Inflammatory effects of peritoneal dialysis: evidence of systemic monocyte activation.

We evaluated in peritonitis-free patients undergoing continuous ambulatory peritoneal dialysis (CAPD) the release of both interleukin-6 (IL-6) and beta-2-microglobulin (beta 2m) by cultured peripheral blood mononuclear cells (PBMC), as well as the levels of serum amyloid A (SAA), that is, the main hepatic acute phase protein during inflammation. The same measurements were obtained in hemodialysis (HD) patients, uremic non-dialyzed patients (ESRD) and healthy controls (CON). In CAPD, IL-6 production from PBMC was markedly increased in comparison to the control value (600.7 +/- 104.3 vs. 14.2 +/- 3.6 pg/3 x 10(6) PBMC/24 hr, P < 0.005). Similarly, a striking enhancement of the PBMC release of beta 2m was detected in CAPD with respect to CON (10.1 +/- 2.6 vs. 0.063 +/- 0.013 micrograms/3 x 10(6) PBMC/24 hr, P < 0.001). Also, the SAA levels were significantly greater in CAPD patients (21.3 +/- 8.7 micrograms/dl) than in controls (3.14 +/- 0.17 micrograms/dl, P < 0.05). Analogous increases of both IL-6 and beta 2m cell releases, as well as of SAA levels, were observed in HD patients. No difference concerning the three parameters was detected between CON and ESRD. In conclusion, CAPD induces per se PBMC activation with an enhanced release of both IL-6 and beta 2m; this is associated to higher levels of SAA. These systemic inflammatory effects are comparable to those observed in HD patients indicating that CAPD is similar to HD in terms of biocompatibility of the treatment.