Accumulation of advanced glycation end products and beta 2-microglobulin in fibrotic thickening of the peritoneum in long-term peritoneal dialysis patients

作者:Nakamoto Hirotaka; Hamada Chieko*; Shimaoka Tetsutaro; Sekiguchi Yoshimi; Io Hiroaki; Kaneko Kayo; Horikoshi Satoshi; Tomino Yasuhiko
来源:Journal of Artificial Organs, 2014, 17(1): 60-68.
DOI:10.1007/s10047-013-0741-1

摘要

Characteristics of pathological alterations in long-term peritoneal dialysis (PD) are thickening of submesothelial compact (SMC) zone, small-vessel vasculopathy, and loss of mesothelial cells. Bioincompatible PD fluid plays crucial roles in peritoneal injury. Encapsulating peritoneal sclerosis (EPS), a rare and serious complication, occurred in patients on long-term PD or frequent peritonitis episodes, and similar to 50 % of EPS developed after PD cessation. We hypothesized that PD-related peritoneal injury factors induced by bioincompatible PD fluid accumulated in the peritoneum and might induce EPS. We therefore examined the accumulation of advanced glycation end products (AGE) and beta 2-microglobulin (beta 2M) in peritoneum and evaluated the relationship between their accumulation, clinical parameters, and outcome after PD cessation. Forty-five parietal peritoneal specimens were obtained from 28 PD patients, 14 uremic patients, and three patients with normal kidney function. The peritoneal equilibration test was used for peritoneal function. AGE- and beta 2M-expressing areas were found in vascular walls, perivascular areas, and the deep layer of the SMC in short-term PD patients and extended over the entire SMC in long-term patients. Peritonitis and prolonged PD treatment aggravated peritoneal thickening and the proportion of AGE-expressing areas. The proportion of beta 2M-expressing areas was increased in long-term PD patients. Thickening of the SMC and the proportions of AGE- and beta 2M-expressing areas were not related to ascites or EPS after PD withdrawal. It appears that the increased proportion of AGE and beta 2M deposition induced by long-term exposure of PD fluid may be a marker of peritoneal injury.

  • 出版日期2014-3