Publication: Renal tubular function in β-thalassemia
2
Issued Date
1998-01-01
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ISSN
0931041X
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2-s2.0-0031800233
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Mahidol University
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SCOPUS
Bibliographic Citation
Pediatric Nephrology. Vol.12, No.4 (1998), 280-283
Suggested Citation
Achra Sumboonnanonda, Prida Malasit, Voravarn S. Tanphaichitr, Sompong Ong-ajyooth, Sunthorn Sunthornchart, Sa Nga Pattanakitsakul, Siripan Petrarat, Amara Assateerawatt, Arun Vongjirad Renal tubular function in β-thalassemia. Pediatric Nephrology. Vol.12, No.4 (1998), 280-283. doi:10.1007/s004670050453 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/18592
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Title
Renal tubular function in β-thalassemia
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Abstract
Studies of the renal involvement in thalassemic syndromes have been varied and few. This study was designed to define the renal abnormalities associated with β-thalassemia and to correlate the renal findings with clinical parameters. One hundred and four β-thalassemic children with various disease severity were studied. The patients were divided into three groups: 48 with severe anemia [hematocrit (Hct) < 25%], 31 on a hypertransfusion program and desferrioxamine treatment, and 25 with moderate anemia (Hct > 25%). The results were compared with 15 normal children. Significantly higher levels of proteinuria and low molecular weight proteinuria were found in all patients compared with normal children. Aminoaciduria was detected in one-third of patients. Thalassemic patients had significantly lower morning urine osmolarity, higher urine N-acetyl-β-D-glucoseminidase and malondialdehyde (MDA, an indicator of lipid peroxidation). Patients with severe anemia had significantly higher low-molecular weight proteinuria and MDA, and lower urine osmolarity than those with moderate anemia. Our data confirmed the high frequency of renal abnormalities in P-thalassemia patients and indicated some degree of proximal tubular dysfunction. Severity of the abnormalities correlated with the degree of anemia and were least severe in patients on hypertransfusion and desferrioxamine therapy. This suggested that the damage might be caused by anemia and increased oxidation induced by excess iron deposits.