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Logo of canjkhdCanadian Journal of Kidney Health and Disease
Can J Kidney Health Dis. 2016; 3: 2054358116669126.
Published online 2016 September 27. doi:  10.1177/2054358116669126
PMCID: PMC5332078

Language: English | French

Arteriovenous Access Failure, Stenosis, and Thrombosis

Jennifer M. MacRae,1 Christine Dipchand,2 Matthew Oliver,3 Louise Moist,4 Charmaine Lok,5 Edward Clark,6 Swapnil Hiremath,6 Joanne Kappel,7 Mercedeh Kiaii,8 Rick Luscombe,9 Lisa M. Miller,10 and on behalf of the Canadian Society of Nephrology Vascular Access Work Group


Vascular access–related complications can lead to patient morbidity and reduced patient quality of life. Some of the common arteriovenous access complications include failure to mature, stenosis formation, and thrombosis.

Keywords: primary failure, primary patency, secondary patency, peripheral stenosis, angioplasty, access thrombosis, access monitoring, access surveillance


Les complications liées à la création d’un accès vasculaire peuvent s’avérer une cause de morbidité et entraîner une réduction de la qualité de vie du patient. Les complications artérioveineuses les plus répandues incluent un défaut de maturation et le développement d’une sténose ou d’une thrombose.

Vascular access–related complications can lead to patient morbidity and reduced patient quality of life. An individual’s likelihood of developing various vascular access complications varies over time.3 Some of the common arteriovenous access complications include failure to mature, stenosis formation, and thrombosis. Management and treatment of these complications are outlined below.

Arteriovenous Fistula Primary Failure

The definitions of fistula maturation and primary failure vary greatly in the literature. The definition usually relates to anatomical changes (size and flow), the ability to cannulate the fistula for hemodialysis, and whether interventions were required to promote maturation of the fistula. The period of follow-up is also an important component of the definition because longer follow-up reduces failure rates in slow to mature fistulas.

Clinical studies generally use more objective definitions of primary failure. For example, the National Institute of Health, NIH fistula maturation study4 (see “Arteriovenous Access Selection and Evaluation Fistula Maturation” section) uses the primary outcome of unassisted clinical maturation, defined as fistula use with 2 needles for more than 75% of dialysis sessions over a continuous 4-week period and either (1) 4 consecutive sessions during the 4-week period in which 2 needles are used and the mean dialysis machine blood pump speed is greater than 300 mL/min, or (2) a measured single-pool Kt/V greater than 1.4 or urea reduction ratio greater than 70% during any session in which 2 needles are used within the 4-week period. The clinical maturation criteria can be satisfied at any time within 9 months of fistula creation surgery or within 8 weeks of dialysis therapy initiation, whichever comes later. This lengthy definition speaks to the complexities of defining fistula maturation in clinical research.

Table thumbnail

The frequently cited study by Dember et al5 defined fistula suitability as the ability to use the fistula for dialysis with 2 needles and maintain a dialysis machine blood flow rate adequate for optimal dialysis (≥300 mL/min) during 8 of 12 dialysis sessions occurring during a 30-day suitability ascertainment period. An alternate definition would be whether the fistula provided reliable enough use to avoid the use of a catheter. This is a much more objective definition (the patient either has a catheter in place or they do not), and catheter avoidance is the goal of fistula creation so it should be the measure of success. Regardless of the definition used, it is very important to understand exactly how maturation (lack of primary failure) was defined in studies when interpreting risks and counseling patients.

A good estimate of risk of fistula primary failure is reported in a meta-analysis by Al-Jaishi et al6 examining fistula studies published in the year 2000 and later. This study defined primary failure as immediate failure of fistulae within 72 hours of surgery and early dialysis suitability failure, or late dialysis suitability failure based on definitions proposed by the North American Vascular Access Consortium.7,8 The overall risk of primary failure was 23% but increased to 37% in the elderly. The studies had a high degree of heterogeneity, however, reflecting the different definitions of primary failure.

Predictors of Primary Failure

Patient factors that predict primary failure include age, sex, race, diabetes, history of coronary artery disease, peripheral vascular disease, obesity, and location of the fistula.7-9 Lok et al9 developed and validated a risk predication model for fistula failure that included patient age greater than or equal to 65 years, peripheral vascular disease, coronary artery disease, and race. The risk of primary failure was 69% in the highest risk category suggesting that the benefits of fistula creation are uncertain. However, caution should be exercised when applying risk models to specific patient populations as widespread applicability is limited.10 Furthermore, surgical factors such as extent of surgical training,11 the type of anesthesia during access creation,12 and the anastomosis angle13 may also impact primary failure rates (see “Impact of Primary Failure” section in MacRae et al14).

Prevention of Fistula Primary Failure

Interventions for the prevention of primary failure include (1) health care process or team interventions, (2) medical interventions, (3) endovascular or surgical manipulations, and (4) device interventions.

Health care processes

Primary failure may be mitigated by vein preservation programs prior to access placement, although evidence for this strategy is lacking. Ontario and British Columbia have implemented “Save My Veins” and “Vein Preservation” ( programs, respectively, with the intent of preventing vein damage from venipuncture, intravenous cannulation, and peripherally inserted central catheters (PICC).

Not only are preoperative surgical factors becoming increasingly recognized as important for the successful maturation of fistula (as mentioned above), but standardized postoperative care may also play a role. Specifically, involvement of an experienced and interested surgeon may also prevent failure. For example, McLafferty et al15 found that a surgeon-directed follow-up program detected 69% of fistulae with maturation problems and salvaged 83% of them for use.

The patient should also play a role in fistula maturation with careful protection of the fistula extremity from external trauma.

Medical interventions

There are currently no proven pharmacologic therapies to prevent primary failure of fistula. Clopidogrel was previously tested in a randomized trial and found to reduce the risk of early fistula thrombosis from 19.5% to 12.2% but did not increase overall suitability of the fistulas for hemodialysis.5 However, a meta-analysis that included more than 3000 patients explored the role of antiplatelet agents around the time of fistula creation and found that access failure was significantly reduced in fistulas but not grafts. Most of the improvement occurs in the reduction in early thrombotic events.7 A large multicenter trial is underway to determine the effect of fish oil either alone or in combination with aspirin to prevent primary failure (Australia New Zealand Clinical Trials Registry 12607000569404).

Exercise, either prior to surgery or after fistula creation, may play a role in promoting fistula maturation. However, the studies are generally small and despite showing improvements in vessel diameter with isometric exercise, this has not yet been shown to influence maturation fistula outcomes.16,17

Infrared therapy may upregulate nitric oxide synthesis and result in improved endothelial function and subsequent vascular dilation leading to improved fistula maturation. In a recent meta-analysis of 4 randomized trials including 666 patients with fistulas, the unassisted primary patency at 12 months after creation appears to be improved with infrared therapy (probability ratio for patency of 1.23, 95% confidence interval [CI], 1.12-1.35).18

Management of Primary Failure

Endovascular or surgical manipulations

The main anatomic reasons for fistula nonmaturation are insufficient arterial inflow, insufficient venous dilation, and obstructions to the venous outflow tract. A particular common abnormality is juxta-anastomotic stenosis which develops after fistula creation in approximately 50% of newly created fistulas after 4 to 6 weeks of follow-up.19 However, stenosis of the arterial anastomosis and draining veins, including cephalic arch stenosis, can also develop. Endovascular treatment of these lesions can facilitate maturation in many cases. For example, Beathard et al20 reported 98% to 100% immediate technical success rates for angioplasty and eventual fistula use in 92% of their cases. Other procedures such as obliteration of collateral veins, elevation of fistula, and transposition of fistula can also facilitate maturation.

Future device interventions

Many other medical devices and therapeutic treatments are in development to reduce the risk of fistula failure caused by underlying stenosis. These include new types of anastomotic connectors, hybrid grafts, sirolimus- and paclitaxel-coated materials, and bioengineered vessels, all of which are designed to reduce stenosis formation.21 The impact of these devices and therapies is unknown at present but are a clear sign of the efforts underway to reduce fistula failure.

Key Relevant Arteriovenous Access Patency Rates

Table 1 outlines the patency rates for grafts and fistulas.

Table 1.
Comparison of Fistula Versus Graft Survival.

Arteriovenous Fistula

As indicated in Table 1, the primary failure rate of a fistula varies significantly in the literature, which leads to heterogeneity in published primary patency rates. In addition, the primary patency rates of fistula vary according to whether the primary failure rate is incorporated into the denominator and, in a 2014 meta-analysis, ranged from 60% at 1 year, 51% at 2 years (primary failure rate included) or 67% at 1 year and 51% at 2 years (excluding primary failure rate).6 Secondary patency rates for fistula were much higher at 82% at 1 year and 73% at 2 years.6

Arteriovenous Grafts

The primary failure rate for grafts is less than that for fistulas. However, given the increased number of interventions required for graft maintenance, the primary patency rate for grafts is less than that for fistulas. The secondary patency rates for grafts range widely in the literature from 57% at 1 year with standard polytetrafluoroethylene, PTFE33 to 82% with a bovine mesenteric graft (excluding primary failure rate).34 In general, PTFE forearm grafts have lower secondary patency as compared with upper arm grafts.35


  • Primary failure is a common complication for fistulas; the reported rates vary widely in the literature.
  • Interventions aimed at reducing the risk of primary failure include promoting early vein preservation, consideration of antiplatelet agents to reduce early thrombosis, and intervention with endovascular or surgical techniques to facilitate maturation.
  • Grafts tend to have a lower primary failure rate than fistulas but a worse primary patency rate as compared with fistulas. Fistulas tend to have superior primary patency rates but equivalent secondary patency rates, compared with grafts.

Arteriovenous Access (Peripheral Vein) Stenosis

The development of peripheral vein stenosis is the primary cause of fistula and graft thrombosis. The formation of stenosis is initiated by endothelial cell injury which leads to smooth muscle proliferation and neointimal hyperplasia.36-38 The following factors may lead to endothelial injury: shear stress from turbulent blood flow,38-40 mechanical trauma from venipuncture, and angioplasties.41 The most common site for stenosis in grafts occurs at the graft-vein anastomosis in 80% to 85% of the time followed by intragraft stenosis 11% to 15% and the graft-artery anastomosis 2% to 5% of the time.42 Fistulas tend to develop stenosis most commonly either at the juxta-anastomotic site and the outflow vein (70%-85%). In the remaining 15% to 30% of the time, the lesion develops on the arterial site, which includes the feeding artery and anastomosis.

Clinical Features

In a newly created fistula, maturation failure and sometimes thrombosis occur as a result of an inflow or outflow stenosis. Venous stenosis may also be discovered during access flow surveillance whereby a decrease in the access flow from the usual baseline triggers an angiogram of the arteriovenous access. In some cases, the access may present with difficulty needling, prolonged bleeding times after dialysis, or elevated venous and arterial pressures. Depending on the site of the stenosis, the fistula may have physical exam findings43,44 as described in Table 2.

Table 2.
Physical Examination of Fistula.

Treatment Options

The treatment of choice for stenotic lesions of graft and fistula is percutaneous angioplasty. Randomized studies have not demonstrated that preemptive (elective) angioplasty of stenotic lesions improves graft survival.45,46 Despite this, many programs continue to treat graft stenosis, partly because so few grafts are utilized in Canada that it is easier to use the same surveillance protocols as for fistulas (see “Prevention: Role of arteriovenous access monitoring and surveillance” section). Furthermore, some believe that the elective treatment of graft stenosis decreases the need for catheter placement. Older studies demonstrated that surgical management has better patency than angioplasty but more recent endovascular studies suggest equivalent outcomes.

Percutaneous angioplasty

Percutaneous angioplasty has a 90% initial technical success rate for both graft and fistula stenosis.47 The primary unassisted patency is worse for graft than fistula with 25% to 30% patency at 1 year for graft as compared with 67% patency for fistula.6 The secondary (assisted) patency rates are similar for both graft and fistula at approximately 82% patency at 1 year and 70% patency at 2 years.6,8 The complication rate for angioplasty is approximately 4% with hematoma formation as the most common side effect followed by oxygen desaturation and reaction to medication.47

Options for percutaneous angioplasty of recurring stenotic lesions

Angioplasty using high or ultrahigh pressure balloons has an improved immediate success rate (100%)48 compared with standard pressure balloon (92%)48 but higher risk of vein rupture. Angioplasty using a cutting balloon may increase the time to next intervention49,50 and may eliminate the need for the use of a high-pressure balloon. However, a recent randomized trial reported patency rates equivalent to those of conventional angioplasty, but greater risk of venous rupture and dissections with the use of a cutting balloon.49

Angioplasty with a drug-eluting balloon provides an antiproliferative medication such as paclitaxel to the entire area of the stenosis. This technique may have a higher 6-month patency rates (70% vs 20%) using paclitaxel eluting balloon angioplasty as compared with standard balloon angioplasty; in 1 small randomized study.51 At this time, longer term data are lacking, but a large randomized trial is underway.52

Angioplasty using stents does not appear to improve the patency rate for AV access. The main types of stents used in dialysis vascular access include self-expandable stents, covered stents (stent grafts), or drug-eluting stents. Stent grafts are increasingly used for pseudoaneurysms or in areas that are to be cannulated. Stents are only recommended when the stenotic lesion has failed conventional angioplasty with a significant amount of recoil postplasty and if surgery is not an option. Stents are also used as a treatment for vessel rupture associated with angioplasty. Drug-eluting stents (sirolimus, paclitaxel, nitinol, and others) may reduce neointimal hyperplasia and improve patency.53,54 A meta-analysis of stent placement versus angioplasty in arteriovenous access55 suggests that 6-month patency may be improved with nitinol as compared with bare metal stents although these findings are limited by significant heterogeneity and small sample size.

Concerns with using stents

The main concerns regarding the use of stents include possible vein depletion with reduced options for future surgeries, limited area of cannulation, stent migration or stent fracture, and intrastent thrombosis.56 There are no guidelines or studies on the use of anticoagulation or antiplatelet agents as prophylaxis. Furthermore, the cost of stents is prohibitive in some programs.


The surgical revision of peripheral stenosis generally provides results that are comparable57 or better than angioplasty. Surgery, however, often cannot be provided as rapidly as a percutaneous approach and has the further disadvantage that it sometimes leads to a loss of a small portion of the vein. Surgery is best considered in resistant cases when percutaneous angioplasty is not successful or when the lesion is felt to not to be amenable to angioplasty (long lengths of stenosis or significant elastic recoil).


  • Peripheral venous stenosis is the most common cause of fistula and graft dysfunction and may lead to access thrombosis
  • First-line treatment of stenosis should be balloon angioplasty
  • Stent placement in the peripheral vein is generally not recommended except in special circumstances
  • Resistant lesions should be revised surgically when the lesion is not amenable to angioplasty (long lengths of stenosis or significant elastic recoil).

Arteriovenous Access Thrombosis

A fistula can thrombose either early or late after its creation. Early thrombosis of a fistula is most often due to an inflow problem (juxta-anastomosis stenosis or accessory vein) while late thrombosis tends to be due to an outflow stenosis. If either of these lesions is left untreated, this results in thrombosis of the fistula. There are 2 types of thrombosis that can occur: soft, friable clot that disintegrates and a firm fibrin plug.58

Similar to fistulas, graft thrombosis is most often due to neointimal hyperplasia which forms stenosis and subsequent decrease in access flow and thrombosis. The most common lesion is juxta-anastomotic stenosis.

Systemic factors such as hypotension, higher hemoglobin target,59 and hypercoagulabiity60 result in increased risk of access thrombosis for both fistulas and grafts. Patient factors such as sex (female) and diabetes increase risk of fistula thrombosis as well. Thrombosis can be a complication of needling, with a 25% increased risk of thrombosis associated with hematoma from a needle complication.61

Clinical Features

A history of recent onset of difficulty needling, a significant drop in access flow (>25% drop from baseline), a new onset of low access flow (<500 mL/min) or significant recirculation all may be clues to an impending fistula thrombosis. Often there is a history of increased venous and/or arterial pressures noted with a pump speed of 200 mL/min during the first few minutes of dialysis (pressure trend monitoring). Grafts, however, often present with no warning symptoms prior to thrombosis.

The physical examination of a thrombosed fistula or graft demonstrates a lack or a reduced thrill along with an absent or abnormal bruit. The anastamosis may be pulsatile. At times, fistula thrombosis may be confused with cellulitis due to erythema and tenderness at the site. The diagnosis of access thrombosis is usually made on clinical grounds but an ultrasound can confirm the presence of thrombus and a low flow state. Treatment should be initiated as soon as possible.

Treatment Options


Surgery is an established technique for salvage of a thrombosed access. The surgical technique involves the use of a Fogarty thrombectomy combined with retrograde manual removal of clot. Initial success rates for surgical thrombectomy of arteriovenous access range from 70% to 94%62-64 with a 12-month patency rate that ranges from 68% to 88% for either fistula62 or graft.64 For patients who undergo surgical thrombectomy, a venogram with angioplasty of culprit lesions is always recommended; this may be one reason that many centers prefer an endovascular salvage of thrombosed fistula or graft. The identification and correction of underlying stenosis is an important part of postthrombosis care.

Ideally, both fistula and graft thrombosis should be treated within 48 hours in order to avoid placement of a catheter. Furthermore, older thrombi are adherent to the wall and very difficult to remove. Grafts can be salvaged up to 1 week after thrombosis, but fistulas have a shorter window of opportunity, typically 48 hours.

Endovascular intervention

An endovascular approach involves pharmacologically or mechanically disrupting and removing the thrombus, then correcting the underlying lesion. This typically involves infusion of a thrombolytic such as tissue plasminogen activator, tPA in conjunction with using a lacerating device or a balloon catheter to remove the clot. Following mechanical or pharmacologic thrombolysis, an angioplasty is done to correct any underlying stenosis.

An endovascular approach to thrombosed fistulas is associated with an 80% to 90% success rate and improved primary patency rates of 34% to 50% at 12 months.8,62,65 An endovascular approach to thrombosed graft is associated with an initial success rate of 73% with a primary patency rate of only 32% at 1 month.66

Prevention: Role of arteriovenous access monitoring and surveillance

Physical examination and clinical monitoring and assessment are the keys to AV access maintenance and should be a part of the standard care of dialysis patients.15,67-71 Physical examination and clinical monitoring of the arteriovenous access should include an assessment at each dialysis treatment and include LOOK, LISTEN for bruit, and FEEL for thrill. Clinical findings that have been associated with arteriovenous access dysfunction include physical findings of persistent swelling of the arm, presence of collateral veins, prolonged bleeding after needle withdrawal, or altered characteristics of pulse or thrill in outflow vein or graft.67 Any additional surveillance of arteriovenous access using technology is intended to supplement clinical monitoring.

The goal of clinical monitoring and access surveillance is to identify early access dysfunction and correct it with preemptive angioplasty or surgery prior to access thrombosis or loss. Access surveillance and management is an interdisciplinary team function. The patient, nephrologist, nephrology nurse, technician, interventional radiologist/nephrologist, surgeon, and primary care physician should all be participants of the team.

An ideal surveillance method should quickly, accurately, noninvasively, and economically evaluate access anatomy (eg, stenosis) and function. Measurement of dynamic venous pressure (DVP), measurement of access flow (Qa) and access recirculation, and duplex Doppler ultrasound (usually performed in radiology) are noninvasive methods of measuring the blood flow in the arteriovenous access and may be useful ancillary tests that can help confirm clinical suspicion of stenosis or access dysfunction. Access flow (Qa) and DVP are, however, surrogates for stenosis rather than direct measurements. Although these tests are associated with thrombosis, they lack the predictive accuracy needed to be the sole basis for intervention referrals. Thus, Qa and DVP should be emphasized as ancillary tests to be used in combination with information obtained from clinical monitoring. Duplex Doppler ultrasound has the advantage of directly visualizing stenosis while providing flow and velocity measurements that help determine the physiological significance of stenosis. Thus, duplex Doppler ultrasound may avoid inaccuracies inherent in surrogate measurements. However, the few available randomized controlled trials did not demonstrate improved outcomes in grafts when this form of monitoring was compared with either clinical72 or access flow monitoring.46

Access monitoring and surveillance detects underlying fistula and graft stenosis

An accurate physical exam (monitoring) combined with an access surveillance method (including lower access flows) can successfully reveal an underlying access stenosis, particularly when the stenosis is at the venous anastomosis. The duplex Doppler ultrasound accuracy for identifying stenosis was reported as 81% in fistulas,73 with a sensitivity of 93% and specificity of 60%.74 The accuracy for grafts has been reported as 86% for in-graft stenosis and 96% for outflow stenosis,73 and a 100% sensitivity and 50% specificity using duplex ultrasound.74

Access surveillance does not predict graft thrombosis

Access flow and DVP surveillance were both found to be inaccurate predictors of graft thrombosis.75-77 To date, there have been several randomized controlled trials that do not show any benefit of access flow surveillance as a means to improve graft survival,45,46,78 although the time to thrombosis may be reduced. For example, Ram et al75 studied 176 patients who underwent a total of 1957 monthly Qa measurements over 6 years. They evaluated the accuracy of monthly Qa measurements, or percentage decrease in Qa, in predicting thrombosis within the next month. They found that Qa had a sensitivity of 74% and specificity 71% using a threshold of a flow less than 1200 mL/min and a decrease in flow by more than 20%. The mean Qa for grafts that did not thrombose over the next month was 1345 mL/min (range, 90-4000), and the mean Qa for grafts that did thrombose was 895 mL/min (range, 105-2115): values overlapped widely. Moreover, the majority of thromboses were not preceded by a decrease in Qa measurement, usually because thrombosis occurred before a second measurement could be taken.

Access surveillance reduces risk of fistula thrombosis and access loss

In a 2008 meta-analysis of 12 randomized studies of which 4 included fistula only, Tonelli et al79 found that access flow surveillance of fistulas was associated with a significantly reduced relative risk of thrombosis (relative risk [RR], 0.47; 95% CI, 0.28-0.77) but not access loss (RR, 0.65; CI, 0.28-1.51).

A more recent meta-analysis80 including 7 randomized studies in fistulas reported a similar reduction in access thrombosis (RR, 0.50; CI, 0.35-0.71) as well as access loss (RR, 0.50; CI, 0.29-0.86). The reduction in access loss is based on 4 studies72,81-83 of which 3 studies81-83 are from the same center. The preemptive correction of a stenosis in 1000 patients using a fistula will prevent thrombosis in 200 patients; however, this approach will lead to a significant increase in the number of radiologic interventions with an additional 234 fistulograms.


The 2006 National Kidney Foundation Kidney Disease Quality Outcomes Initiative, NKF-KDOQI guidelines84 recommend surveillance of fistulas and grafts monthly for hemodynamically significant stenosis, when combined with correction of the anatomic stenosis, in the hope that this will improve patency rates and decrease the incidence of thrombosis. However, there is a growing body of evidence that surveillance with access flow measurements with subsequent angioplasty in the arteriovenous access with low blood flows may not improve access survival, is costly, and may even be harmfull.79,85-87 Future larger randomized trials are needed to determine the true benefits and potential harms of access flow surveillance. At this time, the frequency and the method of access surveillance are a subject of ongoing controversy.

Prevention: Role of antiplatelet and anticoagulation medication

Antiplatelet agents (aspirin, ticlopidine, and clopidogrel) have been studied for their role in prevention of fistula thrombosis; a recent meta-analysis7 demonstrated a protective effect from early thrombosis and loss of patency in fistula but unclear effect on graft patency. There does not appear to be an increased risk in major bleeding events for single antiplatelet use.7 The long-term effect of antiplatelet therapy on arteriovenous access patency remains unclear. Warfarin appears to have no role in the prevention of thrombosis.88 Fish oil appears to have a protective role for graft thrombosis; the randomized trial by Lok et al89 showed a 50% reduction in the number of thrombotic episodes (1.71 vs 3.41 per 1000 access days) as well as a reduced number of interventions required to maintain the graft (2.89 vs 4.92 per 1000 access days).


  • Access clinical monitoring using history and physical exam is the standard of practice for arteriovenous access.
  • Access surveillance involves the use of tools like dynamic or static venous pressure monitoring or access flow measurements.
  • Intervention based on surveillance does not prevent thrombosis or prolong survival in grafts but in fistulas leads to fewer thrombosis at the expense of increased interventions and does appear to prolong survival.
  • Thrombosed arteriovenous access is a medical emergency, and a salvage attempt should be made as soon as possible in order to avoid catheter placement and admission.

Central Vein Stenosis

Manifestations of central vein stenosis often become apparent when a patient has an ipsilateral access that drains into the side of the central vein stenosis. Signs of venous hypertension, with arm and hand swelling, dusky, rubor (red color) of the hand, and dilated veins on the arm and or chest wall are common. The development of central vein stenosis is thought to be related to a history of catheter90 pacemaker91,92 or PICC insertion,93,94 but cases of central vein stenosis do occur in absence of these risk factors.

The treatment of choice for symptomatic central vein stenosis is percutaneous angioplasty, with long-term patency often requiring repeated interventions.95 The role of stenting is not clear and should be reserved for lesions that have significant elastic recoil or for lesions that recur within 3 months of treatment.84 Asymptomatic lesions do not require intervention and should be monitored (see “Management of Central Vein Stenosis” in Miller et al96).


The authors thank Kirsten Campbell for her editing and management expertise and Adam Bass, Rob Quinn, and Pietro Ravani for reviewer expertise.


Ethics Approval and Consent to Participate: Ethics approval and consent to participate was not required for this trial.

Consent for Publication Availability: Consent for publication was obtained from all authors.

Availability of Data and Materials: There is no data to share.

Author Contributions: J.M.M. conceived, designed, and coordinated the review; drafted the manuscript; and critically revised the manuscript. C.D., M.O., L.M., C.L., E.C., S.H., M.K., J.K., and R.L. helped draft the manuscript and provided critical review. L.M.M. helped design and coordinate the review and provide critical review. All authors read and approved the final manuscript.

Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: The Vascular Access Work Group was supported by the Canadian Society of Nephrology through an unrestricted educational grant from Roche Pharmaceuticals, Canada.


1. Lee T, Mokrzycki M, Moist L, et al. Standardized definitions for hemodialysis vascular access. Semin Dial. 2011;24(5):515-524. [PMC free article] [PubMed]
2. Sidawy AN, Gray R, Besarab A, et al. Recommended standards for reports dealing with arteriovenous hemodialysis accesses. J Vasc Surg. 2002;35(3):603-610. [PubMed]
3. Ravani P, Gillespie BW, Quinn RR, et al. Temporal risk profile for infectious and noninfectious complications of hemodialysis access. J Am Soc Nephrol. 2013;24(10):1668-1677. [PubMed]
4. Dember LM, Imrey PB, Beck GJ, et al. Objectives and design of the hemodialysis fistula maturation study. Am J Kidney Dis. 2014;63(1):104-112. [PMC free article] [PubMed]
5. Dember LM, Beck GJ, Allon M, et al. Effect of clopidogrel on early failure of arteriovenous fistulas for hemodialysis: a randomized controlled trial. JAMA. 2008;299(18):2164-2171. [PMC free article] [PubMed]
6. Al-Jaishi AA, Oliver MJ, Thomas SM, et al. Patency rates of the arteriovenous fistula for hemodialysis: a systematic review and meta-analysis. Am J Kidney Dis. 2014;63(3):464-478. [PubMed]
7. Palmer SC, Di Micco L, Razavian M, et al. Antiplatelet therapy to prevent hemodialysis vascular access failure: systematic review and meta-analysis. Am J Kidney Dis. 2013;61(1):112-122. [PubMed]
8. Turmel-Rodrigues L, Pengloan J, Baudin S, et al. Treatment of stenosis and thrombosis in haemodialysis fistulas and grafts by interventional radiology. Nephrol Dial Transplant. 2000;15(12):2029-2036. [PubMed]
9. Lok CE, Allon M, Moist L, Oliver MJ, Shah H, Zimmerman D. Risk equation determining unsuccessful cannulation events and failure to maturation in arteriovenous fistulas (REDUCE FTM I). J Am Soc Nephrol. 2006;17(11):3204-3212. [PubMed]
10. Lilly MP, Lynch JR, Wish JB, et al. Prevalence of arteriovenous fistulas in incident hemodialysis patients: correlation with patient factors that may be associated with maturation failure. Am J Kidney Dis. 2012;59(4):541-549. [PubMed]
11. Saran R, Elder SJ, Goodkin DA, et al. Enhanced training in vascular access creation predicts arteriovenous fistula placement and patency in hemodialysis patients: results from the Dialysis Outcomes and Practice Patterns Study. Ann Surg. 2008;247(5):885-891. [PubMed]
12. Sahin L, Gul R, Mizrak A, et al. Ultrasound-guided infraclavicular brachial plexus block enhances postoperative blood flow in arteriovenous fistulas. J Vasc Surg. 2011;54(3):749-753. [PubMed]
13. Ene-Iordache B, Cattaneo L, Dubini G, Remuzzi A. Effect of anastomosis angle on the localization of disturbed flow in “side-to-end” fistulae for haemodialysis access. Nephrol Dial Transplant. 2013;28(4):997-1005. [PubMed]
14. MacRae JM, Oliver M, Clark E, et al. ; on behalf of the Canadian Society of Nephrology Vascular Access Work Group. Arteriovenous vascular access selection and evaluation. Can J Kidney Health Dis. In press.
15. McLafferty RB, Pryor RW, III, Johnson CM, Ramsey DE, Hodgson KJ. Outcome of a comprehensive follow-up program to enhance maturation of autogenous arteriovenous hemodialysis access. J Vasc Surg. 2007;45(5):981-985. [PubMed]
16. Leaf DA, MacRae HS, Grant E, Kraut J. Isometric exercise increases the size of forearm veins in patients with chronic renal failure. Am J Med Sci. 2003;325(3):115-119. [PubMed]
17. Kumar S, Seward J, Wilcox A, Torella F. Influence of muscle training on resting blood flow and forearm vessel diameter in patients with chronic renal failure. Br J Surg. 2010;97(6):835-838. [PubMed]
18. Bashar K, Healy D, Browne LD, et al. Role of far infra-red therapy in dialysis arterio-venous fistula maturation and survival: systematic review and meta-analysis. PLoS One. 2014;9(8):e104931. [PMC free article] [PubMed]
19. Allon M, Robbin ML, Young CJ, et al. Preoperative venous intimal hyperplasia, postoperative arteriovenous fistula stenosis, and clinical fistula outcomes. Clin J Am Soc Nephrol. 2013;8(10):1750-1755. [PubMed]
20. Beathard GA, Arnold P, Jackson J, Litchfield T.; Physician Operators Forum of RMSL. Aggressive treatment of early fistula failure. Kidney Int. 2003;64(4):1487-1494. [PubMed]
21. Riella MC, Roy-Chaudhury P. Vascular access in haemodialysis: strengthening the Achilles’ heel. Nat Rev Nephrol. 2013;9(6):348-357. [PubMed]
22. Allemang MT, Schmotzer B, Wong VL, et al. Arteriovenous grafts have higher secondary patency in the short term compared with autologous fistulae. Am J Surg. 2014;208(5):800-805. [PubMed]
23. Disbrow DE, Cull DL, Carsten CG, III, Yang SK, Johnson BL, Keahey GP. Comparison of arteriovenous fistulas and arteriovenous grafts in patients with favorable vascular anatomy and equivalent access to health care: is a reappraisal of the Fistula First Initiative indicated? J Am Coll Surg. 2013;216(4):679-685; discussion 685-676. [PubMed]
24. Lok CE, Sontrop JM, Tomlinson G, et al. Cumulative patency of contemporary fistulas versus grafts (2000-2010). Clin J Am Soc Nephrol. 2013;8(5):810-818. [PubMed]
25. Swindlehurst N, Swindlehurst A, Lumgair H, et al. Vascular access for hemodialysis in the elderly. J Vasc Surg. 2011;53(4):1039-1043. [PubMed]
26. Schild AF, Perez E, Gillaspie E, Seaver C, Livingstone J, Thibonnier A. Arteriovenous fistulae vs. arteriovenous grafts: a retrospective review of 1,700 consecutive vascular access cases. J Vasc Access. 2008;9(4):231-235. [PubMed]
27. Snyder DC, Clericuzio CP, Stringer A, May W. Comparison of outcomes of arteriovenous grafts and fistulas at a single veterans’ affairs medical center. Am J Surg. 2008;196(5):641-646. [PubMed]
28. Kakkos SK, Andrzejewski T, Haddad JA, et al. Equivalent secondary patency rates of upper extremity Vectra Vascular Access Grafts and transposed brachial-basilic fistulas with aggressive access surveillance and endovascular treatment. J Vasc Surg. 2008;47(2):407-414. [PubMed]
29. Keuter XH, De Smet AA, Kessels AG, van der Sande FM, Welten RJ, Tordoir JH. A randomized multicenter study of the outcome of brachial-basilic arteriovenous fistula and prosthetic brachial-antecubital forearm loop as vascular access for hemodialysis. J Vasc Surg. 2008;47(2):395-401. [PubMed]
30. Weale AR, Bevis P, Neary WD, Lear PA, Mitchell DC. A comparison between transposed brachiobasilic arteriovenous fistulas and prosthetic brachioaxillary access grafts for vascular access for hemodialysis. J Vasc Surg. 2007;46(5):997-1004. [PubMed]
31. Lee T, Barker J, Allon M. Comparison of survival of upper arm arteriovenous fistulas and grafts after failed forearm fistula. J Am Soc Nephrol. 2007;18(6):1936-1941. [PubMed]
32. Rooijens PP, Burgmans JP, Yo TI, et al. Autogenous radial-cephalic or prosthetic brachial-antecubital forearm loop AVF in patients with compromised vessels? a randomized, multicenter study of the patency of primary hemodialysis access. J Vasc Surg. 2005;42(3):481-486; discussion 487. [PubMed]
33. Tordoir JH, Hofstra L, Leunissen KM, Kitslaar PJ. Early experience with stretch polytetrafluoroethylene grafts for haemodialysis access surgery: results of a prospective randomised study. Eur J Vasc Endovasc Surg. 1995;9(3):305-309. [PubMed]
34. Bacchini G, Del Vecchio L, Andrulli S, Pontoriero G, Locatelli F. Survival of prosthetic grafts of different materials after impairment of a native arteriovenous fistula in hemodialysis patients. ASAIO J. 2001;47(1):30-33. [PubMed]
35. Akoh JA. Prosthetic arteriovenous grafts for hemodialysis. J Vasc Access. 2009;10(3):137-147. [PubMed]
36. Swedberg SH, Brown BG, Sigley R, Wight TN, Gordon D, Nicholls SC. Intimal fibromuscular hyperplasia at the venous anastomosis of PTFE grafts in hemodialysis patients. Clinical, immunocytochemical, light and electron microscopic assessment. Circulation. 1989;80(6):1726-1736. [PubMed]
37. Rekhter M, Nicholls S, Ferguson M, Gordon D. Cell proliferation in human arteriovenous fistulas used for hemodialysis. Arterioscler Thromb. 1993;13(4):609-617. [PubMed]
38. Roy-Chaudhury P, Spergel LM, Besarab A, Asif A, Ravani P. Biology of arteriovenous fistula failure. J Nephrol. 2007;20(2):150-163. [PubMed]
39. Sterpetti AV, Cucina A, Santoro L, Cardillo B, Cavallaro A. Modulation of arterial smooth muscle cell growth by haemodynamic forces. Eur J Vasc Surg. 1992;6(1):16-20. [PubMed]
40. Hsieh HJ, Li NQ, Frangos JA. Shear stress increases endothelial platelet-derived growth factor mRNA levels. Am J Physiol. 1991;260(2, pt 2):H642-H646. [PubMed]
41. Chang CJ, Ko PJ, Hsu LA, et al. Highly increased cell proliferation activity in the restenotic hemodialysis vascular access after percutaneous transluminal angioplasty: implication in prevention of restenosis. Am J Kidney Dis. 2004;43(1):74-84. [PubMed]
42. Maya ID, Oser R, Saddekni S, Barker J, Allon M. Vascular access stenosis: comparison of arteriovenous grafts and fistulas. Am J Kidney Dis. 2004;44(5):859-865. [PubMed]
43. Tessitore N, Bedogna V, Melilli E, et al. In search of an optimal bedside screening program for arteriovenous fistula stenosis. Clin J Am Soc Nephrol. 2011;6(4):819-826. [PubMed]
44. Beathard GA, Marston WA. Endovascular management of thrombosed dialysis access grafts. Am J Kidney Dis. 1998;32(1):172-175. [PubMed]
45. Moist LM, Churchill DN, House AA, et al. Regular monitoring of access flow compared with monitoring of venous pressure fails to improve graft survival. J Am Soc Nephrol. 2003;14(10):2645-2653. [PubMed]
46. Ram SJ, Work J, Caldito GC, Eason JM, Pervez A, Paulson WD. A randomized controlled trial of blood flow and stenosis surveillance of hemodialysis grafts. Kidney Int. 2003;64(1):272-280. [PubMed]
47. Beathard GA, Litchfield T.; Physician Operators Forum of Rms Lifeline I. Effectiveness and safety of dialysis vascular access procedures performed by interventional nephrologists. Kidney Int. 2004;66(4):1622-1632. [PubMed]
48. Trerotola SO, Stavropoulos SW, Shlansky-Goldberg R, Tuite CM, Kobrin S, Rudnick MR. Hemodialysis-related venous stenosis: treatment with ultrahigh-pressure angioplasty balloons. Radiology. 2004;231(1):259-262. [PubMed]
49. Vesely TM, Siegel JB. Use of the peripheral cutting balloon to treat hemodialysis-related stenoses. J Vasc Interv Radiol. 2005;16(12):1593-1603. [PubMed]
50. Kariya S, Tanigawa N, Kojima H, et al. Primary patency with cutting and conventional balloon angioplasty for different types of hemodialysis access stenosis. Radiology. 2007;243(2):578-587. [PubMed]
51. Katsanos K, Karnabatidis D, Kitrou P, Spiliopoulos S, Christeas N, Siablis D. Paclitaxel-coated balloon angioplasty vs. plain balloon dilation for the treatment of failing dialysis access: 6-month interim results from a prospective randomized controlled trial. J Endovasc Ther. 2012;19(2):263-272. [PubMed]
52. Karunanithy N, Mesa IR, Dorling A, et al. Paclitaxel-coated balloon fistuloplasty versus plain balloon fistuloplasty only to preserve the patency of arteriovenous fistulae used for haemodialysis (PAVE): study protocol for a randomised controlled trial. Trials. 2016;17(1):241. [PMC free article] [PubMed]
53. Kakisis JD, Avgerinos E, Giannakopoulos T, Moulakakis K, Papapetrou A, Liapis CD. Balloon angioplasty vs nitinol stent placement in the treatment of venous anastomotic stenoses of hemodialysis grafts after surgical thrombectomy. J Vasc Surg. 2012;55(2):472-478. [PubMed]
54. Chan MR, Bedi S, Sanchez RJ, et al. Stent placement versus angioplasty improves patency of arteriovenous grafts and blood flow of arteriovenous fistulae. Clin J Am Soc Nephrol. 2008;3(3):699-705. [PubMed]
55. Fu N, Joachim E, Yevzlin AS, Shin JI, Astor BC, Chan MR. A meta-analysis of stent placement vs. angioplasty for dialysis vascular access stenosis. Semin Dial. 2015;28(3):311-317. [PubMed]
56. Calsina L, Clara A, Collado S, Barbosa F, Martinez R, Mateos E. Treatment of arteriovenous haemodialysis graft thrombosis associated to venous anastomotic stenosis by surgical thrombectomy, covered stenting and high-pressure angioplasty. Nefrologia. 2013;33(4):564-570. [PubMed]
57. Tessitore N, Mansueto G, Lipari G, et al. Endovascular versus surgical preemptive repair of forearm arteriovenous fistula juxta-anastomotic stenosis: analysis of data collected prospectively from 1999 to 2004. Clin J Am Soc Nephrol. 2006;1(3):448-454. [PubMed]
58. Shah A, Ansari N, Hamadeh Z. Cardiac arrest secondary to bilateral pulmonary emboli following arteriovenous fistula thrombectomy: a case report with review of the literature. Case Rep Nephrol. 2012;2012:831726. [PMC free article] [PubMed]
59. Besarab A, Bolton WK, Browne JK, et al. The effects of normal as compared with low hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin. N Engl J Med. 1998;339(9):584-590. [PubMed]
60. Salmela B, Hartman J, Peltonen S, Alback A, Lassila R. Thrombophilia and arteriovenous fistula survival in ESRD. Clin J Am Soc Nephrol. 2013;8(6):962-968. [PubMed]
61. Lee T, Barker J, Allon M. Needle infiltration of arteriovenous fistulae in hemodialysis: risk factors and consequences. Am J Kidney Dis. 2006;47(6):1020-1026. [PubMed]
62. Lipari G, Tessitore N, Poli A, et al. Outcomes of surgical revision of stenosed and thrombosed forearm arteriovenous fistulae for haemodialysis. Nephrol Dial Transplant. 2007;22(9):2605-2612. [PubMed]
63. Ponikvar R. Surgical salvage of thrombosed native arteriovenous fistulas for hemodialysis by interventional nephrologists. Ther Apher Dial. 2009;13(4):340-344. [PubMed]
64. Ponikvar R, Premru V, Kersnic B. Surgical thrombectomy of thrombosed arteriovenous grafts by interventional nephrologists. Ther Apher Dial. 2011;15(3):306-310. [PubMed]
65. Schon D, Mishler R. Pharmacomechanical thrombolysis of natural vein fistulas: reduced dose of TPA and long-term follow-up. Semin Dial. 2003;16(3):272-275. [PubMed]
66. Kakkos SK, Haddad GK, Haddad JA, Scully MM. Secondary patency of thrombosed prosthetic vascular access grafts with aggressive surveillance, monitoring and endovascular management. Eur J Vasc Endovasc Surg. 2008;36(3):356-365. [PubMed]
67. Paulson WD, Moist L, Lok CE. Vascular access surveillance: an ongoing controversy. Kidney Int. 2012;81(2):132-142. [PubMed]
68. Schuman E, Ronfeld A, Barclay C, Heinl P. Comparison of clinical assessment with ultrasound flow for hemodialysis access surveillance. Arch Surg. 2007;142(12):1129-1133. [PubMed]
69. Leon C, Orozco-Vargas LC, Krishnamurthy G, et al. Accuracy of physical examination in the detection of arteriovenous graft stenosis. Semin Dial. 2008;21(1):85-88. [PubMed]
70. Asif A, Leon C, Orozco-Vargas LC, et al. Accuracy of physical examination in the detection of arteriovenous fistula stenosis. Clin J Am Soc Nephrol. 2007;2(6):1191-1194. [PubMed]
71. Leon C, Asif A. Physical examination of arteriovenous fistulae by a renal fellow: does it compare favorably to an experienced interventionalist? Semin Dial. 2008;21(6):557-560. [PubMed]
72. Scaffaro LA, Bettio JA, Cavazzola SA, et al. Maintenance of hemodialysis arteriovenous fistulas by an interventional strategy: clinical and duplex ultrasonographic surveillance followed by transluminal angioplasty. J Ultrasound Med. 2009;28(9):1159-1165. [PubMed]
73. Sands JJ, Ferrell LM, Perry MA. Systemic barriers to improving vascular access outcomes. Adv Ren Replace Ther. 2002;9(2):109-115. [PubMed]
74. Vardza Raju A, Kyin May K, Htet Zaw M, et al. Reliability of ultrasound duplex for detection of hemodynamically significant stenosis in hemodialysis access. Ann Vasc Dis. 2013;6(1):57-61. [PMC free article] [PubMed]
75. Ram SJ, Nassar R, Work J, Abreo K, Dossabhoy NR, Paulson WD. Risk of hemodialysis graft thrombosis: analysis of monthly flow surveillance. Am J Kidney Dis. 2008;52(5):930-938. [PubMed]
76. Paulson WD, Ram SJ, Birk CG, Work J. Does blood flow accurately predict thrombosis or failure of hemodialysis synthetic grafts? a meta-analysis. Am J Kidney Dis. 1999;34(3):478-485. [PubMed]
77. McDougal G, Agarwal R. Clinical performance characteristics of hemodialysis graft monitoring. Kidney Int. 2001;60(2):762-766. [PubMed]
78. Dember LM, Holmberg EF, Kaufman JS. Randomized controlled trial of prophylactic repair of hemodialysis arteriovenous graft stenosis. Kidney Int. 2004;66(1):390-398. [PubMed]
79. Tonelli M, James M, Wiebe N, Jindal K, Hemmelgarn B.; Alberta Kidney Disease Network. Ultrasound monitoring to detect access stenosis in hemodialysis patients: a systematic review. Am J Kidney Dis. 2008;51(4):630-640. [PubMed]
80. Ravani P, Quinn RR, Oliver MJ, et al. Preemptive correction of arteriovenous access stenosis: a systematic review and meta-analysis of randomized controlled trials. Am J Kidney Dis. 2015;67(3):446-460. [PubMed]
81. Tessitore N, Bedogna V, Poli A, et al. Should current criteria for detecting and repairing arteriovenous fistula stenosis be reconsidered? interim analysis of a randomized controlled trial. Nephrol Dial Transplant. 2014;29(1):179-187. [PubMed]
82. Tessitore N, Lipari G, Poli A, et al. Can blood flow surveillance and pre-emptive repair of subclinical stenosis prolong the useful life of arteriovenous fistulae? a randomized controlled study. Nephrol Dial Transplant. 2004;19(9):2325-2333. [PubMed]
83. Tessitore N, Mansueto G, Bedogna V, et al. A prospective controlled trial on effect of percutaneous transluminal angioplasty on functioning arteriovenous fistulae survival. J Am Soc Nephrol. 2003;14(6):1623-1627. [PubMed]
84. Vascular Access Work Group. Clinical practice guidelines for vascular access. Am J Kidney Dis. 2006;48(suppl 1):S176-247. [PubMed]
85. Paulson WD, Work J. Controversial vascular access surveillance mandate. Semin Dial. 2010;23(1):92-94. [PubMed]
86. Paulson WD, White JJ. Should arteriovenous fistulas and synthetic grafts undergo surveillance with pre-emptive correction of stenosis? Nat Clin Pract Nephrol. 2008;4(9):480-481. [PubMed]
87. Allon M, Robbin ML. Hemodialysis vascular access monitoring: current concepts. Hemodial Int. 2009;13(2):153-162. [PMC free article] [PubMed]
88. Crowther MA, Clase CM, Margetts PJ, et al. Low-intensity warfarin is ineffective for the prevention of PTFE graft failure in patients on hemodialysis: a randomized controlled trial. J Am Soc Nephrol. 2002;13(9):2331-2337. [PubMed]
89. Lok CE, Moist L, Hemmelgarn BR, et al. Effect of fish oil supplementation on graft patency and cardiovascular events among patients with new synthetic arteriovenous hemodialysis grafts: a randomized controlled trial. JAMA. 2012;307(17):1809-1816. [PMC free article] [PubMed]
90. MacRae JM, Ahmed A, Johnson N, Levin A, Kiaii M. Central vein stenosis: a common problem in patients on hemodialysis. ASAIO J. 2005;51(1):77-81. [PubMed]
91. Saad TF, Ahmed W, Davis K, Jurkovitz C. Cardiovascular implantable electronic devices in hemodialysis patients: prevalence and implications for arteriovenous hemodialysis access interventions. Semin Dial. 2015;28(1):94-100. [PubMed]
92. Tan CS, Jie C, Joe J, et al. The impact of transvenous cardiac devices on vascular access patency in hemodialysis patients. Semin Dial. 2013;26(6):728-732. [PubMed]
93. Allen AW, Megargell JL, Brown DB, et al. Venous thrombosis associated with the placement of peripherally inserted central catheters. J Vasc Interv Radiol. 2000;11(10):1309-1314. [PubMed]
94. Gonsalves CF, Eschelman DJ, Sullivan KL, DuBois N, Bonn J. Incidence of central vein stenosis and occlusion following upper extremity PICC and port placement. Cardiovasc Intervent Radiol. 2003;26(2):123-127. [PubMed]
95. Surowiec SM, Fegley AJ, Tanski WJ, et al. Endovascular management of central venous stenoses in the hemodialysis patient: results of percutaneous therapy. Vasc Endovascular Surg. 2004;38(4):349-354. [PubMed]
96. Miller L, MacRae JM, Kiaii M, et al. ; on behalf of the Canadian Society of Nephrology Vascular Access Work Group. Hemodialysis tunneled catheter noninfectious complications. Can J Kidney Health Dis. In press.

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