الفهرس 
Chronic Kidney diseaseOnly 14 pages are availabe for public view
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Abstract
Advanced glycation end products (AGEs) are a potential candidate for accumulated non-traditional risk factor associated with the development of long- term complications of chronic kidney disease. AGEs contribute to a variety of microvascular and macrovascular complications through the formation of cross-links between molecules in the basement membrane of the extracellular matrix and by engaging the receptor for advanced glycation end products (RAGE). The C-truncated RAGE variant, a 50-kd protein, is mainly produced in endothelial cells by means of regulated alternative splicing or carboxyterminal truncation through metalloproteinases. This receptor is known as soluble RAGE (sRAGE) or endogenous secretory RAGE, a naturally occurring inhibitor of the AGE–RAGE interaction The aim of the present work is to study the association between serum glycated end products and their soluble receptors [assessed by carboxymethyllysein and soluble receptor of glycated end products (sRAGE)] and the presence of cardiovascular dysfunction in non-diabetic chronic kidney disease patients The study was conducted on forty 120 subjects classified into two groups: group (I) 80 CKD patients (estimated glomerular filteration rate (eGFR) ≤ 60 and > 15 mL/min/1.73m²) and group (II) 40 control subject with preserved kidney function defined by normal blood urea and serum creatinine. group (I) CKD patients was further subclassifed according to presence or absence of Left ventricular hypertrophy and carotid intima thickness.
Thorough history and examination was done stressing on cardiovascular complication and absence of exclusion criteria especially stage 5 CKD patients or history of renal replacement therapy. Routine and specific investigation was done. group (I) CKD patients and group (II) Control patients were compared regarding clinical, laboratory and radiological features. Results of the present study revealed statistical significant difference between the studied groups as regard clinical, laboratory and radiological features. There was high significant Correlation between Carboxymethyllsein (CML) (pg/dl) and Carotid intima thickness (IMT) in group (I) (r = 0.617, P value < 0.001) and negative significant Correlation between Soluble receptor of advanced glycated end products (sRAGE) and Carotid intima thickness (IMT) in group (I) (r = -0.27, P value < 0.05) (table 22). There was high significant Correlation between Left Ventricular Hypertrophy measured by LVMI (g/m²) and carotid intima thickness (r=0.54, P value <0.001) (table 23). There was high significant Correlation between Carboxymethyllsein (CML) (pg/dl) and Left Ventricular hypertrophy measured by (Left Ventricular Mass Index) LVMI (g/m²) in group (I) (r = 0. 755, P value < 0.001) (table 24). Carboxymethyllysein was the independent risk factor of Left Ventricular Hypertrophy (LVH) in group I (CKD) patients with odd ratio (OR) 23.1(CI:3.4-158.8) followed by mean arterial blood pressure (MAP) with odd ratio 10.04 (CI:1.3-77.5) (table 26). .
The most protective factor of Left Ventricular Hypertrophy (LVH) in group I (CKD) patients was the soluble receptor of advanced glycated end products with odd ratio 15.6 (CI: 2.5-98.9) (table 26). Carboxymethyllysein was the independent risk factors of Carotid intima thickness in group I (CKD) patients with odd ratio (OR) 8.2 (CI: 1.05-64.1) (table 27).
Conclusion
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Conclusion It is concluded that: o CML and sRAGE are significantly increased in the studied non-diabetic CKD patients compared to healthy control subjects. This increase is significantly higher in stage 4 than stage 3 CKD. o The significant increase and significant correlation between both CML and sRAGE and each of LVH and IMT could indicate that AGEs can be a good predictor and/or non-traditional risk factor for the occurance of cardiovascular morbidity in non-diabetic CKD patients.