AER.
A statistically significant positive correlation was found between both systolic and diastolic blood pressure and BMI, TBARS (in whole obese subjects) and AER (in obese with proteinuria). A negative correlation was found between both systolic and diastolic blood pressure with adiponectin in obese subjects.