P174 Urinary excretion of Th1, Th2 and Th17 cytokines in idiopathic focal segmental glomerulosclerosis: Preliminary results from a single center
Introduction Idiopathic Focal Segmental Glomerusclerosis (FSGS) usually leads to end stage renal disease. Cytokines excreted in the urine may represent immunological mechanisms and predict response to treatment. Methods First morning urine samples, collected at day of renal biopsy from 20 FSGS patients [M/F 15/5 age 43.4 yrs (16-75)], and 10 healthy controls, were used to detect IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-17, INF-gama, G-CSF, GM-CSF, MCP-1, MIP1b, TNF-beta by a multiplex cytokine assay. Histological findings evaluated were percentage of global sclerosis, mesangial hypercellularity, interstitial infiltration and tubular atrophy. Renal function and degree of proteinuria were estimated at the day of renal biopsy and at the end of follow up. Results FSGS patients, comparing to controls had increased urinary levels of IL-1β (0.02 ± 0.04 vs. 0.008 ± 0.004 fg/dl, p = 0.05), IL-5 (0.02 ± 0.02 vs. 0.01 ± 0.004 fg/dl, p = 0.05) IL-12 (0.08 ± 0.07 vs. 0.04 ± 0.01 fg/dl, p = 0.05) GM-CSF (4.9 ± 9 vs. 0.3 ± 0.7 fg/dl, p = 0.03), and MCP-1 (1.2 ± 0.9 vs. 0.2 ± 0.2 fg/dl, p  Cytokines which showed significant correlations with histology were mainly produced by Th2 cells. Global sclerosis correlated with: IL-10 (r = 0.6, p = 0.009), IL-13 (r = 0.5, p = 0.03), IL-7 (r = 0.5, p = 0.03) and TNF-beta (r = 0.5, p = 0.03). Degree of mesangial hypercelullarity had negative correlation with IL-4 (r = −0.6, p = 0.01), IL-5 (r = −0.6, p = 0.03), IL-10 (r = −0.7, p = 0.002) and GM-CSF (r = −0.5, 0.04). Patients who did not respond to treatment and progressed to ESRD had increased IL-6 (0.13 ± 0.06 vs.0.07 ± 0.04 fg/dl, p = 0.05), MCP-1 (1.7 ± 0.9 vs. 0.9 ± 0.8 fg/dl, p = 0.02) and reduced IL-17 0.03 ± 0.03 vs.0.05 ± 0.1 fg/dl). Conclusion Th2 cytokines seem to participate to the progression of histological lesions in FSGS and their urinary levels may predict disease outcome.