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Antibiotic administration in an animal model of chronic peritoneal dialysate exposure
Siska Mortier1, An S De Vriese, Anne Leyssens
1Renal Unit, Department of Respiratory Diseases, University Hospital, Ghent, Belgium. siska.mortier@ugent.be
Objectives:
The high incidence of intraperitoneal infection remains an important problem in animal models of chronic dialysate exposure. Prophylactic antibiotic administration can be used to resolve this problem, but the isolated effects of antibiotics on peritoneal membrane function and structure are unknown. The present study examined the effects of prophylactic antibiotics on infection rate and peritoneal membrane function and structure in a rat model of chronic dialysate exposure.
Design:
A first group of rats (A; n = 12) received 10 mL 3.86% glucose dialysate twice daily through a heparin-coated catheter. In a second group of animals (B; n = 12), oxacillin 2.5 mg/day and gentamicin 0.04 mg/day were added to the dialysate. Group C (n = 12) was injected twice daily with an identical dose of antibiotics dissolved in 1 mL of buffer solution. Group D (n = 12) was left untreated. Dialysate cultures were obtained regularly. After 8 weeks of exposure, peritoneal transport studies were performed and samples for histology were obtained.
Results:
Technique survival was 92% in group A and 100% in the remaining groups. Five rats in group A but none of the animals in the other groups developed peritonitis. The transport rates of small solutes were elevated and net ultrafiltration was decreased in group A compared to the controls. Fibrosis, as evaluated by quantifying Picro Sirius Red staining with image analysis, was significantly elevated in group A (3.48% +/- 1.06% vs 0.72% +/- 0.51% in group D, p < 0.05) but not in group B (0.29% +/- 0.07%) or in group C (0.52% +/- 0.28%). Vascular density, measured by counting the number of blood vessels that stained positive for endothelial NO synthase, was increased in both groups that were exposed to dialysate: 153.0 +/- 12.9/microm2 in group A and 131.6 +/- 14.3/microm2 in group B, versus 76.76 +/- 12.37/microm2 in group C and 73.2 +/- 10.4/microm2 in group D (p < 0.01).
Conclusions:
Prophylactic administration of oxacillin and gentamicin adequately prevented intraperitoneal infection in an animal model of chronic dialysate exposure. In addition, fibrosis was absent, suggesting intraperitoneal infection rather than dialysate exposure is a causative factor.
Insights
Prophylactic antibiotics prevented infection in a rat model of chronic dialysate exposure. This study suggests infection, not dialysate, causes fibrosis, offering insights into peritoneal membrane health.
Area of Science:
- Nephrology
- Peritoneal Dialysis
- Animal Models
Background:
- Intraperitoneal infection is a significant complication in chronic dialysate exposure models.
- The impact of prophylactic antibiotics on peritoneal membrane function and structure is not well understood.
Purpose of the Study:
- To investigate the effects of prophylactic antibiotics on infection rates.
- To assess the influence of prophylactic antibiotics on peritoneal membrane structure and function in rats undergoing chronic dialysate exposure.
Main Methods:
- Rats received daily glucose dialysate, with some groups receiving oxacillin and gentamicin in the dialysate or via injection.
- Peritoneal transport studies and histological analyses were conducted after 8 weeks.
- Infection rates were monitored through regular dialysate cultures.
Main Results:
- Prophylactic antibiotics (oxacillin and gentamicin) completely prevented peritonitis in treated groups.
- Elevated solute transport and decreased ultrafiltration were observed in the non-antibiotic dialysate group.
- Fibrosis was significantly increased in the non-antibiotic dialysate group but absent in antibiotic-treated groups.
Conclusions:
- Prophylactic oxacillin and gentamicin effectively prevented intraperitoneal infection in this rat model.
- The absence of fibrosis in antibiotic-treated groups indicates infection, not dialysate exposure, is the primary cause of fibrosis.