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Volume 50, Issue 5, Pages 782-790 (November 2007)


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Neointimal Hyperplasia in Early Arteriovenous Fistula Failure

Prabir Roy-Chaudhury, MD, PhD1Corresponding Author Informationemail address, Lois Arend, MD2, Jianhua Zhang, MS1, Mahesh Krishnamoorthy, MS3, Yang Wang, MD1, Rupak Banerjee, PhD3, Antoine Samaha, MD4, Rino Munda, MD5

Received 28 January 2007; accepted 17 July 2007. published online 21 September 2007.

Refers to article:
Early Fistula Failure: Back to Basics
Laura M. Dember, Bradley S. Dixon
American Journal of Kidney Diseases
November 2007 (Vol. 50, Issue 5, Pages 696-699)
Full Text | Full-Text PDF (187 KB)
Background

Hemodialysis vascular access dysfunction currently is a huge clinical problem. Although arteriovenous fistulas (AVFs) are the preferred form of permanent dialysis access, they continue to have significant problems with early AVF failure. Although inadequate dilatation of the venous segment was believed to have a role in early AVF failure, the exact pathogenesis of early AVF failure is unknown despite the magnitude of the clinical problem.

Study Design

Case series.

Setting & Participants

Hemodialysis patients.

Outcomes & Measurements

Stenotic venous segments from 4 patients with early AVF failure were subjected to a detailed histological, morphometric, and immunohistochemical analysis.

Results

All 4 patients had significant luminal stenosis, primarily as a result of eccentric neointimal hyperplasia. This was confirmed through morphometric analysis, which documented intima-media area and thickness ratios that were greater than unity. Cellular phenotyping studies showed that the majority of cells within the region of neointimal hyperplasia were myofibroblasts, with smaller numbers of contractile smooth muscle cells.

Limitations

We described only a limited number of specimens.

Conclusions

We show for the first time that aggressive neointimal hyperplasia is present in venous segment specimens from patients with early AVF failure. Future therapies to address this problem will need to target this pathogenetic pathway.

1 Department of Medicine, Division of Nephrology, Cincinnati Dialysis Access Research Program, University of Cincinnati, Cincinnati, OH

2 Department of Pathology, University of Cincinnati, Cincinnati, OH

3 Department of Mechanical, Industrial, and Nuclear Engineering, University of Cincinnati, Cincinnati, OH

4 Department of Kidney and Hypertension Center, University of Cincinnati, Cincinnati, OH

5 Department of Surgery, University of Cincinnati, Cincinnati, OH.

Corresponding Author InformationAddress correspondence to Prabir Roy-Chaudhury, MD, PhD, Division of Nephrology, University of Cincinnati, MSB G251, 231 Albert Sabin Way, Cincinnati, OH 45267-0585.

 Originally published online as doi:10.1053/j.ajkd.2007.07.019 on September 24, 2007.

PII: S0272-6386(07)01126-2

doi:10.1053/j.ajkd.2007.07.019


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