Systemic Effects of Hemodialysis Access

Systemic Effects of Hemodialysis Access

Systemic Effects of Hemodialysis Access Anil K. Agarwal Patients with advanced chronic kidney disease are at a high risk of cardiovascular events. Pat...

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Systemic Effects of Hemodialysis Access Anil K. Agarwal Patients with advanced chronic kidney disease are at a high risk of cardiovascular events. Patients with end-stage renal disease have a particularly high morbidity and mortality, in part attributed to the complications and dysfunction related to vascular access in this population. Creation of an arteriovenous access for HD is considered standard of care for most patients and has distinct advantages including less likelihood of infections, less need for intervention, and positive impact on survival as compared with usage of a catheter. However, creation of an arteriovenous shunt incites a series of events that significantly impacts cardiovascular and neurohormonal health in both positive and negative ways. This article will review the short- and long-term effects of dialysis access on cardiovascular, neurohormonal, and pulmonary systems as well as a brief review of their effect on survival on HD. Presence of other comorbidities in a patient with dialysis access can amplify these effects, and these considerations are of paramount importance in individualizing the approach to not only the choice of vascular access but also the modality of kidney replacement therapy. Q 2015 by the National Kidney Foundation, Inc. All rights reserved. Key Words: Systemic effects of dialysis access, High-flow fistula, Vascular access, Pulmonary hypertension

INTRODUCTION Patients with ESRD suffer from failure of a vital organ with diverse roles in maintenance of “milieu interieur,” often with concomitant suboptimal function of other vital organs, in the backdrop of multiple comorbidities including diabetes mellitus, hypertension, heart failure, and infections. Kidneys regulate cardiovascular hemodynamics through regulation of blood volume and BP as well as mineral metabolism. Ineffective regulation of these essential functions leads to cardiovascular consequences including left ventricular (LV) hypertrophy, volume overload, and endothelial dysfunction. Consequently, the patient with kidney dysfunction is considered to be at the highest level of cardiovascular risk. AVF for HD remains a singular important advance that made chronic HD feasible.1 However, creation of AV access for HD imparts another degree of complexity to this already complex physiology. Aside from making obvious alterations in the vascular anatomy, the AV accesses cause changes in cardiovascular hemodynamics, including the systemic and pulmonary circulations that have been recognized for over half a century, starting soon after the placement of the first AVF.2,3 These alterations result in adaptations and maladaptations of cardiac structure, function, and pulmonary circulation that impact normal function, quality of life, and survival of patients on HD. Use of AV grafts and catheters has been noted to be associated with higher levels of circulating pro-inflammatory cytokines. Vascular access can lead to other systemic complications including ischemia (steal), thromboembolic phenomenon, infections, and psychological complications. Dialysis catheters can cause central vein stenosis (CVS) in addition to a high incidence of infections. This review will focus primarily on hemodynamic alterations associated with AV accesses and their downstream effects because most studies have examined AVF or mixed AV accesses. AV grafts are likely to cause similar hemodynamic consequences as AVF. However, AV grafts are associated with a higher level of inflammation than AVF. Systemic effects of central venous catheters (CVCs) will be briefly mentioned, primarily related to infectious and mechanical effects not related to physiologic changes, because of their adverse impact on survival and quality of life of patients on HD.

Cardiovascular and Neurohormonal Effects Creation of AVF has immediate and late effects on systemic circulation.2–6 The procedure is followed by an increase in cardiac contractility and decrease in peripheral resistance, which result in increased cardiac output (CO). There is also an increase in blood volume and LV end-diastolic volume along with restrictive physiology in diastole. At the same time, vascular endothelium undergoes structural and functional changes responding to the shear stress and increase in blood flow. There is production of nitric oxide and vasorelaxation. The diameters of the artery and the vein increase as a result of increased flow through this newly created low-resistance parallel circuit. Short-term effects of AVF creation have been studied extensively. An echocardiographic study of 16 patients with chronic kidney failure assessed echocardiographic changes before and 3, 7, and 14 days after creation of AVF 4 Concentrations of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were also checked on day 1, 3, 6, 10, and 14. The study showed that within 10 days to 2 weeks after creation of AVF, CO increased by 15%, fractional shortening increased by 8%, and LV enddiastolic diameter increased 4%. There was shortening of the deceleration time of the early diastolic filling wave (212%) and the ratio of the peak velocity of early diastolic to atrial filling (E-A ratio) increased (118%). The difference in duration of LV inflow and pulmonary venous flow at atrial contraction, a marker of LV end-diastolic pressure, significantly shortened by day 14 after the operation (237%). The authors concluded that the creation of an AV fistula induced LV diastolic dysfunction and a restrictive filling pattern. There was an increase in ANP and From the Section of Nephrology at University Hospital East, The Ohio State University Wexner Medical Center, Columbus, OH. Financial Disclosure: The author declares that he has no relevant financial interests. Address correspondence to Anil K. Agarwal, MD, FACP, FASN, FNKF, Section of Nephrology at University Hospital East, The Ohio State University Wexner Medical Center, Columbus, OH 43210 E-mail: Anil.agarwal@osumc. edu Ó 2015 by the National Kidney Foundation, Inc. All rights reserved. 1548-5595/$36.00 http://dx.doi.org/10.1053/j.ackd.2015.07.003

Advances in Chronic Kidney Disease, Vol 22, No 6 (November), 2015: pp 459-465

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BNP levels with maximal increase after 10 days (ANP, with no change in aldosterone levels. Plasma angiotensin 148%; BNP, 168%; Fig. 1). The increase in CO was associII, angiotensin-converting enzyme, and endothelin levels ated with elevation of ANP levels but not BNP levels. The did not change. The authors concluded that creation of increase in E-A ratio correlated only with BNP level elevaAV access is independently associated with further protion. gression of already existing LVH. Acute and chronic hemodynamic changes at 24 hour and AVF can affect cardiac load by increasing preload and 8 weeks after placement of a radiocephalic AVF were studdecreasing afterload. In 10 patients with AVF, a ied in 17 subjects at 24 hours with a Swan-Ganz catheter.5 60-second compression and reconstruction of aortic presAt baseline, all patients had normal right atrial pressure; sure waves from finger pressure recordings showed a pulmonary artery wedge pressure, stroke volume index small increase in LV oxygen demand, but a larger decline (SVI), high normal heart rate (HR), and systemic vascular in cardiac oxygen supply.7 During fistula compression, systolic, diastolic, and mean arterial pressures increased, resistance index (SVRI). The PAP, MAP, cardiac index (CI), and HR decreased significantly. Although stroke volume and pulmonary vascular resistance index (PVRI) were decreased slightly, there was a significant decrease in CO high at baseline. At 24 hours after the AV fistula creation, and increase in SVR. there was an insignificant rise in HR, CI, PAP, and PVRI, It is well recognized that arterial stiffness, as measured and a fall in SVRI and MAP with no change in right atrial by carotid-femoral pulse wave velocity, is increased in pressure, pulmonary artery wedge pressure, and SVI. A dialysis patients and causes increased central BP and rising trend of HR and CI with a fall in SVRI was observed myocardial hypoperfusion. In a small study of 43 patients, in 10 of 17 patients. At the sixth week, the 8 patients stud30 of the 43 patients with successful AVF showed ied showed a significant increase in the systolic pressure decreased total peripheral and MAP and PVRI. Also, resistance, increased SV and there was a rise in SVI in all CLINICAL SUMMARY CO with decreased systolic patients and CI in 6 patients, and diastolic BP 2 weeks afwith insignificant change in  Arteriovenous access for hemodialysis is preferred over ter placement of AV fistula.8 the cardiac filling pressure. catheter access due to the less likelihood of infections and This study demonstrated None of the patients develinterventions and a positive impact on survival as potential benefits of AVF oped congestive heart failure compared to using a catheter. creation in HD patients due to AVF. Increase  Access creation leads to changes in heart rate, blood although overall benefits of (although insignificant) in pressure, blood volume, cardiac output, pulmonary and AV access have to be considCI after AVF despite a systemic resistance, changes in natriuretic peptides as ered in an individual patient. decrease in preload after well as structural changes in vascular endothelium and AVF was not well explained left ventricular mass. Heart Failure by these findings. The au Access flow to cardiac output ratio .0.3 may predict heart thors concluded that the crePresence of AVF, especially failure. when associated with high ation of an AVF for HD does access flow, has been obnot lead to a significant  Potential short and long term effects of AV access should change in the cardiac hemoserved to be associated with be carefully considered in individualizing the approach dynamic parameters and is heart failure, which is generto the choice of vascular access and the modality of renal replacement therapy, especially in patients with ally attributed to an increase not an appreciable factor preexisting cardiovascular morbidity. leading to circulatory conin CO.9 However, relatively gestion or pulmonary edema uncommon occurrence of heart failure with such AVF in these patients. suggests presence of intrinsic heart disease in those who Timing of various changes was also studied in another prospective echocardiographic and neurohormonal study develop heart failure. It is also likely that many cases of heart failure due to AVF are missed and attributed to other of 12 predialysis patients before and 1 and 3 months after risk factors. Upper arm AV access is more likely to have creation of a primary AV access.6 After creation of access, the weight, BP, or hemoglobin level did not change, but higher access flow and result in heart failure as compared CI increased and SVR decreased. LV mass corrected to with an access in forearm although there is no difference height significantly increased from 63.8 6 5.5 to between AVF and AV graft (Fig. 3).10 2 2 68.9 6 4.9 g/m at 1 month and 72.5 6 8.9 g/m at 3 months There are many AV access–associated risk factors for (Fig. 2). The increase in mass was mostly due to an increase occurrence of heart failure. It is well known that a highflow AVF can cause significant adverse changes in CO, BP, in interventricular septal thickness. LV end-diastolic diamand HR. An access flow (Qa) over 2 L per minute is a risk eter and posterior wall thickness did not change. The incidence of LV hypertrophy (LVH) increased from 67% at factor for occurrence of heart failure.10 Another risk factor is the occurrence of a high degree of cardiopulmonary baseline to 83% and 90% at 1 and 3 months, respectively. recirculation. One study showed a strong positive correlaLeft atrial area increased, and early diastolic transmitral flow increased. Inferior vena cava diameter increased at tion between Qa, CO, and CI and a negative correlation with SVR (Fig. 4).11 There was an average Qa:CO ratio of 1 month and did not change at 3 months. A remarkable in14% to 20% in stable long-term HD patients, but a ratio crease in ANP was seen 2 weeks after creation of AVF associated with increased contractility, CO, and decrease in higher than 0.3 was associated with high output heart peripheral resistance. There was decreased renin activity failure.

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Figure 1. Percentage of increase in plasma concentrations of (A) atrial natriuretic peptide (ANP) and (B) brain natriuretic peptide (BNP) after the AVF operation. Values given as mean 6 standard error of the mean. *p , .05. **p , .01 compared with control (pre) for each peptide.4

Similar association of high Qa with heart failure was noted in a surgical study, and the symptoms of heart failure resolved with flow reduction.12 A study of 31 patients undergoing flow reduction surgery showed intraoperative increase in systolic blood pressure (111 6 6-123 6 6 mm Hg, p , .05) and diastolic blood pressure (57 6 4-63 6 5 mm Hg, p , .05) after 15-second clamping of access.13 Mean access flow in these patients was approximately 3000 mL/min. Such increases were modest (16 6 3 and 12 6 2 mm Hg, respectively, p ¼ .37) in control patients with access-associated hand ischemia, who had mean access flow just above 1000 mL/min. Both groups experienced modest reduction in heart rate of approximately 3 beats/min with compression. Authors suggested that an incremental increase in access flow might cause poor cardiac performance. Impact on Myocardial Ischemia and Valvular Disease In patients with preexisting coronary artery disease, creation of an AVF can incite silent subendocardial myocardial

Figure 2. Changes in left ventricular mass indexed to height after creation of an AV access. Each line represents 1 patient. Filled squares represent mean 6 standard error of the mean for the corresponding period.6

ischemia due to increase in sympathetic demand and contractility, which causes an imbalance between subendocardial oxygen supply and increased oxygen demand.14 Also, AVF can potentially steal blood flow from an ipsilateral internal mammary artery bypass graft predisposing to myocardial ischemia and cause decompensation in presence of critical aortic stenosis.15–18 Pulmonary Hypertension Pulmonary hypertension (PH) is quite prevalent in patients with ESRD (40%-50%) but remains an underappreciated cause of cardiovascular morbidity and mortality.19,20 PH is defined as pulmonary artery pressure greater than 25 mm of Hg at rest and 30 mm of Hg during exercise.21 The pathogenesis of PH and possible management have been extensively reviewed, and potential mechanisms of development of PH in dialysis patients have been hypothesized (Fig. 5).22 PH in ESRD patients is generally attributed to increase in pulmonary flow especially in patients with high-flow AVF

Figure 3. Comparison of the cardiac output values among the patients subdivided according to the vascular access flow cutoff values. The horizontal line represents the median, upper, and lower limits of the box including the first and third quartiles, and capped bars indicate minimum and maximum value. The 1-way ANOVA followed by the Tukey’s posthoc test was performed to compare the mean cardiac output values in each access blood flow category identified by the cutoff points previously calculated.10

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PD, which also supports the theory of high pulmonary flow with HD and AV access. PH and CO decrease significantly after compression of AVF.23 Furthermore, kidney failure itself may be a contributing factor as demonstrated by resolution of PH after transplantation despite a patent AV access.27 Prevalent uncontrolled systemic hypertension also contributes to secondary PH in many instances. Treatment of PH includes use of anticoagulants, diuretics, oxygen, vasodilators, and antiproliferative agents. The efficacy of these therapeutic modalities, however, has not been studied in patients with ESRD. PH may reverse after kidney transplantation. Flow reduction in a high-flow AV access should be considered. PD provides an alternative therapy in appropriate patient. Figure 4. Relationship between access flow and cardiac index.11 The dots represent the cardiac index at different access flow. This is how it is in the original article and does not need to be expanded.

and elevation of pulmonary systolic pressure after the creation of AV access.23 Pulmonary artery vasoconstriction can occur due to hormonal and metabolic derangements, whereas increase in pulmonary artery pressure can be a result of anemia, fluid overload, and hemodynamic changes due to AV access. A study of 180 patients with HD, PD, and kidney transplant analyzed demographic, clinical, and echocardiographic findings to create a multivariable linear regression model to find factors associated with pulmonary artery pressure.24 PH was detected in 31.6%, 8.3%, and 5% of the patients on HD, PD, and transplant recipients, respectively (p , .001). In multivariate analysis, HD, age, smoking, systolic cardiac dysfunction, and diastolic cardiac dysfunction were associated with systolic pulmonary artery pressure. Decreased nitric oxide production, presence of inhibitors of nitric oxide, and endothelial dysfunction in HD patients with AVF and PH and elevated levels of inflammatory cytokines such as IL-1 beta, TNF-alpha, and IL-6 have been implicated as well.25 After closure of AVF, improvement has been demonstrated that implicates AV access as a cause of PH in this population.26 PH is uncommon in patients with

Reversing Changes of AV Access Creation: Impact of Kidney Transplantation, AVF Ligation, or Banding Interestingly and importantly, LVH can regress after kidney transplantation and once AVF is nonfunctional. In patients with high-flow AVF, banding of the AVF to reduce the flow, distalization of anastomosis, complete ligation, and abandoning of the access can resolve symptoms and reversal of cardiac changes toward normal.28,29 Ligation of access has the potential to reverse the hemodynamic changes; however, it leaves the patient with no functional access. Reduction of flow in such an access can be achieved using banding or distalization of inflow. Ultrasound-guided banding of AVF in 30 patients with high-flow AVF and cardiac failure or steal syndrome led to expected reduction in flow, size of anastomosis and resolution of symptoms, and no need of reintervention.30 CO was reduced from 8.5 6 2.9 L/min to 6.1 6 1.9 L/min (p , .01). During the median 1-year follow-up, AVF and AV graft patency rates were 100% and 80%, respectively, and there was resolution of clinical complaints. Such banding can be achieved using a variety of techniques that are out of the scope of this article. Distalization of inflow by disconnecting the existing high-flow anastomosis and creating another anastomosis using a smaller distal inflow has been shown to be successful as well.31 There has been a debate about the utility of an AVF after a successful kidney transplant. In a rare case scenario, a lower

Figure 5. Potential pathophysiologic mechanisms of pulmonary hypertension in patients on dialysis.22

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extremity AV access has the potential to steal blood flow from an ipsilateral kidney transplant.32 This can be ameliorated by ligation of access. However, there is more concern about cardiovascular impact of continued functional AV access after transplantation. The risk of surgical closure relates to a potential need of access for HD in case of allograft failure. This can be minimized by a careful selection of patients who have stable allograft function with no significant proteinuria, recurrent rejection, or evidence of recurrence of primary kidney disease.33 An AVF closure after transplantation has the potential benefit of decreasing LV volume and mass. Studies have shown a 6.4% to 8.6% decrease in LV mass 1 month after AVF closure, reaching 11.1% and 15.8% at 3 to 4 and 21 months, respectively.34–36 In these studies, not all patients responded to surgical closure to a similar degree. An increase in SVR and BP during an acute compression of AVF best predicted LV diameter and mass reduction.34 Other similar studies have shown that there is regression of LVH after occlusion of AVF in nontransplant patients. In a study of 25 HD patients with malfunctioning AVF who underwent AVF closure, echocardiographic changes from the baseline were compared at 6 months.29 LV mass decreased from 225 6 55 to 206 6 51 g (p , .001), and LV mass index decreased from 135 6 40 to 123 6 35 g/m2 (p , .001). LV internal diastolic diameter, interventricular septum thickness, and diastolic posterior wall thickness decreased significantly, whereas LV ejection fraction increased from 56 6 7% to 59 6 6% (p , .001). No significant changes were observed in controls that did not undergo AVF closure. In patients with AVF closure, LV morphologic characteristics showed a decrease in both eccentric hypertrophy and concentric hypertrophy in favor of normalization or a pattern of concentric remodeling. AV Access and Mortality Both high- and low-flow AVF can be of importance to survival of patients on HD. High-flow AVF, by causing adverse cardiovascular changes described previously, can contribute to mortality. On the contrary, a low-flow access will also cause under dialysis and impact survival and quality of life. To compare extremes of access flow, a Canadian study of 820 incident dialysis patients with median follow-up period of 28 months, observed 25.1% overall mortality 37 The adjusted risk of mortality was similar between the low and high baseline Qa before and after adjustment for demographic characteristics, comorbidity, and access type. The findings did not suggest an increased risk of death at higher levels of Qa. Despite systemic effects of AV accesses that might be detrimental, such accesses are less inflammatory than a catheter used for dialysis. There is controversy about quantitative associations between vascular access type and clinical outcomes. A systematic review of cohort studies to evaluate such an association identified 3965 citations of which 67 met inclusion criteria.38 The metaanalysis showed that those individuals using catheters had higher risks for all-cause mortality (risk ratio ¼ 1.53 and 1.38), fatal infections (2.12 and 1.49), and cardiovascular events (1.38 and 1.26) as compared with those using AVF and AV graft, respectively. Compared to those with

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fistula, those using graft had increased all-cause mortality (1.18) and fatal infection (1.36), but similar risk for cardiovascular events (1.07). The risk for bias, especially selection bias, was high. Considering recent increase in prevalence of AVF, it is important to consider whether such change in access use could have led to a higher mortality. A study of United States Renal Data System Clinical Performance Measures data comprising of 4854 patients who initiated dialysis between 1999 and 2004, analyzed risk of all-cause and cardiovascular death.39 AVF use was strongly associated with lower all-cause and CV mortality. After adjustment for covariates, AVF use 90 days after dialysis initiation remained significantly associated with lower cardiovascular mortality (hazard ratio 0.69, p ¼ .0004) compared with catheter use. It is interesting to note that although AV access use at the start of ESRD conferred a marginal reduction in CVrelated mortality, AVF use 90 days after dialysis initiation conferred a 31% reduction in CV-related mortality, when compared with CVC use at 90 days. Moreover, it is remarkable to note that the AVF use was protective given the higher prevalence of hypertension among patients reporting AVF use at dialysis initiation, and the comparable prevalence of ischemic heart disease, myocardial infarction, peripheral vascular disease, history of cardiac arrest, and cerebrovascular disease found among AVF, AVG, and CVC patients in this nationally representative cohort. Type of vascular access has been linked to survival on HD with significantly higher mortality with catheter as compared with AVF and AV graft.40 Change in type of vascular access can also affect clinical outcomes. A study of 79,545 patients (43% fistulas, 29% catheters, and 27% grafts) showed unadjusted hazard ratios of death for grafts (1.22, but 1.05 in adjusted models) and catheters (1.76) compared with fistulas.41 Compared with patients who continued using a catheter, those who converted to either a graft or fistula had an hazard ratio of mortality of 0.69, whereas those who converted from a graft or fistula to a catheter had increased hazard ratios to 2.12 (both p , .001). Catheters are notorious for their predisposition to become infected. Infection can often become disseminated and cause metastatic infections and death. There is also a frequent risk of thromboembolism with indwelling catheters. In addition to large vein and intracardiac thrombosis, the catheters can also cause fibrointimal proliferation and stenosis within the central veins. CVS affects blood flow from the ipsilateral extremity and compromises future vascular access on the same side. In presence of bilateral upper extremity CVS, symptoms suggestive of superior vena cava syndrome can be present. Recanalization of CVS is a possibility although not always feasible or successful. However, in presence of a high-flow AVF, recanalization of CVS can sometimes result in precipitation of heart failure due to sudden volume overload. Furthermore, the catheters have been observed to be associated with a high level of inflammation and worse survival than AV accesses. A randomized study of incident dialysis patients developing bacteremia or sepsis requiring hospitalization showed increased risk of subsequent heart disease and heart failure.42 As a high level of inflammation is associated with acceleration of

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atherosclerosis, occurrence of infection and inflammation due to vascular access may confer an increased risk of cardiovascular disease in patients with ESRD.43 In patients with limited life expectancy (elderly, terminal illness) and in those with poor peripheral vasculature, catheters may be an appropriate choice or the only option when HD is the chosen modality. Although catheters do not induce striking changes in hemodynamics compared with AV access, they do have a striking impact on patient survival. These data compel consideration of overall evidence about pros and cons of vascular accesses rather than simply looking at the changes in hemodynamics associated with AV accesses. Approach to Vascular Access: Considering Hemodynamic Consequences Consideration of the incipient hemodynamic changes after creation of AVF is important, especially in those with preexisting cardiac conditions that are not uncommon in ESRD population. The risks of AV access are especially more relevant to those with advanced HF (New York Heart Association class III and IV) and when an upper arm AV access is created. It is reasonable to consider alternatives, including PD and placement of a “planned” tunneled catheter if an AV access is not feasible or considered unsafe. It is also important to consider that catheters are not necessarily devoid of adverse CV events due to their impact on systemic inflammation and their propensity toward infection and sepsis. After creation of AVF, a high-risk patient, such as elderly patient and the patient with HF, PH, valvular disease, and upper arm AV fistula should be monitored carefully for adverse hemodynamic consequences. In case of symptoms and evidence of high access flow, strategies to reduce flow should be considered. Distalization of the anastomosis or banding can be effective in many cases. In intractable cases, ligation of the access may be necessary. The patient should be closely monitored after the ligation of high-flow AV fistula because of the possibility of abrupt increase in SVR and its adverse effect on cardiac performance. In presence of severe aortic stenosis, valve repair or replacement should be considered before the placement of AV access. Individualized approach to the dialysis access is essential to improve outcomes. REFERENCES 1. Brescia MJ, Cimino JE, Appel K, et al. Chronic hemodialysis using venipuncture and a surgically created arteriovenous fistula. N Engl J Med. 1966;275(20):1089-1092. 2. Nakano J, Deschryver C. Effects of arteriovenous fistula on systemic and pulmonary circulations. Am J Physiol. 1964;207(6):1319-1324. 3. Ahearn D, Maher JF. Heart failure as a complication of hemodialysis arteriovenous fistula. Ann Intern Med. 1972;77(2):201-204. 4. 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. 5. Sandhu JS, Wander GS, Gupta ML, Aulakh BS, Nayyar AK, Sandhu P. Hemodynamic effects of arteriovenous fistula in endstage renal failure. Ren Fail. 2004;26(6):695-701. 6. Ori Y, Korzets A, Katz M, et al. The contribution of an arteriovenous access for hemodialysis to left ventricular hypertrophy. Am J Kidney Dis. 2002;40(4):745-752.

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28. Kotaro O, Tsutomu A, Kenichi K, et al. Impact of inflow reduction of arteriovenous fistula on systemic hemodynamics in a patient with high-output heart failure during hemodialysis: a case report. J Cardiol Cases. 2010;1(2):e98-e101. 29. Movilli E, Viola BF, Brunofi G, et al. Long-term effects of AVF closure on echocardiographic functional and structural findings in HD patients: a prospective study. Am J Kidney Dis. 2010;55(4): 682-689. 30. Tellioglu G, Berber I, Kilicoglu G, Seymen P, Kara M, Titiz I. Doppler ultrasonography-guided surgery for high-flow hemodialysis vascular access: preliminary results. Transplant Proc. 2008;40(1):87-89. 31. Parmar CD, Chieng G, Abraham KA, Kumar S, Torella F. Revision using distal inflow for treatment of heart failure secondary to arteriovenous fistula for hemodialysis. J Vasc Access. 2009;10(1): 62-63. 32. Symington E, Afzali B, MacPhee I, Chemla ES. Compromise of renal transplant blood flow by an arteriovenous graft. Nephrol Dial Transplant. 2006;21(9):2644-2646. 33. Unger P, Wissing KM. Arteriovenous fistula after renal transplantation: utility, futility or threat? Nephrol Dial Transplant. 2006;21(2):254-257. 34. Unger P, Wissing KM, De Pauw L, et al. Reduction of left ventricular diameter and mass after surgical arteriovenous fistula closure in renal transplant recipients. Transplantation. 2002;74(1):73-79. 35. De Lima JJ, Vieira ML, Molnar LJ, et al. Cardiac effects of persistent hemodialysis arteriovenous access in recipients of renal allograft. Cardiology. 1999;92(4):236-239.

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36. van Duijnhoven ECM, Cheriex ECM, Tordoir JHM, et al. Effect of closure of the arteriovenous fistula on left ventricular dimensions in renal transplant patients. Nephrol Dial Transplant. 2001;16(2): 368-372. 37. Al-Ghonaim M, Manns BJ, Hirsch DJ, et al. Relation between access blood flow and mortality in chronic hemodialysis patients. Clin J Am Soc Nephrol. 2008;3(2):387-391. 38. Ravani P, Palmer SC, Oliver MJ, et al. Associations between hemodialysis access type and clinical outcomes: a systematic review. J Am Soc Nephrol. 2013;24(3):465-473. 39. Wasse H, Speckman RA, McClellan WM. Arteriovenous fistula use is associated with lower cardiovascular mortality compared with catheter use among ESRD patient. Semin Dial. 2008;21(5):483-489. 40. Dhingra R, Young E, Hulbert-Shearon T, et al. Type of vascular access and mortality in US hemodialysis patients. Kidney Int. 2001;60: 1443-1451. 41. Lacson E, Wang W, Lazarus M, et al. Change in vascular access and mortality in maintenance hemodialysis patients. Am J Kidney Dis. 2009;54(5):912-921. 42. Ishani A, Collins A, Herzog C, Foley R. Septicemia, access and cardiovascular disease in dialysis patients: the USRDS Wave 2 Study. Kidney Int. 2005;68(1):311-318. 43. Honda H, Qurexhi A, Heimburger O, et al. Serum albumin, C-reactive protein, interleukin 6, and fetuin a as predictors of malnutrition, cardiovascular disease, and mortality in patients with ESRD. Am J Kidney Dis. 2006;47(1):139-148.