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 15 ml/min per 1.73 m 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.

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