A mathematical model of venous neointimal hyperplasia formation
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A mathematical model of venous neointimal hyperplasia formation Paula Budu-Grajdeanu1, Richard C Schugart1, Avner Friedman*1, Christopher Valentine2, Anil K Agarwal2 and Brad H Rovin2 Address: 1Mathematical Biosciences Institute, The Ohio State University, Columbus, OH, USA and 2Division of Nephrology, Department of Internal Medicine at The Ohio State University College of Medicine, Columbus, OH, USA Email: Paula Budu-Grajdeanu - [email protected]; Richard C Schugart - [email protected]; Avner Friedman* - [email protected]; Christopher Valentine - [email protected]; Anil K Agarwal - [email protected]; Brad H Rovin - [email protected] * Corresponding author
Published: 23 January 2008 Theoretical Biology and Medical Modelling 2008, 5:2
doi:10.1186/1742-4682-5-2
Received: 18 September 2007 Accepted: 23 January 2008
This article is available from: http://www.tbiomed.com/content/5/1/2 © 2008 Budu-Grajdeanu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: In hemodialysis patients, the most common cause of vascular access failure is neointimal hyperplasia of vascular smooth muscle cells at the venous anastomosis of arteriovenous fistulas and grafts. The release of growth factors due to surgical injury, oxidative stress and turbulent flow has been suggested as a possible mechanism for neointimal hyperplasia. Results: In this work, we construct a mathematical model which analyzes the role that growth factors might play in the stenosis at the venous anastomosis. The model consists of a system of partial differential equations describing the influence of oxidative stress and turbulent flow on growth factors, the interaction among growth factors, smooth muscle cells, and extracellular matrix, and the subsequent effect on the stenosis at the venous anastomosis, which, in turn, affects the level of oxidative stress and degree of turbulent flow. Computer simulations suggest that our model can be used to predict access stenosis as a function of the initial concentration of the growth factors inside the intimal-luminal space. Conclusion: The proposed model describes the formation of venous neointimal hyperplasia, based on pathogenic mechanisms. The results suggest that interventions aimed at specific growth factors may be successful in prolonging the life of the vascular access, while reducing the costs of vascular access maintenance. The model may also provide indication of when invasive access surveillance to repair stenosis should be undertaken.
Background Vascular access dysfunction in chronic hemodialysis patients Healthy kidneys filter wastes from blood and regulate electrolyte, acid-base, and volume homeostasis. When the kidneys fail, one needs treatment to replace the wo
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