Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Observational Study
. 2013 Dec;62(6):1122-9.
doi: 10.1053/j.ajkd.2013.03.040. Epub 2013 Jun 5.

Correlation of pre-existing vascular pathology with arteriovenous graft outcomes in hemodialysis patients

Affiliations
Observational Study

Correlation of pre-existing vascular pathology with arteriovenous graft outcomes in hemodialysis patients

Michael Allon et al. Am J Kidney Dis. 2013 Dec.

Abstract

Background: Arteriovenous grafts (AVGs) are prone to neointimal hyperplasia leading to AVG failure. We hypothesized that pre-existing pathologic abnormalities of the vessels used to create AVGs (including venous intimal hyperplasia, arterial intimal hyperplasia, arterial medial fibrosis, and arterial calcification) are associated with inferior AVG survival.

Study design: Prospective observational study.

Setting & participants: Patients with chronic kidney disease undergoing placement of a new AVG at a large medical center who had vascular specimens obtained at the time of surgery (n = 76).

Predictor: Maximal intimal thickness of the arterial and venous intima, arterial medial fibrosis, and arterial medial calcification.

Outcome & measurements: Unassisted primary AVG survival (time to first intervention) and frequency of AVG interventions.

Results: 55 patients (72%) underwent interventions and 148 graft interventions occurred during 89.9 years of follow-up (1.65 interventions per graft-year). Unassisted primary AVG survival was not associated significantly with arterial intimal thickness (HR, 0.72; 95% CI, 0.40-1.27; P = 0.3), venous intimal thickness (HR, 0.64; 95% CI, 0.37-1.10; P = 0.1), severe arterial medial fibrosis (HR, 0.58; 95% CI, 0.32-1.06; P = 0.6), or severe arterial calcification (HR, 0.68; 95% CI, 0.37-1.31; P = 0.3). The frequency of AVG interventions per year was associated inversely with arterial intimal thickness (relative risk [RR], 1.99; 95% CI, 1.16-3.42; P < 0.001 for thickness <10 vs. >25 μm), venous intimal thickness (RR, 2.11; 95% CI, 1.39-3.20; P < 0.001 for thickness <5 vs. >10 μm), arterial medial fibrosis (RR, 3.17; 95% CI, 1.96-5.13; P < 0.001 for fibrosis <70% vs. ≥70%), and arterial calcification (RR, 2.12; 95% CI, 1.31-3.43; P = 0.001 for <10% vs. ≥10% calcification).

Limitations: Single-center study. Study may be underpowered to demonstrate differences in unassisted primary AVG survival.

Conclusions: Pre-existing vascular pathologic abnormalities in patients with chronic kidney disease may not be associated significantly with unassisted primary AVG survival. However, vascular intimal hyperplasia, arterial medial fibrosis, and arterial calcification may be associated with a decreased frequency of AVG interventions.

Keywords: Arteriovenous graft; intimal hyperplasia; medial fibrosis; vascular calcification.

PubMed Disclaimer

Figures

Fig 1
Fig 1
Hematoxylin-eosin stains of arteries and veins used to create arteriovenous grafts. The maximal intimal thickness was measured between the internal elastic lamina (IEL) and the vascular endothelium. A. Artery without intimal hyperplasia (intimal thickness=2 μm). B. Artery with severe intimal hyperplasia (intimal thickness=134 μm). C. Vein without intimal hyperplasia (intimal thickness=2 μm). D. Vein with severe intimal hyperplasia (intimal thickness=82 μm).
Fig 2
Fig 2
Distribution of arterial and venous intimal thickness, as determined from the Hematoxylin-eosin stains of vessels obtained at the time of arteriovenous grafts. Note the values are not normally distributed.
Fig 3
Fig 3
Association of unassisted primary arteriovenous graft survival with preexisting arterial (A) and venous (B) intimal hyperplasia.
Fig 4
Fig 4
Pathologic abnormalities in the arteries obtained during arteriovenous graft creation. A+B, trichrome stain used to quantify medial fibrosis (collagen stains blue); C+D, Von Kossa stain used to quantify arterial calcification (calcium stains black). A. Artery with mild medial fibrosis (49%). B. Artery with severe medial fibrosis (86%). C. Artery with mild calcification (0.4%). D. Artery with severe calcification (47.1%).
Fig 5
Fig 5
Association of arterial medial fibrosis with unassisted primary arteriovenous graft survival.
Fig 6
Fig 6
Distribution of arterial calcification in arteriovenous grafts placed in the upper extremity and thigh.
Fig 7
Fig 7
Association of unassisted primary arteriovenous graft survival with preexisting arterial calcification.

References

    1. Lynch JR, Wasse H, Armistead NC, McClellan WM. Achieving the goal of the Fistula First Breakthrough Initiative for prevalent maintenance hemodialysis patients. Am J Kidney Dis. 2011;57:78–89. - PMC - PubMed
    1. Allon M. Current management of vascular access. Clin J Am Soc Nephrol. 2007;2:786–800. - PubMed
    1. Allon M, Zhang L, Maya ID, Bray MS, Fernandez JR. Association of factor V gene polymorphism with arteriovenous graft failure. Am J Kidney Dis. 2012;59:682–8. - PMC - PubMed
    1. Roy-Chaudhury P, Kelly BS, Miller MA, et al. Venous neointimal hyperplasia in polytetrafluoroethylene dialysis grafts. Kidney Int. 2001;59:2325–34. - PubMed
    1. Roy-Chaudhury P, Sukhatme VP, Cheung AK. Hemodialysis vascular access dysfunction: A cellular and molecular viewpoint. J Am Soc Nephrol. 2006;17:1112–27. - PubMed

Publication types