TY - JOUR
T1 - Immune mediators in idiopathic nephrotic syndrome
T2 - Evidence for a relation between interleukin 8 and proteinuria
AU - Souto, Marcelo F.O.
AU - Teixeira, Antônio L.
AU - Russo, Remo C.
AU - Penido, Maria Goretti M.G.
AU - Silveira, Kátia D.
AU - Teixeira, Mauro M.
AU - Simões E Silva, Ana Cristina
PY - 2008/12
Y1 - 2008/12
N2 - The pathogenesis of idiopathic nephrotic syndrome (INS) remains unknown. Several findings suggest a role for the immune system. This study aimed to evaluate immune mediators in INS by measuring plasma and urinary levels of transforming growth factor β1 (TGF-β1), monocyte chemoattractant protein-1 (MCP-1/CCL2), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and IL-8 (IL-8/CXCL8) in pediatric patients with INS and in age-matched healthy controls. Patients were divided according to their response to corticosteroids: steroid-sensitive (SS, n = 8), or steroid-resistant (SR, n = 24). Immune mediators were also compared in regard with disease activity (relapse and remission). Immune mediators were measured by ELISA. Plasma TGF-β1 levels in SR patients were approximately 2.8-fold higher than control values (p < 0.05). Urinary IL-8/CXCL8 was 2.9-fold higher in INS patients in relapse (proteinuria >100 mg/m 2/24 h) when compared with patients in remission (p < 0.05), and levels had a positive correlation with individual proteinuria values (p < 0.05). Urinary IL-8/CXCL8 was significantly higher in relapsed SR than in SS patients in remission. No changes in MCP-1/CCL2 and RANTES/CCL5 levels were detected. Our findings suggest that IL-8/CXCL8 and TGF-β1 are involved in the pathogenesis of INS: IL-8/CXCL8 associated with local changes in glomerular permeability and TGF-β1 could be related to worse response to corticosteroids.
AB - The pathogenesis of idiopathic nephrotic syndrome (INS) remains unknown. Several findings suggest a role for the immune system. This study aimed to evaluate immune mediators in INS by measuring plasma and urinary levels of transforming growth factor β1 (TGF-β1), monocyte chemoattractant protein-1 (MCP-1/CCL2), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and IL-8 (IL-8/CXCL8) in pediatric patients with INS and in age-matched healthy controls. Patients were divided according to their response to corticosteroids: steroid-sensitive (SS, n = 8), or steroid-resistant (SR, n = 24). Immune mediators were also compared in regard with disease activity (relapse and remission). Immune mediators were measured by ELISA. Plasma TGF-β1 levels in SR patients were approximately 2.8-fold higher than control values (p < 0.05). Urinary IL-8/CXCL8 was 2.9-fold higher in INS patients in relapse (proteinuria >100 mg/m 2/24 h) when compared with patients in remission (p < 0.05), and levels had a positive correlation with individual proteinuria values (p < 0.05). Urinary IL-8/CXCL8 was significantly higher in relapsed SR than in SS patients in remission. No changes in MCP-1/CCL2 and RANTES/CCL5 levels were detected. Our findings suggest that IL-8/CXCL8 and TGF-β1 are involved in the pathogenesis of INS: IL-8/CXCL8 associated with local changes in glomerular permeability and TGF-β1 could be related to worse response to corticosteroids.
UR - http://www.scopus.com/inward/record.url?scp=57849136036&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=57849136036&partnerID=8YFLogxK
U2 - 10.1203/PDR.0b013e318186ddb2
DO - 10.1203/PDR.0b013e318186ddb2
M3 - Article
C2 - 18679168
AN - SCOPUS:57849136036
SN - 0031-3998
VL - 64
SP - 637
EP - 642
JO - Pediatric Research
JF - Pediatric Research
IS - 6
ER -