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MO682: Serum Total Indoxyl Sulfate is Associated with Intraperitoneal Inflammation and High Peritonitis Episodes in Peritoneal Dialysis Patients


 
 
 The accumulating evidence presented thus far supports the idea that indoxyl sulfate (IS) is a trigger of chronic inflammation in end-stage kidney disease patients. However, although serum IS is one of the most extensively studied uremic toxins, no single study exists which has investigated the association between serum IS and intraperitoneal inflammation in peritoneal dialysis (PD) patients.
 The present study was undertaken to evaluate the association between serum total IS (tIS) concentration and the pro-inflammatory markers in peritoneal dialysis effluent (PDE) and peritonitis episodes in PD patients.
 
 
 
 In this observational cross-sectional study, we analysed serum tIS concentration and 24-h PDE levels of interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein -1 (MCP-1) in 74 PD patients with an average age of 55 (38–64) years and dialysis vintage of 36 (30–58) months. All patients had been undergoing continuous ambulatory PD and had no PD-associated infectious complications for more than 3 months.
 Serum concentrations of tIS were determined using the spectrophotometry method. The concentrations of IL-6, TNF-α and MCP-1 in PDE were analysed using ELISA.
 For the statistical analysis, we stratified this PD patient cohort into two groups depending on experienced peritonitis: the peritonitis group (n = 48) and the peritonitis-free group (n = 26). The data were presented as the median and the interquartile ranges [Me (Q25–Q75)] and compared using the Kruskal–Wallis test. The Spearmen correlation test was performed to assess the association between IS and the pro-inflammatory markers.
 
 
 
 Significant differences were found in serum concentrations of tIS and PDE levels of IL-6 between the peritonitis and the peritonitis-free PD patients (Table 1).
 In addition, serum tIS was significantly associated with number of experienced peritonitis episodes (r = 0.26, P = 0.022).
 Although PDE levels of TNF-a and MCP-1 did not differ between the peritonitis and the peritonitis-free groups in our cohort, they had a direct association with serum tIS similar to those of IL-6 (Fig. 1, 2).
 Moreover, serum tIS was statistically higher in the anuric PD patients compared with the non-anuric patients [33.6 (13.9–74) versus 20.2 (9.3–46) μg/mL, P = 0.043], had a negative association with residual renal function (r = −0.39, P = 0.0017) and, accordingly, total weekly Kt/V (r = −0.27, P = 0.026).
 
 
 
 Serum tIS concentration has a significant direct association with PDE levels of the pro-inflammatory markers, high peritonitis episodes and their outcomes in PD patients. Further well-designed studies are required to establish the effect of serum tIS concentration on intraperitoneal inflammation and clinical outcomes in PD patients.
