Long-term results of children diagnosed with idiopathic nephrotic syndrome; single center experience.

AIM: The aim of this study was to determine the long-term results of children followed up with a diagnosis of nephrotic syndrome in a single center. MATERIALS AND METHOD: The medical data of 33 patients aged between 6 months and 10 years who were diagnosed with idiopathic nephrotic syndrome in our center between January 2000 and December 2012 and followed up for a period of 2-12 years were reviewed (Gulhane Military Medical Academy Ethics committee, 07.11.2012/10). RESULTS: The mean age of disease onset was 3.2±2.04 years (range: 0.5-10 years) and the mean follow-up period was 6±3.4 years (range: 2-12 years). Thirteen (39.4%) of the study group (or the patients) were female and 20 (60.6%) were male. Twenty seven (1.8%) of the patients were sensitive to steroid and 6 (18.1%) were resistant to steroid. Four (12.1%) of the steroid-resistant patients had steroid-dependent nephrotic syndrome, 5 (15.2%) had frequently relapsing nephrotic syndrome and 18 (54.5%) had rarely relapsing nephrotic syndrome. Histopathological diagnoses of six patients who underwent biopsy because of resistance to steroid were as follows: focal segmental glomerulosclerosis (n=3), C1q nephropathy (n=1), diffuse mesangial proliferation (n=1) and membraneous nephropathy (n=1). Fifteen (45.5%) patients entered into full remission and 2 (6%) patients developed chronic renal failure. Treatment complications including decreased bone mineral density in three patients (9%), short stature in 2 patients (6%) and cataract in 2 patients (6%) developed. CONCLUSIONS: Children with nephrotic syndrome carry a risk in terms of short stature, osteoporosis, cataract and renal failure in the long-term follow-up. It was observed that our rates of response to steroid were similar to the literature and the most common histopathological diagnosis was focal segmental glomerulosclerosis in our patients who underwent biopsy because of resistance to steroid. It was thought that multi-center studies should be conducted to demonstrate regional or national differences related with long-term results of childhood nephrotic syndrome.

Malondialdehyde, antioxidant enzymes, and renal tubular functions in children with iron deficiency or iron-deficiency anemia.

We aimed to investigate the effects of iron deficiency (ID) or iron-deficiency anemia (IDA) on oxidative stress and renal tubular functions before and after treatment of children. A total of 30 children with a diagnosis of IDA constituted the IDA group and 32 children with a diagnosis of ID constituted the ID group. Control group consisted 38 age-matched children. Serum ferritin, soluble transferrin receptor (sTfR), serum, and urinary sodium (Na), potassium (K), calcium (Ca), phosphorus (P), creatinine (Cr), uric acid (UA), urinary N-acetyl-ß-D-glucosaminidase (NAG) levels, and intra-erythrocyte malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels were measured before and after iron therapy in the IDA and ID groups, whereas it was studied once in the control group. We have divided the study group in groups according to age (infants <2 years, children 3-9 years, and adolescents 10-15 years). Patients with IDA (infant, adolescent) and ID (infant, children, and adolescent) had a significantly high level of MDA in post-treatment period in comparison to those of healthy control. Patients with IDA (children, adolescent) and ID (infant, children) had a significantly high level of pre-treatment GSH-Px than controls. Post-treatment SOD was lower in IDA (children and adolescent) groups than control and post-treatment CAT was lower in IDA and ID (adolescent) groups than control. These findings show that ferrous sulfate used in the treatment of ID or IDA could lead to oxidative stress; however, a marked deterioration of in proximal renal tubular functions was not seen.

Evaluation of lipid peroxidation and antioxidant system in healthy iron-replete infants receiving iron prophylaxis.

OBJECTIVE: Iron supplementation is commonly recommended for infants; however, there are some reports that it causes oxidative damage. The aim of this study was to investigate the potential effects of iron supplementation at 4 mo of age, for a period of 2 mo, on lipid peroxidation and free radical scavenging enzymes. METHODS: Twenty-seven healthy 4-mo-old infants chosen randomly and given iron supplementation (ferrous sulfate, 10 mg of elemental iron per day) constituted the study group and 26 healthy 4-mo-old infants who were chosen randomly and not given iron supplementation constituted the control group. Weight, height, head circumference, complete blood cell count, serum ferritin level and intraerythrocytic zinc, iron, copper, malondialdehyde, catalase, superoxide dismutase, and glutathione peroxidase levels were measured in the two groups at 4 and 6 mo of life. RESULTS: Compared with controls at 6 mo of age, no significant differences were observed for intraerythrocytic zinc (0.5 ± 0.1 versus 0.6 ± 0.2 µg/mL, P > 0.05), copper (0.2 ± 0.1 versus 0.2 ± 0.2 µg/mL, P > 0.05), iron (130.8 ± 10.9 versus 127.4 ± 11.1 µg/mL, P > 0.05), malondialdehyde (21.4 ± 3.5 versus 22.4 ± 2.3 nmol/g of hemoglobin, P > 0.05), catalase (135.4 ± 23.9 versus 135.1 ± 23.3 MU/g of hemoglobin, P > 0.05), superoxide dismutase (1736.4 ± 141.1 versus 1701.3 ± 103.9 U/g of hemoglobin, P > 0.05), and glutathione peroxidase (8.9 ± 1.6 versus 8.4 ± 1.6 U/g of hemoglobin, P > 0.05) levels. CONCLUSION: Our study indicates that the supplemental use of elemental iron 10 mg/d for a period of 2 mo in healthy iron-replete infants did not cause lipid peroxidation or an impairment of antioxidant status.