title: Immune mediators in idiopathic nephrotic syndrome: evidence for a relation between interleukin 8 and proteinuria.
abstract: 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 beta1 (TGF-beta1), 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-beta1 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/m2/24 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-beta1 are involved in the pathogenesis of INS: IL-8/CXCL8 associated with local changes in glomerular permeability and TGF-beta1 could be related to worse response to corticosteroids.
authors.affiliation: Departamento de Pediatria, Universidade Federal de Minas Gerais, Belo Horizonte, MG, 30130-100, Brazil.
authors.forename: Marcelo F O
authors.initials: MF
authors.lastname: Souto
authors.forename: Antônio L
authors.initials: AL
authors.lastname: Teixeira
authors.forename: Remo C
authors.initials: RC
authors.lastname: Russo
authors.forename: Maria-Goretti M G
authors.initials: MG
authors.lastname: Penido
authors.forename: Kátia D
authors.initials: KD
authors.lastname: Silveira
authors.forename: Mauro M
authors.initials: MM
authors.lastname: Teixeira
authors.forename: Ana C
authors.initials: AC
authors.lastname: Simões E Silva
mesh_terms: D000293:Adolescent; D018932:Chemokine CCL2 / Q000097:blood / Q000652:urine; D018946:Chemokine CCL5 / Q000097:blood / Q000652:urine; D002648:Child; D005260:Female; D006801:Humans; D007155:Immunologic Factors / Q000097:blood / Q000276:immunology / Q000652:urine; D016209:Interleukin-8 / Q000097:blood / Q000276:immunology* / Q000652:urine; D008297:Male; D009404:Nephrotic Syndrome / Q000378:metabolism / Q000503:physiopathology; D011507:Proteinuria / Q000097:blood / Q000276:immunology* / Q000652:urine; D053773:Transforming Growth Factor beta1 / Q000097:blood / Q000652:urine
chemical_list: C111835:CCL2 protein, human; C483024:CCL5 protein, human; D018932:Chemokine CCL2; D018946:Chemokine CCL5; D007155:Immunologic Factors; D016209:Interleukin-8; D053773:Transforming Growth Factor beta1