Abstract
Peritonitis is still a major cause of the death in peritoneal dialysis (PD) patients despite the significant decline of the peritonitis rates in recent years. The present study is designed to evaluate the therapeutic potential of peroxisome proliferator-activated receptor-γ agonist, rosiglitazone, on the structure and function of the peritoneum in a PD rat accompanied with peritonitis induced by lipopolysaccharide (LPS). Our data showed that the peritoneal membrane in the LPS-only group showed increased peritoneal thickness, vessel density, and hypercellularity compared with the PD-only group. Rosiglitazone administration significantly inhibited increase of the three indicators in PD rats with LPS treatment. In line with this, rosiglitazone improved function of the peritoneum in LPS-induced PD rats receiving rosiglitazone, which was reflected by decreased D/P urea and D/P albumin. Mechanistically, rosiglitazone-mediated improvements in the damaged structure and function of the peritoneum in PD rats with LPS treatment were associated with reduced inflammation and preserving mesothelial cell monolayer resulted from up-regulation of AQP-1 and ZO-1. Our findings thus suggest that peroxisome proliferator-activated receptor γ (PPAR-γ) activation might be a reasonable strategy to prevent and ameliorate peritoneal deterioration in PD patients, especially with peritonitis.
Highlights
Peritoneal dialysis (PD) is a renal replacement strategy in patients with end-stage renal failure by using the peritoneum as a semipermeable membrane for ultrafiltration (UF) and diffusion
Rosiglitazone decreased the number of dialysate neutrophil in LPS-induced peritoneal dialysis (PD) rat
There were basically no differences in the lymphocyte counts among these five groups (Table 1). These results suggested that rosiglitazone could inhibit the production of neutrophils in drained dialysate induced by LPS treatment
Summary
Peritoneal dialysis (PD) is a renal replacement strategy in patients with end-stage renal failure by using the peritoneum as a semipermeable membrane for ultrafiltration (UF) and diffusion. Chronic exposure to nonphysiological PD solutions and peritonitis caused by repeated microbial infection results in a loss of the mesothelial cells monolayer, submesothelial fibrosis, angiogenesis, and hyalinizing vasculopathy, which subsequently causes increased rates of small-solute transport and ultrafiltration dysfunction of the peritoneal memc 2018 The Author(s).
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