In patients with beta -thalassemia major, the most important cause of morta
lity and morbidity is organ failure due to deposits of iron.. In this study
, the nature of the kidney injury and possible pathogenetic factors were in
vestigated. Seventy children with beta -thalassemia major and 14 age and se
x-matched healthy children were involved in the study. Blood and timed urin
e samples were obtained for hematological and biochemical tests. The mean v
alues of blood urea nitrogen (BUN), serum creatinine, creatinine clearance,
serum sodium, urine osmolality, fractional excretion of sodium, potassium,
and uric acid were not statistically different between the groups. Serum l
evels of potassium, phosphorus, and uric acid and the urine volume, high ur
inary protein to creatinine (U-P/Cr), urinary N-acetyl-beta -D-glucosaminid
ase to creatinine (U-NAG/Cr), and urinary malondialdehyde to creatinine, (U
-MDA/Cr), and the tubular phosphate reabsorption (TRP) values were statisti
cally different between two groups (P<0.05). Increased serum levels of pota
ssium, phosphorus, and uric acid in the patient group were attributed to th
e rapid erythrocyte turnover. The presence of high U-P/Cr, U-NAG/Cr and U-M
DA/Cr, ratios shows that in these patients with proximal renal tubular dama
ge may be secondary to oxidative lipid peroxidation mediated by the iron ov
erload.