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Kidney Week

Abstract: TH-PO320

Mouse Model of Venous Stenosis

Session Information

  • Vascular Access - I
    November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

  • 704 Dialysis: Vascular Access

Authors

  • DiBartolo, Salvatore, Rush University Medical Center, Chicago, Illinois, United States
  • Altintas, Mehmet M., Rush University Medical Center, Chicago, Illinois, United States
  • Samelko, Beata, Rush University Medical Center, Chicago, Illinois, United States
  • Wasse, Monnie, Rush University Medical Center, Chicago, Illinois, United States
Background

A response of the vein wall to balloon angioplasty results in post-angioplasty restenosis (PARS). PARS impedes normal blood flow leading to a spectrum of complication and morbidities that exacerbates the outcome of vascular diseases, and remains a limiting factor for successful vascular intervention. Previous studies have indicated that mice of different inbred backgrounds have differences in arterial remodeling response, however, have not assessed the venous remodeling response.

Methods

To objectively evaluate the influence of uremia on venous remodeling, we utilized a CKD mouse model and developed a surgical technique that mimics the vascular damage of angioplasty. We recapitulated renal failure by inducing chronic renal function insufficiency via partial nephrectomy (2/3-nephrectomy) model with a high protein diet, and model venous restenosis via wire injury to the external jugular vein (EJV). To provide the basis for a genetic analysis of venous remodeling, we subjected 3 different inbred strains of mice; chosen based on their remodeling response to arterial injury (C57BL6, FVB, and SJL/J), to EJV wire injury to evaluate the cellular response involved in venous remodeling influenced by uremia.

Results

We developed a model that mimics venous stenosis in mice. Our model was validated via assessing vascular composition by immunological and histological staining and geometrical analysis (i.e., the evaluation of the lumen, intimal and medial area) by microscopy of the injured vein.

Conclusion

Our model helps us elucidate and further understand the pathophysiology of venous remodeling that occurs in hemodialysis vascular access dysfunction.

Funding

  • NIDDK Support