Hemodialysis

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Dialysis Main Page

Patient Information

Overview

Components

Dialyzer
Dialysate
Blood Delivery System

Vascular Access

Anticoagulation

Monitoring and Adequacy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2] Seyedmahdi Pahlavani, M.D. [3]

Overview

The goal of hemodialysis is removing toxins and aim to maintain euvolemia. Ninety three percent of ESRD patients in the United States and 89% worldwide, are under hemodialysis.[1] Solute diffusion across a membrane is the basic principle for hemodialysis. Metabolic waste products move across a semipermeable membrane depending on their concentration gradient between plasma and dialysate. Concentration gradient, membrane surface area, the membrane thickness, and size of solute molecule are important factors determining rate of diffusion. Small molecules clear more efficiently than larger molecules. Fluid removal is another advantage of hemodialysis that could be achieved by ultrafiltration. In-center hemodialysis and home hemodialysis are available for ESRD patients requiring renal replacement therapy; the choice of modality is based on patient condition, patient preference, and the availability of equipments.

Components

The Dialyzer

Dialyzer is usually made of bundles of hollow fibers permitting a high flow rate of blood and dialysate simultaneously. Parallel plates are another type of dialyzer that are barely used in recent times. Most of the dialyzers are synthetic with a variety of materials including polyamide, polyarylethersulfone, polyvinylpyrrolidone, polyacrylonitrile, and polysulfone. Biocompatible membranes have the advantage of not activating complement system.

The Dialysate

The dialysate is a paramount composition in hemodialysis. Solutes diffuse across the dialyzer between blood and dialysate. The dialysate composition should be individualized to restore plasma normal values. The main solutes in dialysate include sodium, potassium, calcium, magnesium, chloride, bicarbonate , and glucose. These electrolytes are treated with water during the process. About 100 liters of water is needed for each dialysis session. The water used for hemodialysis should be processed in order to have a balanced concentration of solutes. Also, contaminants including bacteria, viruses, and heavy metals, such as aluminium should be removed from water. This removal could be done either by using reverse osmosis or deionization. Filters may be used to improve water quality by removing particles. The dialyzate temperature could also be adjusted to cause vasoconstriction and improve patient's hemodynamics.

The choice of the dialysate is important to maintain or correct the electrolytes.

  • Sodium: Usually, sodium concentration of 140-145 mEq/L is suitable for most of the patients but, it could be adjusted based on patient's sodium level.
  • Potassium: The potassium concentration in dialysate solution depends on patient potassium level. For example: For patients with hyperkalemia, a potassium concentration of 2-3 mEq/L is appropriate and for patients with hypokalemia, a potassium concentration of 4 mEq/L is appropriate.
  • Calcium: Dialysate concentration for calcium are available with 2.5 ,3, or 3.5 mEq/L. In most of the cases a 2.5 mEq/L solution which is equivalent to 5 mg/dl ionized calcium is used.

Blood Delivery System

The blood pump delivers blood from the arterial line to the dialyzer and then return it to the venous line. It's speed could be adjusted based on patient condition typically between 200 to 600 mL/min. This pump allows creating a transmembrane pressure in dialyzer by sucking dialysate. The dialysate flow rate is between 500 to 800 mL/min.

Vascular Access

  • The establishment and maintenance of reliable vascular access is crucial for long-term hemodialysis.
  • Creating arteriovenous (AV) access by establishing arteriovenous fistula (AVF) is the most reliable vascular access. On the other hand, arteriovenous graft (AVG) may provide access in certain circumstances by placing a prosthetic or biograft. However, majority of patients need temporary access by tunneled catheters for initiating hemodialysis.
  • Insertion of central catheter may cause complications, such as arterial and ventricular dysrhythmias, arterial puncture, hemothorax, pneumothorax, air embolism, perforation of central vein or cardiac chamber, and pericardial tamponade.
  • Infection is another concern regarding catheter care. Migration of bacteria from patient's skin is the mechanism of catheter infection. Skin preparation before procedure by using chlorhexidine at the catheter exit site could prevent catheter infection. Staphylococcus epidermidis, is the most common isolate. Prompt catheter removal is recommended if evidences of site infection is present even in the absence of systemic signs.
  • Catheter thrombosis may cause block blood flow is another aspect of catheter care. Instilling alteplase in the affected catheter lumen for 30 to 120 minutes is the preferred treatment.
  • Central vein stenosis: Subclavian vein catheters have a higher risk of stenosis. Using a dilator and ultrasound guided inserting may decrease the risk of vessel trauma and consequently minimize the likelihood of stenosis.

Vascular Access Complications (AV Fistula and AV Graft)

Arteriovenous access complications can occur immediately after access creation or develop months to years later due to altered hemodynamics and repeated cannulation. Contemporary practice emphasizes tailoring access choice and management to individual patient factors and preserving a functional access while minimizing morbidity.[2]

Epidemiology

Access related hand ischemia occurs in approximately 1 percent to 20 percent of patients after access creation, with 1 percent to 9 percent requiring surgical treatment.[3][4][5][6][7][8]

Pathophysiology

Mechanisms include arterial occlusive disease proximal or distal to the anastomosis, increased blood flow through the access, and inadequate adaptation of distal collateral networks.[3][4][8][9][10]

Risk factors

Peripheral vascular disease, diabetes, coronary artery disease, advanced age, female sex, brachial artery based inflow, multiple prior access procedures, and prior steal increase risk.[3][4][8][9][11]

Clinical features

Symptoms range from coolness and paresthesia to weakness, rest pain, ulceration, and tissue loss, and may worsen during dialysis. Improvement in perfusion findings with manual access compression supports the diagnosis.[6][10]

Diagnostic evaluation

Duplex ultrasonography assesses arterial stenosis or occlusion and may show retrograde flow from the distal artery into the access. Retrograde flow can occur in asymptomatic patients.[12]

Access flow assessment is helpful. High flow is typically greater than 800 mL per minute for autogenous access and greater than 1200 mL per minute for nonautogenous access.[12][13][14]

Digital pressures and digital brachial index can support the diagnosis. A basal digital pressure less than 80 mm Hg and a digital brachial index less than 0.6 to 0.7 have been associated with ischemia, although standardized thresholds are not established.[15][16]

Management

Mild symptoms may be monitored. Lifestyle limiting symptoms or tissue threatening ischemia warrant intervention.[2]

If arterial inflow obstruction is present, endovascular angioplasty with or without stenting is preferred.[2]

For high flow access related ischemia, flow reduction strategies include banding or plication. Precision banding and plication can relieve symptoms but overcorrection can lead to thrombosis and undercorrection can fail to resolve symptoms.[17][18][19]

For severe ischemia, access preserving reconstructive options include distal revascularization with interval ligation, revision using distal inflow, and proximalization of arterial inflow. Outcomes across series show high symptom resolution with variable 1 year patency depending on technique and conduit.[20][21]

For radial artery based forearm access, distal radial artery ligation may improve symptoms in selected patients with adequate ulnar and palmar arch perfusion.[22]

Access ligation is reserved for refractory ischemia, failure of reconstructive options, or limited life expectancy.[23]

Ischemic Monomelic Neuropathy

Ischemic monomelic neuropathy is rare but limb threatening and may occur within hours after access creation, typically with severe pain and global sensory and motor deficits despite preserved distal pulses and a warm hand. Diagnosis is frequently delayed because perfusion can appear normal. Immediate access ligation is recommended to prevent permanent sensorimotor loss affecting the median, ulnar, and radial nerves.[24][25]

Neuropathies in Hemodialysis Patients

Carpal tunnel syndrome

Carpal tunnel syndrome is more common in hemodialysis patients and is associated with dialysis related amyloid deposition and longer dialysis duration. Symptoms are in the median nerve distribution and often worsen at night. Nerve conduction studies confirm the diagnosis. Management ranges from splinting and therapy to surgical decompression. Coexisting access related ischemia or venous hypertension can exacerbate symptoms and should be evaluated.[26][27][28][29]

Ulnar neuropathy

Ulnar neuropathy occurs in a substantial minority of hemodialysis patients and may relate to positioning and compression during dialysis, ischemia from shunting, and amyloid deposition. Electromyography confirms diagnosis. Management is usually conservative, with surgical decompression for severe cases.[30]

Aneurysm and pseudoaneurysm

Arteriovenous fistula aneurysm

Aneurysmal dilation of AVFs is common and associated with repeated cannulation and outflow stenosis. Concerning findings include rapid expansion, prolonged post-dialysis bleeding, skin thinning, ulceration, and adherence of skin to the aneurysm.[31][32][33][34]

Asymptomatic aneurysms generally do not require repair. In symptomatic patients, evaluation for outflow stenosis and treatment of stenosis are important to reduce recurrence.[31]

Open repair is typically favored over endovascular repair due to lower thrombosis, fewer secondary interventions, reduced catheter need, and better long term function in comparative analyses. Techniques include aneurysmorrhaphy, resection with primary anastomosis, and interposition grafting, with aneurysmorrhaphy showing favorable patency in reported series. Staged repair can preserve dialysis function when multiple segments are involved.[32][35][36][37]

Pseudoaneurysm

Pseudoaneurysms occur predominantly in AVGs and are associated with repeated puncture and graft degeneration. Cannulation at the pseudoaneurysm site should be avoided. Small stable pseudoaneurysms may be observed. Indications for repair include enlargement, multiple pseudoaneurysms limiting cannulation sites, threatened skin integrity, or pain. Concern for infection requires graft excision.[33][38]

Bleeding from arteriovenous access

Access bleeding can rapidly become life threatening. Causes include pseudoaneurysm rupture, overlying skin ulceration, trauma, or graft integrity compromise from repeated cannulation, and persistent post cannulation bleeding may indicate venous outflow stenosis.[39]

Initial management includes firm direct pressure for 30 to 40 minutes. Non surgical hemostatic strategies and compression adjuncts have been described.[40]

If manual pressure fails, temporary proximal occlusion using a blood pressure cuff can be used. A superficial figure 8 or purse string stitch may be used as a temporizing measure, avoiding deep placement that could ligate the access. Tourniquet use should be brief to reduce neuromuscular risk. Urgent vascular access evaluation is required, and definitive management depends on etiology.[41]

Infection of arteriovenous access

Infection risk is lower in AVFs and higher in AVGs, with reported ranges approximately 0.56 percent to 5 percent for AVFs and 4 percent to 20 percent for AVGs. Organisms commonly include Staphylococcus species and Pseudomonas, and polymicrobial infections can occur. Virulent organisms increase risk of anastomotic disruption.[8][42]

Imaging may assist diagnosis. CT and ultrasonography can show perigraft fluid and inflammatory changes, and tagged leukocyte imaging has demonstrated higher sensitivity and specificity in vascular graft infection literature when CT is nondiagnostic.[43][44]

Management depends on extent and organism. Localized superficial AVF infection may be treated with broad spectrum antibiotics, while anastomotic involvement often requires ligation or revision with biologic conduit. For AVG infection, partial graft excision with segmental bypass may be considered for localized infection, while extensive infection, anastomotic involvement, occlusion, highly virulent organisms, or recurrent bacteremia generally favor total graft excision for source control.[45][46][47][48]

Anticoagulation

Dialysis patients tend to have greater risk of thrombosis due to increased factor VII activity, increased fibrinolytic activity, and elevated fibrinogen levels. However, uremic state may poses patients to bleeding diathesis. Also, dialysis procedure may increase turbulent blood flows with high shear stress which may activate platelets. All of these concepts emerge the use of anticoagulants during hemodialysis. Heparin (UFH) is the most frequently used form of anticoagulants. The usual heparin dose is 50 to 100 U/kg bolus at the initiation which followed by 100 U/hour. Activated clotting time (ACT) is measured in certain circumstances to assess the level of anticoagulation by maintaining it above 200 to 250 sec. Some patients have a higher risk of bleeding which requires a regional anticoagulation. In this method, extracorporeal dialyzer is heparinized in the arterial line and protamine is administered in the venous line. Another strategy is not using any forms of anticoagulation which hemodialysis is initiated with a high blood flow rate to decrease the risk of thrombosis and using saline flush technique which, the dialyzer is flushed with 50 mL of saline every 15 to 60 minutes.

High output heart failure due to arteriovenous access

Arteriovenous access creation can reduce systemic vascular resistance and increase cardiac output, and in some patients this contributes to high output heart failure. Risk factors include preexisting heart failure, brachial artery based access, larger anastomotic length, and high access flow.[49]

Clinical findings may include Nicoladoni Branham sign, where access compression produces transient hypertension and bradycardia.[50]

Echocardiography may show a hyperdynamic circulation and chamber dilation, and duplex ultrasound may show high access flow, often greater than 2000 mL per minute. Definitive attribution to access is supported when flow reduction improves cardiac function. Management options include flow reduction procedures or ligation, with ligation appropriate in patients who no longer require access after transplant.[51][52][53][54]

Monitoring and Adequacy

The dialysis adequacy is measured by using two factors, Kt/V and the urea reduction rate:

  • Kt/V: measures the ratio of cleared plasma (Kt) to the volume of urea distribution (V). The goal is to keep the ratio above 1.2 however, Kt/V higher than 1.4 may show more efficient dialysis.
  • Urea reduction ratio (URR): It reflects the removal of urea. URR is calculated by using the pre and post dialysis BUN measures. URR = (BUN pre-BUN post) / BUN pre It is recommended to keep URR 65% to 70%.

A typical hemodialysis is usually between 3 to 4 hours and three times a week. Blood flow is between 400 to 500 mL/min. However, for central venous catheter it might be lower about 350 to 400 mL/min. Dialysate flow rate is between 500 to 800 mL/min. Large size dialyzer may improve the adequacy.

References

  1. ↑ Collins AJ, Foley RN, Gilbertson DT, Chen SC (June 2015). "United States Renal Data System public health surveillance of chronic kidney disease and end-stage renal disease". Kidney Int Suppl (2011). 5 (1): 2–7. doi:10.1038/kisup.2015.2. PMC 4455192. PMID 26097778.
  2. ↑ 2.0 2.1 2.2 Lok CE, Huber TS, Lee T, et al; National Kidney Foundation. KDOQI clinical practice guideline for vascular access: 2019 update. Am J Kidney Dis. 2020;75(4)(suppl 2):S1-S164. doi:10.1053/j.ajkd.2019. 12.001
  3. ↑ 3.0 3.1 3.2 Morsy AH, Kulbaski M, Chen C, Isiklar H, Lumsden AB. Incidence and characteristics of patients with hand ischemia after a hemodialysis access procedure. J Surg Res. 1998;74(1):8-10. doi: 10.1006/jsre.1997.5206
  4. ↑ 4.0 4.1 4.2 Lazarides MK, Staramos DN, Panagopoulos GN, Tzilalis VD, Eleftheriou GJ, Dayantas JN. Indications for surgical treatment of angioaccess-induced arterial “steal”. J AmColl Surg. 1998;187(4):422-426. doi:10.1016/S1072-7515(98)00139-2
  5. ↑ HaimovM, Baez A, Neff M, Slifkin R. Complications of arteriovenous fistulas for hemodialysis. Arch Surg. 1975;110(6):708-712. doi: 10.1001/archsurg.1975.01360120026004
  6. ↑ 6.0 6.1 Odland MD, Kelly PH, Ney AL, Andersen RC, Bubrick MP. Management of dialysis-associated steal syndrome complicating upper extremity arteriovenous fistulas: use of intraoperative digital photoplethysmography. Surgery. 1991;110(4):664- 669.
  7. ↑ Davidson D, Louridas G, Guzman R, et al. Steal syndrome complicating upper extremity hemoaccess procedures: incidence and risk factors. Can J Surg. 2003;46(6):408-412.
  8. ↑ 8.0 8.1 8.2 8.3 Ballard JL, Bunt TJ, Malone JM. Major complications of angioaccess surgery. Am J Surg. 1992;164(3):229-232. https://dx.doi.org/10.1016/S0002-9610(05)81076-1
  9. ↑ 9.0 9.1 Valentine RJ, Bouch CW, Scott DJ, et al. Do preoperative finger pressures predict early arterial steal in hemodialysis access patients? a prospective analysis. J Vasc Surg. 2002;36(2):351-356. doi:10. 1067/mva.2002.125848
  10. ↑ 10.0 10.1 Malik J, Tuka V, Kasalova Z, et al. Understanding the dialysis access steal syndrome. a review of the etiologies, diagnosis, prevention and treatment strategies. J Vasc Access. 2008;9(3):155-166. doi: 10.1177/112972980800900301
  11. ↑ Kudlaty EA, Kendrick DE, AllemangMT, Kashyap VS,Wong VL. Upper extremity steal syndrome is associated with atherosclerotic burden and access configuration. Ann Vasc Surg. 2016;35:82-87. doi: 10.1016/j.avsg.2016.01.058
  12. ↑ 12.0 12.1 Sivanesan S, How TV, Bakran A. Characterizing flow distributions in AV fistulae for haemodialysis access. Nephrol Dial Transplant. 1998;13(12):3108- 3110. doi:10.1093/ndt/13.12.3108
  13. ↑ van Hoek F, Scheltinga MRM, Luirink M, Raaymakers LCJ, van Pul C, Beerenhout CH. Access flow, venous saturation, and digital pressures in hemodialysis. J Vasc Surg. 2007;45(5):968-973. doi:10.1016/j.jvs.2006.12.064
  14. ↑ Ravindhran B, Totty JP, SidapraM, et al. Long term outcomes of ‘Christmas tree’ banding for haemodialysis access induced distal ischemia: a 13-year experience. J Vasc Access. 2024;25(3): 863-871. doi:10.1177/11297298221141497
  15. ↑ Modaghegh MHS, Roudsari B, Hafezi S. Digital pressure and oxygen saturation measurements in the diagnosis of chronic hemodialysis access-induced distal ischemia. J Vasc Surg. 2015; 62(1):135-142. doi:10.1016/j.jvs.2015.02.024
  16. ↑ Papasavas PK, Reifsnyder T, Birdas TJ, Caushaj PF, Leers S. Prediction of arteriovenous access steal syndrome utilizing digital pressure measurements. Vasc Endovascular Surg. 2003;37(3):179-184. doi: 10.1177/153857440303700304
  17. ↑ Soo Hoo AJ, Scully RE, Sharma G, et al. Contemporary outcomes of precision banding for high flow hemodialysis access. J Vasc Access. 2023; 24(6):1260-1267. doi:10.1177/11297298221076581
  18. ↑ Yaghoubian A, de Virgilio C. Plication as primary treatment of steal syndrome in arteriovenous fistulas. Ann Vasc Surg. 2009;23(1): 103-107. doi:10.1016/j.avsg.2008.08.009
  19. ↑ Zanow J, Petzold K, Petzold M, Krueger U, Scholz H. Flow reduction in high-flow arteriovenous access using intraoperative flow monitoring. J Vasc Surg. 2006;44(6):1273-1278. doi:10.1016/j.jvs. 2006.08.010
  20. ↑ Kordzadeh A, Parsa AD. A systematic review of distal revascularization and interval ligation for the treatment of vascular access-induced ischemia. J Vasc Surg. 2019;70(4):1364-1373. doi:10.1016/j. jvs.2019.02.060
  21. ↑ Scali ST, Chang CK, Raghinaru D, et al. Prediction of graft patency and mortality after distal revascularization and interval ligation for hemodialysis access-related hand ischemia. J Vasc Surg. 2013;57(2):451-458. doi:10.1016/j.jvs.2012. 08.105
  22. ↑ Fitzgibbon JJ, Heindel P, Hentschel DM, Ozaki CK,Hussain MA. Contemporary outcomes of distal radial artery ligation for access related hand ischemia. J Vasc Access. 2025;26(1):149-155. doi:10. 1177/11297298231195910
  23. ↑ Leake AE, Winger DG, Leers SA, Gupta N, Dillavou ED. Management and outcomes of dialysis access-associated steal syndrome. J Vasc Surg. 2015;61(3):754-760. doi:10.1016/j.jvs.2014.10.038
  24. ↑ Thermann F, Kornhuber M. Ischemic monomelic neuropathy: a rare but important complication after hemodialysis access placement—a review. J Vasc Access. 2011;12(2):113- 119. doi:10.5301/JVA.2011.6365
  25. ↑ Wilbourn AJ, Furlan AJ, HulleyW, Ruschhaupt W. Ischemic monomelic neuropathy. Neurology. 1983;33(4):447-451. doi:10.1212/WNL.33.4.447
  26. ↑ Larson E, Lancaster T, Pelrine E,Werner B, Deal DN. Carpal tunnel release in the dialysis-dependent population: Incidence and outcomes. J Hand Microsurg. 2024;16(3):100056. doi:10.1016/j.jham. 2024.100056
  27. ↑ Kopeć J, Gadek A, Drozdz M, et al. Carpal tunnel syndrome in hemodialysis patients as a dialysis-related amyloidosis manifestation– incidence, risk factors and results of surgical treatment. Med Sci Monit. 2011;17(9):CR505-CR509. doi:10.12659/MSM.881937
  28. ↑ Kwon HK, Pyun SB, ChoWY, Boo CS. Carpal tunnel syndrome and peripheral polyneuropathy in patients with end stage kidney disease. J Korean Med Sci. 2011;26(9):1227-1230. doi:10.3346/jkms. 2011.26.9.1227
  29. ↑ Grant Y, Freilich S, Horwitz MD, Shemesh D, Crane J. Carpal tunnel syndrome in patients with arteriovenous fistula for haemodialysis: a narrative review of the current literature. J Vasc Access. 2021; 22(5):795-800. doi:10.1177/1129729820948690
  30. ↑ Nardin R, Chapman KM, Raynor EM. Prevalence of ulnar neuropathy in patients receiving hemodialysis. Arch Neurol. 2005;62(2): 271-275. doi:10.1001/archneur.62.2.271
  31. ↑ 31.0 31.1 Patel MS, Street T, Davies MG, Peden EK, Naoum JJ. Evaluating and treating venous outflow stenoses is necessary for the successful open surgical treatment of arteriovenous fistula aneurysms. J Vasc Surg. 2015;61(2):444-448. doi: 10.1016/j.jvs.2014.07.033
  32. ↑ 32.0 32.1 Yan Q, Davies MG. Comparison of open and endovascular aneurysm repair in native arteriovenous fistulas. Ann Vasc Surg. 2024;100: 233-242. doi:10.1016/j.avsg.2023.09.102
  33. ↑ 33.0 33.1 Shah AS, Valdes J, Charlton-Ouw KM, et al. Endovascular treatment of hemodialysis access pseudoaneurysms. J Vasc Surg. 2012;55(4):1058- 1062. doi:10.1016/j.jvs.2011.10.126
  34. ↑ Jankovic A, Donfrid B, Adam J, et al. Arteriovenous fistula aneurysm in patients on regular hemodialysis: prevalence and risk factors. Nephron Clin Pract. 2013;124(1-2):94-98. doi:10. 1159/000355548
  35. ↑ Baláž P, Rokošný S, Bafrnec J, Whitley A, O’Neill S. Repair of aneurysmal arteriovenous fistulae: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg. 2020;59(4):614-623. doi:10.1016/j. ejvs.2019.07.033
  36. ↑ Chang R, Alabi O, Mahajan A, et al. Arteriovenous fistula aneurysmorrhaphy is associated with improved patency and decreased vascular access abandonment. J Vasc Surg. 2023;77 (3):891-898.e1. doi:10.1016/j.jvs.2022.10.054
  37. ↑ Yan Q, Davies MG. Outcomes of one-stage and two-stage aneurysm repair in arteriovenous fistulae. J Vasc Surg. 2024;79(3):662-670.e3. doi: 10.1016/j.jvs.2023.10.057
  38. ↑ Dosluoglu HH, Harris LM. Hemodialysis access: nonthrombotic complications. In: Sidawy AN, Perler BA, eds. Rutherford’s Vascular Surgery and Endovascular Therapy. Vol 10. 2nd ed. Elsevier; 2022. doi:10.1016/b978-1-4160-5223-4.00075-5
  39. ↑ Ellingson KD, Palekar RS, Lucero CA, et al. Vascular access hemorrhages contribute to deaths among hemodialysis patients. Kidney Int. 2012;82 (6):686-692. doi:10.1038/ki.2012.185
  40. ↑ Greenstein R, Nawrocki P, Nesbit C. Bottle it up: prehospital management of an AV fistula bleed using a bottle cap. Am J Emerg Med. 2023;67: 197.e1-197.e2. doi:10.1016/j.ajem.2023.03.011
  41. ↑ Hancock HM, Stannard A, Burkhardt GE, et al. Hemorrhagic shock worsens neuromuscular recovery in a porcine model of hind limb vascular injury and ischemia-reperfusion. J Vasc Surg. 2011; 53(4):1052-1062. doi:10.1016/j.jvs.2010.10.104
  42. ↑ Padberg FT Jr, Calligaro KD, Sidawy AN. Complications of arteriovenous hemodialysis access: recognition and management. J Vasc Surg. 2008;48(5)(suppl):55S-80S. doi:10.1016/j.jvs.2008. 08.067
  43. ↑ Reinders Folmer EI, Von Meijenfeldt GCI, Van der Laan MJ, et al. Diagnostic imaging in vascular graft infection: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg. 2018;56 (5):719-729. doi:10.1016/j.ejvs.2018.07.010
  44. ↑ Erba PA, Leo G, Sollini M, et al. Radiolabelled leucocyte scintigraphy versus conventional radiological imaging for the management of late, low-grade vascular prosthesis infections. Eur J Nucl Med Mol Imaging. 2014;41(2):357-368. doi:10.1007/ s00259-013-2582-9
  45. ↑ Schwab DP, Taylor SM, Cull DL, et al. Isolated arteriovenous dialysis access graft segment infection: the results of segmental bypass and partial graft excision. Ann Vasc Surg. 2000;14(1):63- 66. doi:10.1007/s100169910011
  46. ↑ Liu RH, Fraser CD III, Zhou X, Beaulieu RJ, Reifsnyder T. Complete versus partial excision of infected arteriovenous grafts: does remnant graft material impact outcomes? J Vasc Surg. 2020;71(1): 174-179. doi:10.1016/j.jvs.2019.03.062
  47. ↑ Schutte WP, Helmer SD, Salazar L, Smith JL. Surgical treatment of infected prosthetic dialysis arteriovenous grafts: total versus partial graft excision. Am J Surg. 2007;193(3):385-388. doi:10. 1016/j.amjsurg.2006.09.028
  48. ↑ Walz P, Ladowski JS. Partial excision of infected fistula results in increased patency at the cost of increased risk of recurrent infection. Ann Vasc Surg. 2005;19(1):84-89. doi:10.1007/s10016-004-0139-x
  49. ↑ Zahra SA, Choudhury RY, Basharat K, et al. Translational sciences in cardiac failure secondary to arteriovenous fistula in hemodialysis patients. Ann Vasc Surg. 2021;74:431-449. doi:10.1016/j.avsg. 2021.01.071
  50. ↑ Wattanasirichaigoon S, Pomposelli FB Jr. Branham’s sign is an exaggerated Bezold-Jarisch reflex of arteriovenous fistula. J Vasc Surg. 1997;26 (1):171-172. doi:10.1016/S0741-5214(97)70168-X
  51. ↑ Iwashima Y, Horio T, Takami Y, et al. Effects of the creation of arteriovenous fistula for hemodialysis on cardiac function and natriuretic peptide levels in CRF. Am J Kidney Dis. 2002;40(5): 974-982. doi:10.1053/ajkd.2002.36329
  52. ↑ Reddy YNV, Melenovsky V, Redfield MM, Nishimura RA, Borlaug BA. High-output heart failure: a 15-year experience. J AmColl Cardiol. 2016;68(5):473-482. doi:10.1016/j.jacc.2016.05.043
  53. ↑ Stern AB, Klemmer PJ. High-output heart failure secondary to arteriovenous fistula. Hemodial Int. 2011;15(1):104-107. doi:10.1111/j.1542-4758. 2010.00518.x
  54. ↑ Rao NN, Stokes MB, Rajwani A, et al. Effects of arteriovenous fistula ligation on cardiac structure and function in kidney transplant recipients. Circulation. 2019;139(25):2809-2818. doi:10.1161/ CIRCULATIONAHA.118.038505
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