Urinary excretion of il-1β, il-6 and il-8 cytokines during relapse and remission of idiopathic nephrotic syndrome

Abstract

Background/aim: The role of pro-inflammatory cytokines in the immunopathogenesis of idiopathic nephrotic syndrome had been widely postulated. Reports on the release of cytokines, during idiopathic nephrotic syndrome (INS) activation, were conflicting in defining a specific interleukin pattern during relapse and remission of the disease. The aim of this study was to explore the role of IL-1β, IL-6 and IL-8 in the pathophysiology of INS during relapse and remission. Patients and methods: A total of 37 INS patients were included. Their demographic and biochemical data were reviewed. Levels of IL-1 β, IL-6 and IL-8 were measured in the urine of patients during relapse and remission of the disease. Urine samples from 30 age- and sexmatched controls were checked for the same 3 cytokines. Results: Mean age of patients at study was 6.4 ±3.2 years (range: 14 months–12 years). Male:female ratio was 24:13. Mean serum creatinine was 47 ±13 mmol/L, and mean serum albumin was 21 ±7 g/L. Mean urinary IL-1 β, IL6 and IL8 levels, corrected to urinary creatinine, in patients during relapse were 132.94 ±654.97, 217.82 ±1124.31 and 150.227 ±523.97 pg/mmol compared to 9.11 ±40.75, 0.146 ±0.652, and 6.455 ±24.53 pg/μmol in controls, respectively (P = 0.02, 0.03 and 0.014, respectively). No significant difference was reported in the mean level of the 3 cytokines compared to controls during remission (P = 0.94, 0.092 and 0.076). Conclusion: Our results support the role of T-cell activation and the subsequent release of IL-1 β, IL6 and IL8 in the pathogenesis of relapses in INS. The use of steroid-sparing cytokine blockers in managing relapses of INS remains a tempting challenge.