Pentraxin 3 as a new biomarker of peritoneal injury in peritoneal dialysis patients

• Published in: Journal of artificial organs 2013-03, Vol.16 (1), p.66-73
• Main Authors: Kanda, Reo, Hamada, Chieko, Kaneko, Kayo, Nakano, Takanori, Wakabayashi, Keiichi, Io, Hiroaki, Horikoshi, Satoshi, Tomino, Yasuhiko
• Format: Article
• Language: English
• Subjects: Adult; Aged; Antibodies; biomarkers; Biomarkers - metabolism; Biomedical Engineering and Bioengineering; C-Reactive Protein - metabolism; Cardiac Surgery; Dialysis; Effluents; End-stage renal disease; Endothelial cells; Female; Fibroblasts; Fibrosis; Gelatinase A; Hospitals; Humans; Inflammation; Injuries; Interleukin 6; Male; Medicine; Medicine & Public Health; Middle Aged; Nephrology; Original Article; pentraxins; Peritoneal Cavity - pathology; Peritoneal Dialysis - adverse effects; Peritoneal Fibrosis - diagnosis; Peritoneal Fibrosis - etiology; Peritoneal Fibrosis - metabolism; Peritoneum; Peritoneum - metabolism; Peritoneum - pathology; Peritonitis; Serum Amyloid P-Component - metabolism; Vascular diseases
• ISSN: 1434-7229; 1619-0904
• DOI: 10.1007/s10047-012-0663-3

It is well known that bioincompatible peritoneal dialysate plays a central role in the development of peritoneal fibrosis. Peritoneal inflammation continues even after the cessation of peritoneal dialysate stimulation. It is important to establish the definition of persistent inflammation in the peritoneal cavity at the cessation of peritoneal dialysis (PD). The objective of the present study was to determine whether pentraxin 3 (PTX3) in peritoneal effluent (PE) may be a new biomarker in PD patients. Serum, PE, and peritoneal specimens were obtained from 50 patients with end-stage kidney disease at Juntendo University Hospital. Samples of 19 patients were obtained at the initiation of PD and those of 31 patients at the cessation of PD. PTX3, high-sensitivity CRP, and MMP-2 and IL-6 were analyzed. An immunohistological examination using an anti-PTX3 antibody was performed. Expressions of PTX3 were observed in endothelial cells, fibroblasts, and mesothelial cells in the peritoneum. The PTX3 level in PE at the cessation of PD was significantly higher than that at the initiation of PD. Effluent PTX3 levels in patients with a history of peritonitis or a PD duration of more than 8 years were significantly higher than those in patients without peritonitis or patients with a PD duration of