Role of platelet factor 4 in arteriovenous fistula maturation failure: What do we know so far?

Author:

Xiao Yuxuan1ORCID,Vazquez-Padron Roberto I2ORCID,Martinez Laisel2,Singer Harold A1,Woltmann Daniel1,Salman Loay H13ORCID

Affiliation:

1. Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY, USA

2. DeWitt Daughtry Family Department of Surgery, Leonard M. Miller School of Medicine, University of Miami, Miami, FL, USA

3. Division of Nephrology and Hypertension, Albany Medical College, Albany, NY, USA

Abstract

The rate of arteriovenous fistula (AVF) maturation failure remains unacceptably high despite continuous efforts on technique improvement and careful pre-surgery planning. In fact, half of all newly created AVFs are unable to be used for hemodialysis (HD) without a salvage procedure. While vascular stenosis in the venous limb of the access is the culprit, the underlying factors leading to vascular narrowing and AVF maturation failure are yet to be determined. We have recently demonstrated that AVF non-maturation is associated with post-operative medial fibrosis and fibrotic stenosis, and post-operative intimal hyperplasia (IH) exacerbates the situation. Multiple pathological processes and signaling pathways are underlying the stenotic remodeling of the AVF. Our group has recently indicated that a pro-inflammatory cytokine platelet factor 4 (PF4/CXCL4) is upregulated in veins that fail to mature after AVF creation. Platelet factor 4 is a fibrosis marker and can be detected in vascular stenosis tissue, suggesting that it may contribute to AVF maturation failure through stimulation of fibrosis and development of fibrotic stenosis. Here, we present an overview of the how PF4-mediated fibrosis determines AVF maturation failure.

Funder

The John Faunce and Alicia Tracy Roach Fund of the Community

Publisher

SAGE Publications

Subject

Nephrology,Surgery

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