The role of iron-derived free radicals in the development of diabetic nephropathy in patients with beta-thalassemia

R. Loebstein*, D. Lehotay, G. Sher

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Our objectives were to determine if there is an increased incidence or accelerated course of nephropathy in patients with diabetes mellitus secondary to transfusional hemochromatosis and to examine whether free radical activity contributes to its development. We evaluated 9 patients with beta thalassemia complicated by diabetes mellitus for diabetic nephropathy over a 7 year period. Lipid peroxidation was qualified by measuring the presence of 20 aldehydes and results were compared to 5 diabetics without iron overload. Nephropathy developed in 6/9 (66.6%) of the patients after mean duration of overt diabetes of 3.6 ±2.0 years. Three patients had evidence of progressive microalbuminuria over a 7 year period. Two patients with borderline microalbuminuria demonstrated stable albumin excretion rates over the follow up period. Total aldehyde concentration was significantly higher in beta-thalassemia diabetic patients compared to non-thalassemic diabetic controls (8106±1280 vs. 4594±247 nM/L; p<0.0001). The 3 patients with progressive microalbuminuria demonstrated significantly higher total aldehyde concentration compared to other beta-thalassemia diabetic patients with stable albumin excretion (9428±337 vs.7445±1003 nM/L; p<0.01). Serum vitamin E concentrations were significantly lower in beta-thalassemia patients with diabetes compared to diabetic patients without iron overload: 12.1±6.0 micromoles/L vs. 25.9±11.4; p=0.02. We concluded that iron-derived free radical generation might play an important role in the early development and high incidence of nephropathy in diabetic patients with beta-thalassemia.

Original languageEnglish
Pages (from-to)A762
JournalFASEB Journal
Issue number5
StatePublished - 20 Mar 1998
Externally publishedYes


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