The low patency rates of Arteriovenous (AV) fistulae are well documented in the literature [1]. Up to 90% of AV fistula morbidity is caused by stenotic lesion formation and the subsequent development of thrombosis in the Vascular Access (VA) junction [1]. The underlying pathology of these stenotic lesions is intimal hyperplasia (IH) which has been characterized by the degradation of the extra cellular matrix (ECM), migration and proliferation of smooth muscle cells (SMCs) and the infiltration of leukocytes and monocytes into the intima. IH primarily occurs in a number of key locations within the VA junction of AV fistulae which include the suture line of the anastomosis, on the floor of the vein opposite the VA junction and downstream of the anastomosis within the venous conduit of the AV fistula [2].

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