RESUMEN
54 children with nephrotic syndrome and 17 healthy controls were included in the study, among cases studied 40 were males and 14 were females, 36 had history of hypertension and 12 cases had oedema at the time of sampling. Patients were divided into 4 groups, GP 1:10 cases were. steroid responsive in remission, GP 11:12 cases were steroid resistant during activity, GP III:18 cases were steroid dependent of low dose steroids and GP IV:14 cases were steroid dependent on high dose steroids. For all patients' full history, clinical examination and estimation of urinary proteins as well as serum level of IL-13 and sIL-R11 were done. The level of serum JL-13 was significantly lower in cases, compared to control, interquartile range [IQR] was II and 28 respectively [p<0.005] Comparison of the 4 groups revealed a highly significant correlation between groups II and I [p<0.0054]. groups II and IV [p<0.010], there was also a significant difference in serum IL-I 3 level in both sexes but no significant relation to presence of oedema or hypertension. There was a significant negative correlation between IL-13 and serum protein level [r =-0.2686, p<0.05]. On the other hand the serum level of slL-2R was significantly higher in children with NS compared to controls [1Q11=5000, 1244 respectively, p<0.005]. There was a significant difference between patients in GPI vs OP IV [p<0.0 126] and between OP II vs OP Ill [p<0.029] and a highly significant difference between OP II vs OP IV [p<0.0012]. There was no significant difference as regards sex, but a significant difference in children with oedema [p<0.0090] and a highly significant difference in those with hypertension [p<0.0015]. There was also a significant negative correlation between sIL-2R and steroid intake [r =-0.49, 2 0.03]. Results of renal biopsy had no significant correlation with either IL-13 or sIL-2R. In conclusion TL-13 was significantly lower in all studied groups compared to the control, indicating involvement of IL-13 in the pathogenesis of NS. SIL-2R is involved in pathogenic mechanisms involved in activation of NS so it can be used as a clue for disease activity. The exact role of inflammatory cytolcines in pathogenesis of NS in childhood needs further research work to reach proper understanding of the pathogenesis of this syndrome