Objective To investigate if intraperitoneal and systemic interleukin-6 (IL-6) and soluble IL-6 receptor (sIL-6R) are related to each other and to peritoneal solute transport rate (PSTR). Design Longitudinal study in retrospectively selected patients. Setting Peritoneal dialysis (PD) unit of a university-based hospital. Patients and Methods 31 PD patients on treatment with conventional glucose-based solutions participated in a longitudinal study. IL-6 and sIL-6R were measured in plasma and overnight effluent, both at baseline and after 12 ± 2 months on PD. C-reactive protein (CRP) and serum albumin were used as surrogate markers of inflammation. PSTR of small solutes was evaluated using the dialysate-to-plasma ratio (D/P) of creatinine after a 4-hour dwell; PSTR of large solutes was evaluated using the 24-hour D/P ratio of albumin. Results D/P creat increased over time (0.67 ± 0.15 vs 0.80 ± 0.11, p < 0.0001) and correlated to D/P albumin only at the baseline evaluation. Patients with plasma IL-6 ≥median had higher ( p < 0.005) D/P creat at baseline [0.74 (0.62 – 0.87)] compared to patients with IL-6 < median [0.57 (0.47 – 0.66)]. Dialysate IL-6 at baseline was also higher ( p < 0.05) in patients with plasma IL-6 ≥median [24.7 (16.5 – 38.5) pg/mL] compared to patients with IL-6 < median [14.1 (10 – 25.7) pg/mL]. Neither CRP nor albumin changed over time on PD, although they were closely linked to plasma IL-6 levels. A strong positive correlation was found between D/P creat and dialysate IL-6 (rho = 0.77, p < 0.0001) at baseline, but not at 1 year. In contrast, there was a significant correlation between D/P creat and dialysate sIL-6R (rho = 0.39, p < 0.05) at 1 year, but not at baseline. At 1 year, 17 patients with increasing PSTR had higher increases in dialysate IL-6 (28 ± 26 vs –21 ± 78 pg/mL, p < 0.05) and levels of dialysate sIL-6R (693 ± 392 vs 394 ± 274 pg/mL, p = 0.05) compared to patients with stable PSTR ( n = 11). Patients who had peritonitis presented higher baseline serum IL-6 concentration (6.8 ± 1.0 pg/mL) compared with patients without peritonitis (4.0 ± 0.6 pg/mL, p < 0.05). Finally, both at baseline and after 1 year, there were significant correlations between plasma and dialysate IL-6 (rho = 0.46, p < 0.05, and rho = 0.40, p < 0.05) respectively. Conclusions These findings indicate that, ( 1 ) intraperitoneal and systemic inflammation increase in PD patients during the first year of therapy; ( 2 ) intraperitoneal and systemic inflammation may be interrelated and the IL-6 system may be the link; ( 3 ) the IL-6 system (both intraperitoneal and systemic) is associated with PSTR, particularly in the early phase of PD treatment, in which small and large solute transport are linked. Signs of a transition between acute and chronic inflammation were observed in the follow-up evaluation. Inflammation may, at least in part, be responsible for the development of a high PSTR, and this could be one reason for the high mortality in patients with high PSTR.

Initial fast transport was not associated with systemic inflammation and atherosclerosis. In a population with preserved RRF and absence of baseline serious co-morbidity, it was not predictive of worse prognosis. Other determinants of early peritoneal fast transport deserve investigation.

Biofilms are commonly associated with an increased risk of patient infection. In peritoneal dialysis (PD), catheter associated infection, especially peritonitis, remains a clinically relevant problem. Although the presence of a biofilm is recognized in relapsing, repeat, and catheter-related peritonitis, it remains poorly characterized. In this review, an update on the role of biofilms in PD infections is presented. The emerging concept that host cells and tissue associated biofilms, in addition to the biofilms on the catheters themselves, contribute to the recalcitrance of infections is discussed. Furthermore, the evidence of biofilms on PD catheters, their developmental stages, and the possible influence of the PD environment are reviewed. The focus is given to ex vivo and in vitro studies that contribute to the elucidation of the interplay between host, microbial, and dialysis factors. The key issues that are still to be answered and the challenges to clinical practice are discussed.