Changes of cytokine profiles during peritonitis in patients on continuous ambulatory peritoneal dialysis

Continuous ambulatory peritoneal dialysis (CAPD) has emerged as an importan t dialysis treatment modality worldwide. One of the major complications is bacterial peritonitis, which may result In subsequent technique failure bec ause of loss of peritoneal clearance or peritoneal fibrosis. Bacterial peri tonltis leads to the release of proinflammatory cytokines from resident and infiltrating cells in the peritoneal cavity. We studied 35 patients underg oing CAPD with acute bacterial peritonitis. All patients treated with antib iotics for 2 weeks after the clinical diagnosis of peritonitis had a good r ecovery. Peritoneal dialysate effluent (PDE) was collected on days 1, 3, 5, 10, 21, and 42 after the start of treatment. Cell populations were monitor ed by flow cytometry. PDE levels of interleukin-1 beta (IL-l), IL-6, transf orming growth factor-beta (TGF-beta), and basic fibroblast growth factor (F GF) were measured by enzyme-linked immunosorbent assay. Gene transcription of TGF-beta in macrophages from PDE was measured by quantitative polymerase chain reaction. Bacterial peritonitis was associated with a sharp increase In total cell and neutrophil counts (400-fold) in PDE up to 3 weeks after peritonltis despite clinical remission (P < 0.0001). There was an increased absolute number of macrophages during the first 3 weeks despite the reduce d percentage of macrophages among total cells in PDE compared with noninfec tive PDE. There was a progressive increase in the percentage of mesothelial cells or dead cells in the total cell population in PDE over the entire B week period. PDE levels of IL-1,IL-6, TGF-P, and FGF increased markedly on day 1 before their levels decreased gradually PDE levels of these cytokines or growth factors were significantly greater than those in noninfective PD E (n = 76) throughout the study period (P < 0.01). Similarly, TGF-P complem entary DNA (cDNA) molecules per macrophage were significantly greater than those of macrophages in noninfective PDE throughout this period (P < 0.01). There was no significant correlation between PDE levels of TGF-P and TGF-P cDNA molecules per macrophage, suggesting that peritoneal macrophages are not the only source of TGF-P in PDE. We conclude there Is an active release of proinflammatory cytokines and scierogenic growth factors through at lea st 6 weeks despite apparent clinical remission of peritonitis. The peritone al cytokine networks after peritonltis may potentially affect the physiolog ical properties of the peritoneal membrane. (C) 2000 by the National Kidney Foundation, Inc.