Abstract: TH-PO0703
Modeling Chronic Peritonitis in Rodents with Preexisting AKI
Session Information
- AKI: Prevention, Diagnostics, and Management
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Floyd, Deana, VA Eastern Colorado Health Care System, Aurora, Colorado, United States
- Budnick, Isadore, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
- Colbert, James, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Montford, John R., VA Eastern Colorado Health Care System, Aurora, Colorado, United States
Background
Infection is a common complication after AKI and leads to high rates of death and disability. We have previously shown that bacterial peritonitis can be modeled in mice with preexisting AKI by inoculation with high doses of a donor-derived cecal slurry (CS) solution. We developed a complementary model of chronic bacterial peritonitis using a modified protocol of daily, low dose CS administration to mice with established AKI to improve the translational investigation of AKI-induced immunodysfunction.
Methods
C57BL/6J mice underwent 3 days of aristolochic acid injections at 2.25mg/kg IP to create AKI by day 7 (N=10). Separate control animals were given a vehicle solution (N=8). On day 7, all mice were administered low dose CS (10mg of a 100mg/mL solution) IP daily for 10 days to induce chronic peritonitis. Changes in animal weight, body temperature, and survival were recorded. Plasma BUN, creatinine, cystatin C, NGAL, and spleen weight were measured from specimens obtained at collection.
Results
As compared with controls, infected AKI mice experienced significantly diminished survival starting by two days after CS injections (0% mortality vs median 7.5 day survival, controls vs AKI, p=0.002). Infected AKI mice suffered more weight loss (-6.8% vs -14% mean weight loss vs. baseline, p<0.0001 and lower body temperatures (37.2 vs 35.1 degC, p=0.009). Plasma BUN (20 vs 73 mg/dL, p=0.004), cystatin C (258 vs 515 ng/mL, p=0.013), and NGAL (1618 vs 6339 ng/mL, p=0.047) were significantly higher in infected-AKI mice at collection. Additionally, CS-induced splenic engorgement was noted in control mice and diminished in AKI mice (0.11% vs 0.06% spleen weight/body weight, p=0.002).
Conclusion
Chronic peritonitis can be successfully modeled in rodents with preexisting AKI, who have significantly worse clinical outcomes and biochemical sepsis severity versus infected controls. This model will aid investigators in further preclinical investigation into the nature of immune defects imparted by AKI.
Acknowledgment
JM grant support through a VA Merit Award (I01 BX006356)
Figure 1
Funding
- Veterans Affairs Support