Expression of heat shock proteins 47 and 70 in the peritoneum of patients on continuous ambulatory peritoneal dialysis

Background. Peritoneal sclerosis, characterized by collagen accumulation, i s a serious complication in continuous ambulatory peritoneal dialysis (CAPD ) therapy. Heat shock protein 47 (HSP47) is a collagen-specific molecular c haperon and is closely associated with collagen synthesis. Methods. We determined the expression of HSP47 and HSP70 (nonspecific for c ollagen synthesis) by immunohistochemistry in peritoneal tissues of patient s on CAPD. The tissue for collagen III, alpha-smooth muscle actin (alpha-SM A), and CD68 (a marker for macrophages) were also stained. Thirty-two perit oneal samples were divided into three groups (group A1, 11 patients who had no ultrafiltration loss; group A2, 9 patients who had ultrafiltration loss ; and group B, 12 specimens who had endstage renal disease prior to inducti on of CAPD. Results. In group B, staining for HSP47, HSP70, and collagen III in periton eal tissues was faint, and only a few cells were positive for alpha-SMA and CD68. In contrast, HSP47, HSP70, and collagen III were expressed in areas of thickened connective tissues in fibrotic peritoneal specimens of CAPD pa tients. The expression level of HSP47, HSP70, collagen III, and alpha-SMA a nd the number of CD68-positive cells in group A2 were significantly higher than those in groups A1 and B. HSP47/HSP70-positive cells were mesothelial cells, adipocytes, and alpha-SMA-positive myofibroblasts. Furthermore, the expression level of HSP47 was significantly higher in peritoneal specimens from patients with refractory peritonitis than without it and was significa ntly higher in patients with more than 60 months of CAPD therapy than that in patients with less than 60 months of CAPD. Conclusion. Our results indicate that CAPD therapy may induce HSPs in the p eritoneal tissue, and that peritonitis in CAPD patients may be associated w ith the progression of peritoneal sclerosis at least through HSP47 expressi on and chronic macrophage infiltration. Our data also suggest that the prog ression of peritoneal sclerosis in such patients is associated with deterio ration of peritoneal ultrafiltration function.