Regular hemodialysis reverses gastric mucosal atrophy of patients with chronic renal failure

Abstract

Background/aims: Gastric mucosa of patients with chronic renal failure on regular hemodialysis is known to retain fundic glands relatively intact, but no evidence for regeneration of fundic glands by hemodialysis has been provided to date. This study was performed to investigate endoscopically and histopathologically if hemodialysis to treat renal failure would regenerate the background gastric mucosa and to elucidate factors associated with the mucosal regeneration.

Methodology: First, the relationship between duration of hemodialysis and the degree of atrophy of the background gastric mucosa was investigated in patients with chronic renal failure treated and not treated by hemodialysis. Treated patients were further divided into long-term group treated for 4 years or longer and short-term group treated for shorter than 4 years. The degree of atrophy of gastric mucosa was evaluated by hematoxylin-eosin staining, PAS-alucian blue staining and immunohistochemical staining to detect Ki-67 expression using biopsy specimens obtained from gastric mucosa. The labeling index is the proportion of positively labeled cells with respect to the total number of cells. The proliferative index was calculated by multiplying the labeling index and the proliferative zone (length of the area between the uppermost and lowest labeled cells). Serum gastrin, glucagon and cholecystokinin were assayed as well as urine epidermal growth factor to elucidate factors associated with regeneration of gastric mucosa. Helicobacter pylori infection was examined by ELISA.

Results: In the long-term group, the degree of atrophy of gastric mucosa was endoscopically evaluated to be C1 type. In both of the two hemodialysis groups, endoscopically identified fundic gland region was histologically confirmed to be fundic glands by both hematoxylin-eosin staining and PAS-alucian blue staining. Epithelial cell proliferative index was significantly higher in long-term and short-term hemodialysis group than non-hemodialysis group (P=0.0001). No significant difference in serum gastrin, glucagon and cholecystokinin as well as urine epidermal growth factor was detectable among the three groups. Most patients of both hemodialysis groups were H. pylori-negative.

Conclusions: A possibility of regeneration of the background gastric mucosa in proportion to the duration of hemodialysis was suggested on the basis of histopathological evidence. The observed regeneration of gastric mucosa was ascribable to elimination of factors associated with atrophy of gastric mucosa including H. pylori by hemodialysis.