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The Effects of Deferasirox on Renal, Cardiac and Hepatic Iron Load in Patients with β-Thalassemia Major: Preliminary Results

The iron loading related to erythrocyte transfusions is the major cause of morbidities and mortalities in patients with β-thalassemia major (β-TM). Deferasirox, an orally active iron chelator, has been reported to cause serum creatinine increases in addition to acute renal failures in elderly patients with comorbidities. The nefrotoxicities in patients using deferasirox, despite the facts that the drug is minimally excreted from kidneys and its effective chelation of iron from liver and heart, may rise the question of decomparmentalization of iron from these organs to kidneys. Thirteen patients with β-TM were included in the study (mean age 18.5 ± 7.5 years [9–33 years]). The patients received deferasirox in a dose of 34.3 ± 6.5 mg/kg [17–37 mg/kg]. Four patients (31%) exhibited consecutive increases in serum creatinine greater than 33% above baseline twice during the follow-up period. The results indicated that the earliest iron chelation starts in liver in patients receiving deferasirox. Additionally, by the 6th month of deferasirox, the status of cardiac and renal iron in chronically transfused patients with β-TM were preserved. This may indicate that the serum creatinine increases may not be attributed to iron decompartmantalization from other organs to kidneys.