WORLD JOURNAL OF ADVANCE
HEALTHCARE RESEARCH

Zainab Mohammed Hussein Abd Al-Ameer* and Hind Shaker

ABSTRACT

Background: Beta Thalassemia is an autosomal recessive hereditary hemoglobinopathy characterized by reduced or absent beta-globin chain production. Management primarily involves regular blood transfusions, which can lead to iron overload affecting organs such as the heart, liver, endocrine glands, and kidneys. Renal dysfunction in Beta Thalassemia may result from iron overload, oxidative stress, thrombosis, or as a side effect of iron chelation therapy. β-2 microglobulin, a low-molecular-weight protein filtered by glomeruli and reabsorbed in proximal tubules, serves as a sensitive marker for renal tubular injury and oxidative stress. Aims of Study: To measure serum β-2 microglobulin levels in adults with Beta Thalassemia major and assess its utility as a sensitive renal function marker. To evaluate correlations between β-2 microglobulin, hematological parameters, transfusion frequency, and serum ferritin levels. Patients and Methods: A case-control study was conducted from January to October 2024, including 60 adult Beta Thalassemia major patients and 20 healthy controls. Blood samples were collected before transfusion for CBC, urea, creatinine, ferritin, and β-2 microglobulin, the latter measured via ELISA. Results: Mean age was 22.4±5.3 years; 60% were male. Patients had significantly lower hemoglobin, MCV, and MCH, with higher RDW, platelet count, ferritin, and β-2 microglobulin levels (p<0.001). β-2 microglobulin negatively correlated with GFR and positively with serum ferritin, urea, creatinine, and transfusion frequency. Conclusions: Iron overload, chronic anemia, and chelation toxicity contribute to renal impairment in Beta Thalassemia major. Elevated β-2 microglobulin levels indicate renal dysfunction and correlate with transfusion burden and iron overload, highlighting its role as a sensitive renal marker.