Peritoneal fibrosis is a major complication of
peritoneal dialysis that can lead to ultrafiltration failure. This study investigates the protective effects of
calcitriol on
chlorhexidine digluconate-induced
peritoneal fibrosis in rats.
Peritoneal fibrosis was induced in Sprague-Dawley rats by daily administration of 0.5mL 0.1%
chlorhexidine digluconate in
normal saline via
peritoneal dialysis for 1week. Rats received daily
intravenous injections of
calcitriol (low-dose, 10ng/kg; or high-dose, 100ng/kg) for 1week. After 7days, conventional 4.25% Dianeal (30mL) was administered via
peritoneal dialysis over 4h. Peritoneal solute transport was calculated from the
dialysate concentration relative to its concentration in the initial infused
dialysis solution (D4/D0
glucose) for
glucose, and the
dialysate-to-plasma concentration ratio (D4/P4
urea) at 4h for
urea. Rats were then sacrificed and the liver peritoneum was harvested for immunohistochemical analysis via microscopy. After dialysis, the D4/P4
Urea level was reduced; increases were observed in the D4/D0
glucose level and the levels of active transforming growth factor-β1 and
angiotensin II in serum and
dialysate; the liver peritoneum and muscle peritoneum was markedly thickened, and the expression of α-SMA,
fibronectin,
collagen,
vascular endothelial growth factor,
angiotensin II, transforming growth factor-β1, and phosphorylated Smad2/3 (P-Smad2/3)-positive cells in the liver peritoneum was elevated in the
peritoneal fibrosis group compared with the vehicle group.
Calcitriol decreased the serum and
dialysate active transforming growth factor-β1 and
angiotensin II level, decreased the thickness of the liver peritoneum and muscle peritoneum, and decreased the expression of α-SMA,
fibronectin,
collagen,
vascular endothelial growth factor,
angiotensin II, transforming growth factor-β1, and P-Smad2/3-positive cells in liver peritoneum cells. High-dose
calcitriol exhibited better protective effects against
peritoneal fibrosis than did the lower dose.
Calcitriol protected against
chlorhexidine digluconate-induced
peritoneal fibrosis in rats by decreasing transforming growth factor-β1 and
angiotensin II production.