CONTEXT: Mast cells (MCs) have been implicated in fibrogenesis, angiogenesis, and immunity against bacteria. These 3 mechanisms participate in the peritoneal pathology secondary to peritoneal dialysis (PD) treatment. Despite their potential relevance to PD-related pathology, few studies have focused on MCs. OBJECTIVE: To evaluate possible variations in the number of MCs during PD treatment. DESIGN: A quantitative study of tissue MCs in normal and pathologic peritoneum. Parietal peritoneal biopsies were collected from 4 groups: (1) normal controls (n = 9), (2) uremic non-PD patients (n = 16), (3) uremic patients on PD (n = 26), and (4) non-renal patients with inguinal hernia (n = 20). MCs were evaluated using immunohistochemistry for the detection of tryptase. The total number of cross sections of vessels per peritoneal field was examined in 22 of the 26 peritoneal biopsies of PD patients. RESULTS: PD tissue samples showed fibrosis, mesothelial cell loss, and variable hyalinizing vasculopathy. The number of MCs was similar in normal controls and non-PD uremic patients (mean +/- SE: 7.13 +/- 0.67 and 7.74 +/- 0.74 MCs/mm2, respectively). Peritoneal dialysis patients showed a reduction (4 +/- 0.38 MCs/mm2, P < .001), whereas hernia sac samples showed an increase (10.59 +/- 3.48 MCs/mm2). MC reduction showed no correlation with time on dialysis, fibrosis, number of vessels, or previous episodes of peritonitis. CONCLUSIONS: The peritoneum of patients receiving PD treatment shows a reduction of MCs. Despite such a reduction, fibrosis takes place, suggesting that MCs do not play a critical role in fibrosis genesis. Mast cell loss may be a contributory factor to peritonitis episodes in PD patients.
CONTEXT: Mast cells (MCs) have been implicated in fibrogenesis, angiogenesis, and immunity against bacteria. These 3 mechanisms participate in the peritoneal pathology secondary to peritoneal dialysis (PD) treatment. Despite their potential relevance to PD-related pathology, few studies have focused on MCs. OBJECTIVE: To evaluate possible variations in the number of MCs during PD treatment. DESIGN: A quantitative study of tissue MCs in normal and pathologic peritoneum. Parietal peritoneal biopsies were collected from 4 groups: (1) normal controls (n = 9), (2) uremic non-PDpatients (n = 16), (3) uremic patients on PD (n = 26), and (4) non-renal patients with inguinal hernia (n = 20). MCs were evaluated using immunohistochemistry for the detection of tryptase. The total number of cross sections of vessels per peritoneal field was examined in 22 of the 26 peritoneal biopsies of PDpatients. RESULTS:PD tissue samples showed fibrosis, mesothelial cell loss, and variable hyalinizing vasculopathy. The number of MCs was similar in normal controls and non-PD uremicpatients (mean +/- SE: 7.13 +/- 0.67 and 7.74 +/- 0.74 MCs/mm2, respectively). Peritoneal dialysis patients showed a reduction (4 +/- 0.38 MCs/mm2, P < .001), whereas hernia sac samples showed an increase (10.59 +/- 3.48 MCs/mm2). MC reduction showed no correlation with time on dialysis, fibrosis, number of vessels, or previous episodes of peritonitis. CONCLUSIONS: The peritoneum of patients receiving PD treatment shows a reduction of MCs. Despite such a reduction, fibrosis takes place, suggesting that MCs do not play a critical role in fibrosis genesis. Mast cell loss may be a contributory factor to peritonitis episodes in PDpatients.
Authors: Vanessa Marchant; Antonio Tejera-Muñoz; Laura Marquez-Expósito; Sandra Rayego-Mateos; Raul R Rodrigues-Diez; Lucia Tejedor; Laura Santos-Sanchez; Jesús Egido; Alberto Ortiz; Jose M Valdivielso; Donald J Fraser; Manuel López-Cabrera; Rafael Selgas; Marta Ruiz-Ortega Journal: Biomolecules Date: 2020-09-24