LAUSR

Elevated uric acid (UA), a byproduct of purine metabolism, is known to contribute to oxidative stress and inflammation. In patients undergoing peritoneal dialysis (PD), efficient clearance of UA is crucial for regulating systemic UA levels. However, the potential effects of UA on the peritoneal membrane function remain unclear. This study investigates the relationship between peritoneal uric acid clearance (pUACl), markers of systemic and intraperitoneal inflammation, and the peritoneal membrane function measured by peritoneal transport status, ultrafiltration (UF) rate and peritoneal Kt/V. We hypothesized that increased pUACl in normouricemic PD patients could exacerbate intraperitoneal inflammation and impair peritoneal membrane function. A total of 120 patients aged 50 (38-64) years with a dialysis vintage of 36 (17-60.5) months, who had been undergoing continuous ambulatory PD for at least 3 months before enrollment, were included in this cross-sectional study. Key parameters measured included serum, urine, and dialysate uric acid (UA) concentrations, weekly peritoneal (pUACl), urinary (uUACl) and total UA (tUACl) clearances, creatinine clearance (CrCl), peritoneal UF rate and Kt/V, interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1) in serum and dialysate, and serum C-reactive protein (CRP) levels. Weekly pUACl was calculated using the following formula: Data were presented as medians with interquartile ranges (Me [25th–75th percentiles]) and analyzed using the Kruskal-Wallis test. Correlations between variables were assessed using Spearman's test, and logistic regression analysis was performed to identify factors associated with a peritoneal Kt/V <1.7. The median serum UA levels and pUACl were significantly lower in women compared to men: 283.3 (248.9–304.5) vs. 315.7 (272.0–333.5) μmol/L (P < 0.0001) and 30.1 (23.4–42.8) vs. 36.4 (32.7–47.3) L/week/1.73 m² (P = 0.008), respectively. Moreover, pUACl were significantly lower in patients with high peritoneal transport status compared to high-average and low-average transporters: 26.7 (20.6–34.5) vs. 32.2 (24.8–41.3) vs. 38.5 (35.1–47.2) L/week/1.73 m², respectively (P = 0.01). Patients with preserved diuresis exhibited lower pUACl values compared to those with anuria (29.7 [25.9–35] vs. 39.2 [24.1–47.2] L/week/1.73 m², P = 0.01). No significant association was found between pUACl and uUACl (r = 0.021, P = 0.81). Both pUACl (r = −0.21, P = 0.03) and uUACl (r = 0.45, P < 0.0001) correlated with serum UA, whereas no correlation was observed between tUACl and serum UA (r = −0.06, P = 0.49) in our normourecemic cohort. pUACl showed a strong positive correlation with dialysate UA levels (r = 0.87, P < 0.0001), creatinine clearance (CrCl) (r = 0.41, P < 0.0001), and ultrafiltration rate (r = 0.21, P = 0.01), but a negative correlation with peritoneal Kt/V (Fig. 1). Additionally, pUACl was positively associated with dialysate IL-6 (r = 0.38, P < 0.0001), MCP-1 (r = 0.42, P < 0.0001), and serum MCP-1 (r = 0.39, P < 0.0001) and CRP levels (r = 0.37, P = 0.006). Logistic regression, adjusted for age, dialysis vintage, diuresis, diabetes, peritoneal transport status, and dialysate cytokines, identified pUACl as a significant predictor of peritoneal Kt/V <1.7 (OR 1.07, 95% CI 1.02–1.19). Our findings suggest that while higher pUACl may contribute to better overall UA removal, it might also be associated with increased systemic and intraperitoneal inflammation and potential deterioration of peritoneal membrane function. Further research is warranted to elucidate the mechanisms underlying these associations.