NEPHROLOGY 2005; 10, 427–429 doi:10.1111/j.1440-1797.2005.00484.x © 2005 Asian Pacific Society of Nephrology. Blackwell Science, LtdOxford, UKNEPNephrology1320-53582005 Asian Pacific Society of NephrologyOctober 2005105427429Original Article Renal tubular function and β-thalassemia minorS Kalman et al. Correspondence: Dr Süleyman Kalman, Gülhane Military Medical Faculty, Department of Pediatrics, Division of Nephrology, Etlik 06018, Ankara, Turkey. Email: suleymankalman@yahoo.com Accepted for publication 12 July 2005. Original Article Renal tubular function in children with β-thalassemia minor SÜLEYMAN KALMAN, 1 A AVNI ATAY, 2 ONUR SAKALLIO LU, 1 TANER ÖZGÜRTAS, 3 FAYSAL GÖK, 1 ISMAIL KURT, 3 A EMIN KÜREKÇI, 2 OKAN ÖZCAN 4 and ERDAL GÖKÇAY 4 1 Division of Pediatric Nephrology, 2 Division of Pediatric Hematology, 3 Department of Biochemistry and 4 Department of Pediatrics, Gülhane Military Medical Faculty, Ankara, Turkey SUMMARY: Background: β-thalassemia minor is a common heterozygous haemoglobinopathy that is characterized by both microcytosis and hypochromia. It requires no treatment. It has been postulated that low-grade haemolysis, tubular iron deposition and toxins derived from erythrocytes might cause renal tubular damage in adult patients with β-thalassemia minor. Our aim was to investigate the renal tubular functions in children with β-thalassemia minor and to determine its possible harmful effects. Methods: The study was conducted on 32 children (14 female and 18 male) at the age of 5.8 ± 3.1 years (range 2–14 years) with β-thalassemia minor. The patients were classified as anaemic (haemoglobin (Hb) ≤ 11 g/dL) (Group 1, n = 14) and non-anaemic (Hb > 11 g/dL) (Group 2, n = 18). A control group was formed with 18 healthy children whose ages and sexes match those in other groups (Group 3, n = 18). Fractional excretion of sodium (FE Na , %), fractional excretion of magnesium (FE Mg , %), fractional excretion of uric acid (FE UA , %) and tubular phosphorus reabsorption (TPR,%) were calculated with standard formulas. Urinary calcium excretion (mg/kg per 24 h), zinc (Zn) (μg/dL), glucosuria (mg/dL), β-2 microglobulin (mg/dL) and N-acetyl-β–D-glycosaminidase (NAG, U/mmol creatinine) levels were measured through biochemical methods. Results: There was no statistically significant difference among the three groups in terms of the results of FE Na (%), FE Mg (%), FE UA (%), TPR (%), calciuria (mg/kg per 24 h), NAG, urine Zn, proteinuria, glucosuria or urine β- 2 microglobulin levels (P > 0.05). Conclusion: On the contrary of children with β-thalassemia major, renal tubular dysfunction has not been determined in children with β-thalassemia minor in the present study. KEY WORDS: β β-thalassemia minor, N-acetyl-β β–D-glycosaminidase, renal tubular functions. G – β-thalassemia minor (β-thalassemia trait or heterozygotes β- thalassemia) is a haemoglobinopathy that is characterized with microcytosis and hypochromia. It originates from the existence of β-thalassemia mutation on a single chromo- some. 1 The prevalence of β-thalassemia minor is high among people from the Mediterranean basin, Africa and Asia. It is seen in 2–3% of the Turkish population. 2 Both multiple system and organ involvement, including the kidneys, can be observed in β-thalassemia major. 3,4 Per- sons with β-thalassemia minor are usually symptomless, but the peripheral blood picture reveals minimal anaemia and microcytosis. Serious organ and system involvement were not demonstrated in β-thalassemia minor. Recently, how- ever, renal tubular dysfunctions have been detected in adults with β-thalassemia minor. 5,6 It has also been reported that the risk for osteoporosis is evident in these patients because of metabolic bone disorders induced by hypercalciuria. 7 The children with β-thalassemia minor have not been investigated so far in the literature in terms of renal dys- function. For this reason, we investigated the renal tubular function in this patient group. SUBJECTS AND METHODS The study consisted of 32 children (14 females, 18 males) diagnosed with β-thalassemia minor at the age of 5.8 ± 3.1 years (range 2– 14 years) and 18 healthy children (eight female, 10 male) for the con- trol group at the age of 6.7 ± 2.1 years (range 2–10 years). Patients with renal disorders, urinary tract infections, anaemia as a result of aetiolo- gies other than β-thalassemia minor or those patients who underwent any kind of treatment were all excluded from the study. All subjects had similar eating habits, normal blood urea nitrogen (BUN), creatinine level, normal ultrasonographic findings and were normotensive at the time of study. The diagnosis of β-thalassemia minor was made accord- ing to the results of complete blood count (CBC), peripheral smear, and haemoglobin electrophoresis. The cases were classified as Group 1