Early Detection Of Glomerular Dysfunction In Beta Thalassemia Major Patients Undergoing Chelation Therapy

Abstract

Background: Thalassemia is one of the prevalent hemoglobinopathies caused by gene mutation leading to chronic anemia. Iron overload and direct nephrotoxic effects of chelators are the largely accepted explanations for the mechanisms of renal glomerular impairment in BTM. The aim of this study was to early detection of glomerular dysfunction in BTM patients receiving iron chelators using novel biomarker. Methods: The study included 60 patients with BTM receiving iron chelators: group 1 receiving Deferoxamine (DFO) and group 2 receiving Deferasirox (DFX). Control group include 30 healthy people where matched age and sex with patients. Serum Cystatin C, serum creatinine, blood urea, albumin/creatinine ratio (ACR) in urine was measured in patients and controls. Results: There is no statistically significant difference in blood urea levels between patients and controls. Patients' and controls' serum creatinine levels are statistically significantly different. Serum Cystatin C shows a significant difference between patients and the control group (higher in patients) and is slightly higher in the Deferoxamine group than the Deferasirox group. Patients in the study had higher Albumin-Creatinine Ratio (ACR) values than controls, which is statistically significant. Conclusions: Serum Cystatin C and urinary ACR consider as early markers of glomerular dysfunction. Both Deferasirox and Deferoxamine can produce changes in glomerular function markers.