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Kidney Week

Abstract: TH-PO324

Activation of Formyl Peptide Receptor 1 Causes Arteriovenous Fistula Failure in Rats

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


  • Martinez, Laisel, University of Miami, Miami, Florida, United States
  • Vazquez-Padron, Roberto I., University of Miami, Miami, Florida, United States
  • Hernandez, Diana Rosa, University of Miami, Miami, Florida, United States
  • Tabbara, Marwan, University of Miami, Miller School of Medicine, Miami, Florida, United States
  • Duque, Juan Camilo, University of Miami, Miami, Florida, United States
  • Salman, Loay H., Albany Medical College, Albany, New York, United States

Formyl peptide receptor 1 (FPR1) is a recognition receptor for damage-associated molecular patterns. It is best known for mediating myeloid cell chemotaxis and activation to bacterial formylated peptides. However, it can also recognize mitochondria-derived proteins from apoptotic/necrotic cells due to the evolutionary origins of mitochondria. In a recent transcriptomics analysis of human arteriovenous fistulas (AVFs) that matured or failed after creation, higher expression of FPR1 in the native vein was associated with non-maturation. Immunohistochemistry analyses demonstrated that FPR1 was expressed in smooth muscle cells (SMCs) in the media, where it possibly sensed apoptotic/necrotic cells as a result of vascular trauma after AVF creation. In this study, we tested the effects of FPR1 activation in the maturation of experimental fistulas. We hypothesized that activation of FPR1 at the time of AVF creation would increase the frequency of fistula failure.


AVFs were created in Sprague Dawley rats (n=16) by anastomosing the superficial epigastric vein to the nearby common femoral artery. Twenty nanograms (20 ng) of the FPR1 agonist fMLF were applied perivascularly to eight AVFs in 200 uL of Matrigel at the time of fistula creation. The remaining eight fistulas received Matrigel plus vehicle (control group). AVFs were harvested at 21 days after creation.


Five out of eight AVFs (62.5%) failed to mature in the fMLF-treated subgroup, compared to one out of eight (12.5%) in control animals. Blood flow decreased from 19.2 [8.5-32.4] mL/min in control AVFs to 0.0 [0.0-6.6] mL/min in fMLF-treated fistulas (P=0.018). Venous distensibility was also significantly lower in the latter than in control AVFs, both in the juxta-anastomotic area and in the distal fistula (P<0.05).


Together with the human transcriptomics data, these results suggest that FPR1 activation is implicated in AVF maturation failure.