Pathogenesis of nephrotic syndrome (NS) in children is still unknown, recent data suggest involvement of T cell dysfunction with altered cytokine production. Several papers revealed increased production of TNF during the acute phase of NS as well as its relationship to the severity of the disease. The recent study paper was designed to characterize the association of single nucleotide polymorphism of the TNF gene in position -308 (TNF G-308A) with the natural course of NS in children. DNA samples were collected from 102 children (64 boys and 38 girls with NS aged 3–15 years (median 7 years) – 78 of them had NS sensitive to steroids (SSNS), while in the rest of the cases were resistant to steroid treatment (SRNS). There were no significant differences between the groups of children with SSNS and SRNS as to their sex, age and age at disease onset respectively. Prevalence of allele TNF -308A in the whole group of children with NS did not differ significantly from that in the control group (26.4% vs. 22.0%, n.s.). However, prevalence of allele TNF -308A was significantly higher in children with SRNS as compared to patients with SSNS (12/24, 50.0% vs. 15/78, 19.2%, OR: 4.2, ČI: 1.64–11.17, p <0.01) and the control group respectively. Our data, thus reveled an increased risk of developing SRNS in carriers of the TNF -308A allele and thus support previous data on the role of TNF in the course of childhood nephrotic syndrome. However, another prospective study of more patients should be performed to validate these results and their value to predict the pathological type of NS and the response of patients to steroid therapy.

        Key words: TNF, polymorphism, nephrotic syndrome