الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
β -thalassemia is considered as one of the most common genetic disorders in the world, caused by reduction or absence of β globin chain synthesis. Approximately, 1.5% of the global population are heterozygotes (carriers) of the β- thalassemia gene. The life of patients with β-thalassemia major depends on blood transfusion. Regular blood transfusion improves their general physical condition, and it prevents ineffective hematopoiesis complications. Repeated transfusions in these patients lead to hemosiderosis in the heart, liver, and endocrine glands. In addition to the iron deposits in various body organs, it can cause the premature death of these patients. For this reason, these patients need to use an iron chelator to remove excess iron from the body. Historically, renal disease has not been a major issue in patients with thalassemia because survival was limited by severe cardiac iron loading from chronic transfusion therapy leading to premature early death. With the introduction of effective chelating agents that can reduce the iron burden and its consequences, and extending patients’ survival, renal disease has become a more common occurrence. It has been reported that anemia causes tissue hypoxia in kidneys earlier and at a higher hemoglobin concentration than in other organs. Clinically, serum creatinine and urea levels are commonly used to diagnose kidney injury. However, a disadvantage is that these parameters are affected by age, sex, muscle mass, dehydration, and drugs. In addition, creatinine level does not increase unless at least half of the renal function is lost. Distinct molecules are being investigated in the search for an ideal biomarker that could provide a window for intervention between cell disruption, renal damage, and clinical manifestations. Markers of proximal tubular response, neutrophil gelatinase-associated lipocalin (NGAL)], and tubular enzymes [N-acetyl-β-D glucosaminidase (NAG)] in urine have all emerged as predictors of AKI before renal function decline can be detected clinically. The urinary enzyme N-acetyl-β-D-glucosaminidase (NAG) exists in the lysosomes of proximal tubule epithelial cells. Increased NAG excretion in urine is caused exclusively by proximal tubular cell injury and has recently been recognized as a tubular injury marker related to DKD. This biomarker is known for its high molecular weight that cannot be filtered by the glomerulus; thus, it is released in the tubular lumen as a consequence of proximal tubular damage. Early identification of kidney injury may enable particular interventions to reduce renal damage. Therefore, the aim of this work was to evaluate renal function using predictive biomarkers such as urinary, neutrophil gelatinase-associated lipocalin (NGAL), and N-acetyl-β-D glucosaminidase (NAG) in children with β- thalassemia compared to traditional renal function (Serum urea, creatinine). This prospective case-control study was conducted on a total of 40 children suffering from β-thalassemia major (Thalassemic group) and 40 age- and gender-matched healthy non –anemic controls without any potential diseases affecting renal function (Control group).