The U.S. Renal Data System reported that >30,000 patients are diagnosed with end stage renal disease (ESRD) annually.1 The prevalence of chronic kidney disease has continued to increase exponentially, from <5% in 2007 to 14.5% in 2017 in the United States.1 Over 80% of these receive renal replacement therapy via hemodialysis access. 1 Central venous stenosis (CVS) is one of the most challenging complications in patients with upper extremity hemodialysis access, since it can threaten the patency of the arteriovenous access and cause debilitating symptoms.2 These lesions often involve the subclavian and innominate veins and may cause venous hypertension, massive arm edema, and eventual failure of the distal fistula.3 Repeated catheterization with central lines and implantable devices with venous wires as well as progressive intimal changes from high-flow turbulence predisposes patients to the development of CVS.4,5 The prevalence of CVS in dialysis patients is estimated to be 15-30%, with more than half symptomatic.6 However, the specific prevalence of subclavian stenosis secondary to thoracic outlet compression is unknown in this patient population.

The National Kidney Foundation anticipates the number of patients requiring long-term hemodialysis will continue to rise, perhaps also leading to an increase in number of patients with CVS.7 Some of the central venous lesions threatening ipsilateral AV access patency may be due to compression at the costoclavicular junction. Management of these dialysis-associated lesions mimics that of venous thoracic outlet syndrome (TOS) and may benefit from first rib or clavicle resection.8 This paper reviews management of subclavian vein stenosis secondary to compression thoracic outlet space in patients with ipsilateral arteriovenous access.