Stenosis complicating vascular access for hemodialysis: indications for treatment

INTRODUCTION

Vascular access (VA) for hemodialysis (HD) is the mainstay of adequate dialysis delivery (1, 2). Its complications account for significant morbidity and mortality (3, 4), along with increased financial costs (5) in end-stage renal disease (ESRD) patients.

The aim of the multidisciplinary team committed to the care of the VA is to prolong as much as possible the functional patency of the angioaccess (6, 7). To this purpose the crucial point is the timely recognition of complications menacing patency of the access and their treatment, but to date the ideal tool has yet to be found (8, 9).

Stenosis is definitely the most frequent complication of arteriovenous (AV) VA (both AV fistula and AV graft) (10). The associated clinical consequences depend on its location along the VA (Fig. 1). Whereas the best surveillance strategy is still a matter of debate (11), some evidence is now available about treatment indication and options.

Fig. 1 -

It is now clear how indications for treatment differ significantly, depending on the site of the stenosis and the hemodynamics of the access conduit (7).

The available body of evidence on the best strategy facing stenosis of VA for HD is reviewed; the authors’ opinion (interventional nephrologist/VA surgeon: [NP]; interventional radiologist: [JGM]; and nephrologist: [MH]), has been added, when no definite evidence is available.

INFLOW STENOSIS

The term refers to stenosis occurring in the arterial limb from the origin of the subclavian artery to the anastomotic and juxta-anastomotic region (12-13-14), due to both atherosclerotic lesion and Monckeberg’s medial calcification.

ARTERIAL STENOSIS

The clinical picture is generally characterized by a delayed maturation in both distal and proximal access (13) (Tab. I).

TABLE I -

Clinical consequences of different site stenoses.

INFLOW STENOSIS: INDICATION AND THERAPEUTIC OPTIONS

	Site of the stenotic lesion	Clinical picture	Indications for treatment	Treatment option
HAIDI = hemodialysis access-induced distal ischemia; PTA = percutaneous transluminal angioplasty.
*Stenosis of proximal arteries (above humeral bifurcation).
†Stenosis of ulnar artery (anastomosis on radial artery).
INFLOW STENOSIS	Arterial	- delayed maturation ("flat fistula")	- Early treatment failure	PTA
		- HAIDI	- Ischemia treatment*†,
	Anastomotic and juxta-anastomotic vein	- delayed maturation	- Early treatment failure	PTA or Surgical proximalization of anastomosis
		- drop of flow	- Restore normal flow and dialysis dose
		- asymptomatic

It could be a rare cause of ischemia induced by VA (hemodialysis access-induced distal ischemia, HAIDI) (15, 16). The physical examination (17) reveals a low-flow (“flat”) fistula. Problems in dialysis are difficult cannulation and low delivered dialysis dose (because of low blood pump flow). At ultrasound examination, reduced flow is found along with the typical ultrasound findings of an arterial stenosis (18).

Treatment options

Percutaneous transluminal angioplasty (PTA) is the best and easiest treatment (Fig. 2) (1). Even in small and calcified distal artery at the forearm, excellent results have been reported (19-20-21). Functional patency has been achieved in a high percentage of cases, with 1 year primary and secondary patency of 65%-83% and 86%-96%, respectively.

Fig. 2 -

ANASTOMOTIC AND JUXTA-ANASTOMOTIC VEIN STENOSIS

This is the most frequent lesion found in AV fistula (13), caused by the dramatic increase of shear stress along with surgical traumatism due to anastomosis creation (22, 23).

Immature fistula

The clinical picture is similar for distal and proximal AVF: pulsating anastomosis, low flow at ultrasound, difficult cannulation and reduced dialysis dose (17); therapeutic options differ, depending on the site of the anastomosis.

Distal VA

Both surgical proximalization of the anastomosis and PTA are technically feasible. Several reports, however, clearly indicate an increased number of endovascular procedures needing to be repeated, to obtain similar assisted 1 year patency compared to surgical treatment [restenosis 0.168 vs 0.519/AVF-year for surgery vs PTA (p=0.009)] (24, 25). Therefore, surgical proximalization is the treatment of choice except when multiple stenoses coexist, or whenever the length of the access is a concern.

Proximal VA

There is no available evidence regarding this complication, probably because it is a rare clinical picture (26, 27). Anecdotically and in the opinion of experts (28), PTA is the preferred treatment. Surgical proximalization above the elbow would likely require extended vein dissection and transposition to brachial artery or the use of a bypass graft. Unfortunately, a comparative study is lacking.

Mature fistula

Distal and proximal

When anastomotic or juxta-anastomotic vein stenosis symptomatically affects a distal or proximal AVF by decreasing blood flow, indication for treatment is clear and procedures and options are the same as indicated for immature AVFs.

On the other hand, a debate is going on as to whether prophylactic treatment should be performed in asymptomatic case (normal blood flow, no complication during dialysis) for both distal and proximal AVFs. Some studies (29) seem to show a beneficial effect on access survival after treatment, but in all cases the blood flow and its modification before and after treatment are the most important parameter (30); indeed, final evidence is still lacking.

In the authors’ opinion, provided that no low flow (<500 mL/min) or significant drop (>20%) in two consecutive assessments are recorded (31), no treatment should be done. First, because in the absence of low flow, no risk of thrombosis exists, necessitating no correction (32). Second, as treatment of the stenosis would lead to an increase in flow (33), high flow would likely be caused, with the risk of heart failure (34) or HAIDI (35), especially in proximal access.

MID-VEIN STENOSIS

The clinical picture is similar in both distal and proximal AVF: pulsatile conduit from the anastomosis to the stenosis, risk of aneurism degeneration (36), as well as bleeding after dialysis and skin necrosis (37) (Tab. II). It rarely affects AVF maturation, in mature VA both cannulation and dialysis dose are usually not affected because the stenosis generally falls between the arterial and venous needles. Indications for treatment are low flow and hemostatic complication (37), whereas coexistence of subclinical/clinical HAIDI contraindicates it.

TABLE II -

Inflow stenosis. A) Stenosis of radial artery (arrow) proximally to the distal left radiocephalic anastomosis (transbrachial contrast injection). B) Detail of radial artery angioplasty (4 mm x 40 mm, 15 atm) by retrograde access through the cephalic vein. C) Final angiogram.

MID-VEIN STENOSES: INDICATION AND THERAPEUTIC OPTION

	Site of the stenotic lesion	Clinical picture	Indications for treatment	Treatment option
PTA = percutaneous transluminal angioplasty.
*“Arterial” needle.
MID-VEIN STENOSIS	Between the “arterial” and “venous” needles	- delayed maturation	- Early treatment failure	PTA
		- prolonged bleeding time* (+/- drop of flow)	- Restore normal flow	(Surgical bypass)
		- aneurism degeneration* (+/- drop of flow)	- Prevent aneurism and skin necrosis

Treatment option includes surgery or PTA: some studies, evaluating the results of treatment of stenosis and thrombosis, failed to demonstrate a better treatment option (38, 39). Guidelines on VA do not indicate a preferred approach (1, 2). In the authors’ opinion, when available, PTA should be preferred because of its mini-invasive approach and better preservation of the VA length, along with future options compared to surgery.

OUTFLOW STENOSIS

GRAFT-TO-VEIN ANASTOMOTIC STENOSIS

It is the most common complication of AV graft (17). The clinical picture is characterized by prolonged bleeding after dialysis (37) and low dialysis dose (40). Blood flow measurement shows a low or decreased flow (41).

In such a situation thrombosis is the major risk and prompt stenosis resolution is mandatory.

PTA is the widely preferred treatment (1, 2), even if recurrence after treatment is high (38). To date, no definitive indication for the best surveillance tool exists (11).

CEPHALIC ARCH – END OF BASILIC VEIN TRANSPOSITION STENOSIS

The clinical picture is similar for both AVFs (Table III). The conduit access is entirely pulsatile, prolonged bleeding time is possible, along with accelerated aneurismal degeneration (42). Indication for treatment depends on access blood flow.

TABLE III -

OUTFLOW STENOSIS: INDICATION AND THERAPEUTIC OPTION

	Site of the stenotic lesion	Clinical picture	Indications for treatment	Treatment option
AVF = arteriovenous fistula; PTA = percutaneous transluminal angioplasty.
OUTFLOW STENOSIS	Graft-to-vein anastomosis	- low dialysis dose	- restore blood flow	PTA
		- prolonged bleeding time	- reduce recirculation	(surgical bypass)
			- prevent skin necrosis
	Cephalic arch – end of basilica vein transposition	- low dialysis dose	- restore blood flow	- PTA (primary stenting still debated)
		- prolonged bleeding time	- reduce recirculation
		- aneurismal degeneration	- Prevent skin necrosis	(surgical bypass)
				- blood flow reduction if high-flow AVFs
	Central vein stenosis (subclavian, brachiocephalic trunk, superior vena cava)	- Asymptomatic/paucisymptomatic (mild edema, chest collateral vein)	- no treatment needed
		- painful swelling of the upper arm	Symptoms relief	PTA (surgical bypass)
		- skin ulceration
		- intracranial hypertension

Low-normal flow

When outflow stenosis leads to low access flow, the primary indication for treatment is to prevent thrombosis (43). Moreover, by decreasing high intra-access pressure, both aneurismal degeneration and skin necrosis risk are reduced (37).

Treatment options include PTA (Fig. 3) and surgical correction. As for mid-vein stenosis, even in the absence of a demonstrated superiority, the former seems the better choice, when locally available.

Fig. 3 -

Conflicting results exist about the primary use of the stent, which seems to prolong the primary patency after treatment, but with a similar secondary patency compared to isolated PTA, along with the risk of axillary vein obstruction (44).

Normal-high flow

When a high flow exists, treatment of the stenosis is risky because of the potential of both heart failure (34) and HAIDI (35) induction. Nevertheless, those accesses could present serious hemostatic concern (37), which could be resolved just by treatment of the stenosis. A combined approach has recently been proposed, consisting of PTA associated with surgical reduction of blood flow (45).

CENTRAL VEIN STENOSIS

Subclavian, brachiocephalic and superior vena cava stenosis, mainly induced by central venous catheter or pacemaker wire (46-47-48-49), can become symptomatic if an ipsilateral angioaccess is created. Two pictures are possible, depending on the balance between upper arm blood flow and venous drainage capacity.

“Asymptomatic”

This is the picture of a documented central vein stenosis on the same side of a VA, in the absence of major symptoms. The residual lumen and collateral veins developed are sufficient to ensure adequate upper arm venous drainage. Collateral vein on the chest and a slight edema of the hand and forearm could be evident.

Some evidences (50, 51) suggest that no intervention should be performed in these cases. Indeed no clinical beneficial effect would be obtained, whereas worsening of the lesion may be induced. Renaud et al (51) recently showed that just 40% of untreated patients, followed up for an asymptomatic/paucisymptomatic mean 80% stenosis, became severely symptomatic at 4 years. They even observed a better secondary overall access and central vein patency at 3 years in untreated asymptomatic patients compared to treated symptomatic patients.

Symptomatic

When upper arm blood flow drainage becomes insufficient, major symptoms may ensue. Painful swelling of the whole upper arm, breast and head (52), skin ulceration and intracranial hypertension (53) could be present.

In such cases, relief from the debilitating symptoms is requested. Treatment options include angioaccess ligation or stenosis treatment by surgical or endovascular means. Surgical procedures (54, 55) are not recommended as the first choice, because of significant morbidity and mortality (2).

Conversely, PTA is the treatment of choice (Fig. 4) as it allows preservation of VA function along with the resolution of symptomatic venous hypertension. Unfortunately, high tendency to early restenosis leads to an average 1 year primary patency of about 40%. It still is a matter of debate if primary stenting would improve outcomes (56, 57). Until clear evidence will be provided, it seems that in clinical practice the use of stents should be reserved to elastic recoil after PTA, and for early or frequent restenoses (2).

Fig. 4 -

CONCLUSIONS

Stenosis is the most frequent complication of VA, significantly affecting patients’ morbidity and mortality. Indications and technical options for treatment differ depending on the location of the lesion and the hemodynamics of the VA. When treatment is required, PTA seems by far the preferred approach, since it is less invasive, highly repeatable and more access length sparing, compared to surgery. Careful preoperative evaluation should prevent high flow-induced heart failure and HAIDI.

Outflow stenosis. A) Cephalic arch 90% stenosis (arrow), causing elevated venous pressure during dialysis in a patient with a left brachial-cephalic fistula (blood flow 700 ml/min). B) Dilation with an 8 mm x 40 mm high-pressure balloon catheter (30 atm). C) Final angiogram: absence of residual stenosis (blood flow 1.200 mL/min).

Outflow stenosis. A) Right brachiocephalic vein occlusion (arrows), causing painful arm swelling in a 65-year-old man on hemodialysis with a brachial-cephalic fistula. B) Balloon dilatation by antegrade access through the arteriovenous fistula (14 mm x 40 mm, 17 atm). C) Successful percutaneous transluminal angioplasty resulted in immediate relief of symptoms (note disappearance of collaterals).

• 1. Tordoir J.,Canaud B.,Haage P. EBPG on vascular access. Nephrol Dial Transplant 2007; 22: ii88-ii117
• 2. K/DOQI Clinical Practice Guidelines and Clinical Practice Recommendations for 2006 Updates: hemodialysis adequacy, peritoneal dialysis adequacy, vascular access. Am J Kidney Dis 2006; 48: S1-S322
• 3. Rayner HC.,Pisoni RL.,Bommer J. Mortality and hospitalization in haemodialysis patients in five European countries: results from the DOPPS study. Nephrol Dial Transplant 2004; 19: 108-120
• 4. Polkinghorne KR.,McDonald SP.,Atkins RC.,Kerr PG. Vascular access and all-cause mortality: a propensity score analysis. J Am Soc Nephrol 2004; 15: 477-486
• 5. Sehgal AR.,Dor A.,Tsai AC. Morbidity and cost implications of inadequate hemodialysis. Am J Kidney Dis 2001; 37: 1223-1231
• 6. Turmel-Rodrigues L.,Pengloan J.,Bourquelot P. Interventional radiology in hemodialysis fistulae and grafts: a multidisciplinary approach. Cardiovasc Interv Radiol 2002; 25: 3-16
• 7. Besarab A Jariatul K Stan F Vascular Access monitoring and surveillance. In: Asif A Agarwal AK Yevzlin AS Wu S Bethard G Eds. Interventional nephrology New York McGraw-Hill 2012 121 141
• 8. Besarab A.,Lubkowski T.,Frinak S.,Ramanathan S.,Escobar F. Detecting vascular access dysfunction. ASAIO J 1997; 43: M539-M543
• 9. Tessitore N.,Bedogna V.,Melilli E. In search of an optimal bedside screening program for arteriovenous fistula stenosis. Clin J Am Soc Nephrol 2011; 6: 819-826
• 10. Beathard G Complications of vascular access. In: Lamiere N Metha R Eds. Complications of Dialysis – Recognition and Management New York Marcel Dekker, Inc. 2000 1
• 11. Paulson WD.,Moist L.,Lok CE. Vascular access surveillance: an ongoing controversy. Kidney Int 2012; 81: 132-142
• 12. Asif A.,Gadalean FN.,Merrill D. Inflow stenosis in arteriovenous fistulas and grafts: a multicenter, prospective study. Kidney Int 2005; 67: 1986-1992
• 13. Turmel-Rodrigues L.,Mouton A.,Birmelé B. Salvage of immature forearm fistulas for haemodialysis by interventional radiology. Nephrol Dial Transplant 2001; 16: 2365-2371
• 14. Duijim LE.,Liem YS.,van der Rijt RHH. Inflow stenosis in dysfunctional hemodialysis fistulae and graft. Am J Kidney Dis 2006; 48: 98-105
• 15. DeCaprio JD.,Valentine RJ.,Kakish HB.,Awad R.,Hagino RT.,Clagett GP. Steal syndrome complicating hemodialysis access. Cardiovasc Surg 1997; 5: 648-653
• 16. Arif A.,Leon C.,Merril D. Arterial Steal syndrome: a modest proposal for an old paradigm. Am J Kidney Dis 2006; 48: 88-97
• 17. Beathard GA. Physical examination of the dialysis vascular access. Semin Dial 1998; 11: 231-236
• 18. Franco G. [Contribution of ultrasonography in late maturation of native fistulae for chronic hemodialysis.] J Mal Vasc 2003; 28: 194-199
• 19. Guerra A.,Raynaud A.,Beyssen B.,Pagny JY.,Sapoval M.,Angel C. Arterial percutaneous angioplasty in upper limbs with vascular access devices for haemodialysis. Nephrol Dial Transplant 2002; 17: 843-851
• 20. Turmel-Rodrigues L.,Boutin JM.,Camiade C.,Brillet G.,Fodil-Chérif M.,Mouton A. Percutaneous dilation of the radial artery in nonmaturing autogenous radial-cephalic fistulas for haemodialysis. Nephrol Dial Transplant 2009; 24: 3782-3788
• 21. Raynaud A.,Novelli L.,Bourquelot P.,Stolba J.,Beyssen B.,Franco G. Low-flow maturation failure of distal accesses: treatment by angioplasty of forearm arteries. J Vasc Surg 2009; 49: 995-999
• 22. Pirozzi N.,Apponi F.,Napoletano AM.,Luciani R.,Pirozzi V.,Pugliese F. Microsurgery and preventive haemostasis for autogenous radial-cephalic direct wrist access in adult patients with radial artery internal diameter below 1.6 mm. Nephrol Dial Transplant 2010; 25: 520-525
• 23. Bharat A.,Jaenicke M.,Shenoy S. A novel technique of vascular anastomosis to prevent juxta-anastomotic stenosis following arteriovenous fistula creation. J Vasc Surg 2012; 55: 274-280
• 24. Tessitore N.,Mansueto G.,Lipari G. 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: 448-454
• 25. Long B.,Brichart N.,Lermusiaux P. Management of perianastomotic stenosis of direct wrist autogenous radial-cephalic arteriovenous accesses for dialysis. J Vasc Surg 2011; 53: 108-114
• 26. Hakaim AG.,Nalbandian M.,Scott T. Superior maturation and patency of primary brachiocephalic and transposed basilic vein arteriovenous fistulae in patients with diabetes. J Vasc Surg 1998; 27: 154-157
• 27. Maya ID.,O’Neal JC.,Young CJ.,Barker-Finkel J.,Allon M. Outcomes of brachiocephalic fistulas, transposed brachiobasilic fistulas, and upper arm grafts. Clin J Am Soc Nephrol 2009; 4: 86-92
• 28. Turmel-Rodrigues L. Dilatation is usually the best treatment for stenosis of the arteriovenous hemodialysis fistula. Nat Clin Pract Nephrol 2008; 4: 116-117
• 29. Tessitore N.,Mansueto G.,Bedogna V. A prospective controlled trial on effect of percutaneous transluminal angioplasty on functioning arteriovenous fistulae survival. J Am Soc Nephrol 2003; 14: 1623-1627
• 30. van der Linden J.,Smits JH.,Assink JH. Short- and long-term functional effects of percutaneous transluminal angioplasty in hemodialysis vascular access. J Am Soc Nephrol 2002; 13: 715-720
• 31. May RE.,Himmelfarb J.,Yenicesu M. Predictive measures of vascular access thrombosis: a prospective study. Kidney Int 1997; 52: 1656-1662
• 32. Schwab SJ.,Oliver MJ.,Suhocki P.,McCann R. Hemodialysis arteriovenous access: detection of stenosis and response to treatment by vascular access blood flow. Kidney Int 2001; 59: 358-362
• 33. Napoli M.,Prudenzano R.,Russo F.,Antonaci AL.,Aprile M.,Buongiorno E. Juxta-anastomotic stenosis of native arteriovenous fistulas: surgical treatment versus percutaneous transluminal angioplasty. J Vasc Access 2010; 11: 346-351
• 34. Basile C.,Lomonte C.,Vernaglione L.,Casucci F.,Antonelli M.,Losurdo N. The relationship between the flow of arteriovenous fistula and cardiac output in haemodialysis patients. Nephrol Dial Transplant 2008; 23: 282-287
• 35. Bourquelot P Access induced distal ischemia. In: Asif A Agarwal AK Yevzlin AS Wu S Bethard G Eds. Interventional nephrology. New York McGraw-Hill 2012 601 614
• 36. Beathard G Pseudoaneurism and aneurism formation. In: Asif A Agarwal AK Yevzlin AS Wu S Bethard G Eds. >Interventional nephrology. New York McGraw-Hill 2012 259 267
• 37. Pirozzi N.,Pettorini L.,Scrivano J.,Menè P.,Karam L.,Bourquelot P. Limberg skin flap for treatment of necrosis and bleeding at haemodialysis arteriovenous angioaccess puncture sites. Eur J Vasc Endovasc Surg 2013; 46: 383-387
• 38. Turmel-Rodrigues L.,Pengloan J.,Baudin S. Treatment of stenosis and thrombosis in haemodialysis fistulas and grafts by interventional radiology. Nephrol Dial Transplant 2000; 15: 2029-2036
• 39. Tordoir JH.,Bode AS.,Peppelenbosch N.,van der Sande FM.,de Haan MW. Surgical or endovascular repair of thrombosed dialysis vascular access: is there any evidence? J Vasc Surg 2009; 50: 953-956
• 40. Collins DM.,Lambert MB.,Middleton JP. Fistula dysfunction: effect on rapid hemodialysis. Kidney Int 1992; 41: 1292-1296
• 41. May RE.,Himmelfarb J.,Yenicesu M. Predictive measures of vascular access thrombosis: a prospective study. Kidney Int 1997; 52: 1656-1662
• 42. Badero OJ.,Salifu MO.,Wasse H.,Work J. Frequency of swing-segment stenosis in referred dialysis patients with angiographically documented lesions. Am J Kidney Dis 2008; 51: 93-98
• 43. Falk A.,Teodorescu V.,Lou WY.,Uribarri J.,Vassalotti JA. Treatment of ‘swing point stenoses’ in hemodialysis arteriovenous fistulae. Clin Nephrol 2003; 60: 35-41
• 44. Haage P.,Vorwerk D.,Wildberger JE.,Piroth W.,Schürmann K.,Günther RW. Percutaneous treatment of thrombosed primary arteriovenous hemodialysis access fistulae. Kidney Int 2000; 57: 1169-1175
• 45. Bourquelot P.,Gaudric J.,Turmel-Rodrigues L.,Franco G.,Van Laere O.,Raynaud A. Transposition of radial artery for reduction of excessive high-flow in autogenous arm accesses for hemodialysis. J Vasc Surg 2009; 49: 424-428
• 46. Yevzlin AS. Hemodialysis catheter-associated central venous stenosis. Semin Dial 2008; 20: 522-527
• 47. Gonsalves CF.,Eschelman DJ.,Sullivan KL. Incidence of central vein stenosis and occlusion following upper extremity PICC and port placement. Cardiovasc Interv Radiol 2003; 11: 1309-1314
• 48. Asif A.,Salman LH.,Lopera GG.,Carrillo RG. The dilemma of transvenous cardiac rhythm devices in hemodialysis patients: time to consider the epicardial approach? Kidney Int 2011; 79: 1267-1269
• 49. Mickley V. Central vein obstruction in vascular access. Eur J Vasc Endovasc Surg 2006; 32: 439-444
• 50. Levit RD.,Cohen RM.,Kwak A. Asymptomatic central venous stenosis in hemodialysis patients. Radiology 2006; 238: 1051-1056
• 51. Renaud CJ.,Francois M.,Nony A.,Fodil-Cherif M.,Turmel-Rodrigues L. Comparative outcomes of treated symptomatic versus non-treated asymptomatic high-grade central vein stenoses in the outflow of predominantly dialysis fistulas. Nephrol Dial Transplant 2012; 27: 1631-1638
• 52. Mickley V.,Rich J.,Rilinger N. Stenting of central venous stenoses in hemodialysis patients: long-term results. Kidney Int 1997; 51: 277-280
• 53. Nishimoto H.,Ogasawara K.,Miura K.,Ohmama S.,Kashimura H.,Ogawa A. Acute intracranial hypertension due to occlusion of the brachiocephalic vein in a patient undergoing hemodialysis. Cerebrovasc Dis 2005; 20: 207-208
• 54. Gradman WS.,Bressman P.,Sernaque JD. Subclavian vein repair in patients with an ipsilateral arteriovenous fistula. Ann Vasc Surg 1994; 8: 549-556
• 55. El-Sabroutra .,Duncan JM. Right atrial bypass grafting for central venous obstruction associated with dialysis access: another treatment option. J Vasc Surg 1999; 29: 472-478
• 56. Mickley V. Central vein obstruction in vascular access. Eur J Vasc Endovasc Surg 2006; 32: 439-444
• 57. Bakken AM.,Protack CD.,Saad WE.,Lee DE.,Waldman DL.,Davies MG. Long-term outcomes of primary angioplasty and primary stenting of central venous stenosis in hemodialysis patients. J Vasc Surg 2007; 45: 776-783