Renal tubular function in children with β-thalassemia minor
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 (FENa, %), fractional excretion of magnesium (FEMg, %), fractional excretion of uric acid (FEUA, %) 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 FENa (%), FEMg (%), FEUA (%), 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.
