title: Decreased IL-10 mRNA expression in patients with advanced renal failure undergoing conservative treatment.
abstract: Chronic renal failure (CRF) is characterized by persistent systemic inflammatory response. We tested the hypothesis that the balance between synthetic capacity of pro-inflammatory, as tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, and anti-inflammatory cytokines, as IL-10, may become progressively impaired during decline of renal function. Cytokine mRNA transcript levels (fraction of GAPDH mRNA) were detected by real time RT-PCR technique in whole blood cells of patients with far-advanced or less-advanced CRF (glomerular filtration rate lower or greater than 15ml/min per 1.73m(2), respectively) undergoing conservative treatment and in healthy controls. TNF-alpha mRNA levels were greater (p<0.05) in the patients with far-advanced CRF than in those with less-advanced CRF. IL-6 mRNA levels were not significantly different in the two groups. Both groups of patients exhibited greater (p<0.05) TNF-alpha and IL-6 mRNA levels than the healthy controls. IL-10 mRNA levels were greater (p<0.05) in the patients with less-advanced CRF (65+/-18) than in the healthy controls (12+/-2). Nonetheless, in the patients with far-advanced CRF, IL-10 mRNA levels (20+/-10) were lower (p<0.05) than in the patients with less-advanced CRF and not significantly different than in the healthy controls. In conclusion, advanced renal failure is characterized by unbalanced synthetic capacity of pro- and anti-inflammatory cytokines. A progressive decrease in IL-10 synthetic capacity during the course of CRF could contribute to increasing cardiovascular risk.
authors.affiliation: Department of Clinical, Morphological and Technological Sciences, Division of Internal Medicine, University of Trieste, Clinica Medica, Ospedale di Cattinara, Strada di Fiume 447, 34149 Trieste, Italy.
authors.forename: Alessandra
authors.initials: A
authors.lastname: Bosutti
authors.forename: Gabriele
authors.initials: G
authors.lastname: Grassi
authors.forename: Nicola
authors.initials: N
authors.lastname: Fiotti
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Guarnieri
authors.forename: Gianni
authors.initials: G
authors.lastname: Biolo
mesh_terms: D000368:Aged; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009133:Muscular Atrophy / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D012333:RNA, Messenger / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: C508609:IL10 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10