الفهرس 
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Abstract
Beta-thalassemia syndromes are the most common inherited monogenic disorders worldwide. They are heterogeneous disorders caused by reduced or absent beta-globin synthesis, a major component of adult hemoglobin A leading to an imbalance of the globin chains. Consequently, beta-thalassemia leads to reduced hemoglobin production and accumulation of α-globins. The clinical and hematological spectrum of beta-thalassemia disease ranges from mild to clinically overt conditions, including transfusion dependent beta-thalassemia major and non-transfusion dependent betathalassemia intermedia or thalassemia minor. Renal disease is considered one of the most common causes of morbidity in patients with β-TM. Renal disease may present in many forms, such as renal tubular acidosis, glomerular dysfunction, urine concentration failure, proteinuria, renal tubular damage and excess secretion of proximal tubule damage markers. Thus, the early identification of patients at risk of developing renal impairment is essential to prevent and/or reverse the deterioration in renal function, improving the prognosis and reducing the incidence of end-stage renal disease and mortality. Retinol binding protein (RΒP) is a low molecular weight protein that synthesizes in the liver. Its main function is to transport vitamin A. RΒP acts as a biomarker for diagnosis of proximal tubular dysfunction. So our study aimed to evaluate renal dysfunction using (urinary retinol-binding protein) in patients with transfusion dependent betathalassemia. This cross sectional– case control study was conducted on 50 patients with transfusion dependent beta thalassemia and 50 healthy individuals aged >18 years.