Chronic kidney disease refers to an irreversible, progressive reduction of the renal function of kidneys. When there is a significant loss of renal function a replacement therapy is sought. A kidney transplant is the optimal replacement. However, the demand for kidney transplantation exceeds the supply of transplantable organs and most patients will never receive a kidney transplant. As a consequence, these patients are often referred to hemodialysis to filter blood. To facilitate efficient and adequate dialysis an access capable of supplying high flow rates is required. An arteriovenous fistula is the access modality of choice for patients requiring hemodialysis. This access is formed from the anastomosis of an artery and vein which generates the high flow rates needed for efficient dialysis. Despite the preference of this access, the modality suffers from drastically poor primary and secondary patency rates which necessitate urgent improvement. Following the creation of the access a period of time is required to ensure adequate remodelling and maturation of the fistula occurs prior to cannulation. Non-maturation contributes significantly to the dismal patency rates of this access. Impaired outward remodelling and aggressive intimal hyperplasia are both considered to contribute to fistula non-maturation and the abnormal hemodynamics arising from fistula creation are believed to provide a stimulus for both facets of remodelling. Increasing an understanding of this relationship forms the primary focus of this dissertation. The primary aim of this thesis is to accurately characterise the hemodynamics of an arteriovenous fistula using experimental and numerical models. An unsteady incompressible Navier Stokes solver strategy was implemented and validated as a reliable computational approach to accurately estimate the pressure drop across a representative fistula. Both in-vitro and numerical models demonstrated a quadratic relationship between pressure drop and flow rate across the anastomosis. Instabilities were found to develop within the anastomosis and generated high frequency oscillations of the pressure drop signal. These instabilities were most prevalent during the end of the systole and throughout diastole phase of the cycle.
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