INFLAMMATORY EFFECTS OF PERITONEAL-DIALYSIS - EVIDENCE OF SYSTEMIC MONOCYTE ACTIVATION

We evaluated in peritonitis-free patients undergoing continuous ambula tory peritoneal dialysis (CAPD) the release of both interleukin-6 (IL- 6) and beta-2-microglobulin (beta(2)m) by cultured peripheral blood mo nonuclear cells (PBMC), as well as the levels of serum amyloid A (SAA) , that is, the main hepatic acute phase protein during inflammation. T he same measurements were obtained in hemodialysis (HD) patients, urem ic non-dialyzed patients (ESRD) and healthy controls (CON). In CAPD, I L-6 production from PBMC was markedly increased in comparison to the c ontrol 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(2)m was detected in CAPD with respect to CON (10.1 +/- 2.6 vs. 0 .063 +/- 0.013 mu g/3 x 10(6) PBMC/24 hr, P < 0.001). Also, the SAA le vels were significantly greater in CAPD patients (21.3 +/- 8.7 mu g/dl ) than in controls (3.14 +/- 0.17 mu g/dl, P < 0.05). Analogous increa ses of both IL-6 and beta(2)m cell releases, as well as of SAA levels, were observed in HD patients. No difference concerning the three para meters was detected between CON and ESRD. In conclusion, CAPD induces per se PBMC activation with an enhanced release of both IL-6 and beta( 2)m; this is associated to higher levels of SAA. These systemic inflam matory effects are comparable to those observed in HD patients indicat ing that CAPD is similar to HD in terms of biocompatibility of the tre atment.