Animal Models for Studying Pathophysiology of Hemodialysis Access

Rotmans J.I*, 1, 2
1 Department of Nephrology, Leiden University Medical Center, The Netherlands
2 Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, The Netherlands

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© J.I. Rotmans; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Department of Nephrology, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands; Tel: + 31 71 5262148; Fax: + 31 71 5266868; E-mail:


Despite extensive efforts, most approaches to reduce arteriovenous (AV) access-related complications did not results in substantial improvement of AV access patency thus far. Part of this disappointing progress relates to incomplete understanding of the underlying pathophysiology of hemodialysis access failure. In order to unravel the pathophysiology of hemodialysis access failure, animal models that closely mimic human pathology are of utmost importance. Indeed, it is impossible to study the extremely complex response of the AV access at a molecular and cellular level in great detail in dialysis patients. Over the past decades, numerous animal models have been developed in an attempt to unravel the vascular pathology of AV access failure and to design new therapeutic strategies aimed to improve durability of these vascular conduits. While large animals such as pigs are suitable for intervention studies, murine models have the greatest potential to gain more insight in the molecular mechanisms underlying AV access failure due to the availability of transgenic mice. In the present review, we describe several existing models of AV access failure and discuss the advantages and limitations of these models.

Keywords: Animal models, hemodialysis access failure, intimal hyperplasia, pathophysiology, vascular remodeling..