Arteriovenous ﬁstula (AVF) is regarded as the best vascular access for chronic haemodialysis (HD). Still, AVF inherently causes signiﬁcant haemodynamic changes. Although the necessity for vascular access despite its putative cardiovascular complications favours AVF creation in patients under chronic HD, one may question whether sustaining a functional AVF after successful kidney transplantation extends the haemodynamic threat. Small prospective series suggest that AVF ligation causes rapid and sustained reduction in left ventricular hypertrophy. Still, the beneﬁts of such a cardiac remodelling in long-terms of cardiovascular morbi-mortality still need to be proven. Furthermore, the elevation of diastolic blood pressure and arterial stiffness caused by AVF ligation may blunt the expected cardio-protection. Finally, the closure of a functioning AVF may accelerate the decline of kidney graft function. As a whole, the current management of a functioning AVF in kidney transplant recipients remains controversial and does not rely on strong evidence-based data. The individual risk of graft dysfunction and a return to chronic HD also needs to be balanced. Careful pre-operative functional assessments, including cardio-pulmonary testing and estimated glomerular ﬁltration rate slope estimation, may help better selection of who might beneﬁt the most from AVF closure. Large-scale prospective, ideally multi-centric, trials are essentially needed. Key words: arterial stiffness, arteriovenous ﬁstula, blood pressure, eGFR, kidney transplant recipients, left ventricular, total peripheral resistance Introduction Arteriovenous fistula (AVF) is regarded as the best vascular ac- venous catheters, because with fewer access-related infections cess for chronic haemodialysis (HD) in patients with end-stage and endovascular interventions [3–5]. Efficient HD requires a renal disease (ESRD) [1, 2]. AVF provides better patient access flow rate of 400–600 mL/min. Since the brachial flow only and survival in comparison to arteriovenous grafts and central reaches 60–120 mL/min in physiological conditions, a Received: June 20, 2017; Editorial decision: August 28, 2017 V C The Author 2017. Published by Oxford University Press on behalf of ERA-EDTA. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/ licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact firstname.lastname@example.org Downloaded from https://academic.oup.com/ckj/article-abstract/11/3/406/4557542 by Ed 'DeepDyve' Gillespie user on 20 June 2018 AVF management post-kidney transplantation | 407 permanent vascular access needs to be surgically created on the basis of vessel mapping studies. A distal-to-proximal approach starting from the non-dominant arm is preferred to preserve patients’ quality of life, as suggested in K/DOQI guidelines. AVF referral within 12 months of the estimated time to dialysis performed best among time frame strategies, although the tim- ing of referral is classically guided by the patient’s age and by his/her individual likelihood and rate of progression to ESRD [6, 7]. The AVF flows in the forearm usually reach 500–900 mL/ min, whereas those in the upper arm are 900–1500 mL/min [2, 8]. Inherently, AVF causes significant haemodynamic changes in patients under chronic HD, which may lead to ser- ious complications, including arterial steal, pulmonary hyper- tension (PH) and high-output cardiac failure . As a reminder, high-flow accesses have been defined as flows between 1 and 1.5 L/min and/or >20% of the cardiac output (CO) . Although the necessity for vascular access despite its puta- tive increased risk of cardiovascular complications favours AVF creation in patients under chronic HD, one may question whether sustaining a functional AVF after kidney transplant- ation (KTx) extends such a haemodynamic threat [11–13]. A con- trario, the AVF-associated hyperdynamic circulation has been suggested to reduce blood pressure (BP) and arterial stiffness, as well as to preserve kidney function in patients with advanced chronic kidney disease (CKD) [14–16]. Nowadays, there is no Fig. 1. Schematic summary of haemodynamic changes caused by the creation consensus concerning the strategy between surgical ligation vs. ligation of an arteriovenous ﬁstula. ANP, atrial natriuretic peptide; BP, blood pressure; LV, left ventricle; vasoC, vasoconstrictive. versus watchful preservation of a functioning AVF in kidney transplant recipients (KTRs) with a well-functioning graft . The present review aims at summarizing the scientific evidence This clinical trial included 83 patients randomly allocated in a concerning AVF impacts on renal and cardiovascular functions 1:1 ratio to undergo implantation of an arteriovenous anasto- at the successive stages of kidney disease, i.e. pre-terminal mosis plus current pharmaceutical treatment or to maintain CKD, chronic HD and post-KTx. current treatment alone (controls). Mean systolic 24-h ambula- tory BP reduced by 13.5 mmHg (P<0.0001 versus baseline) in ar- teriovenous coupler recipients and by 0.5 mmHg (P¼0.86 versus Global haemodynamic impacts of AVF baseline) in controls. Physiologically, the addition of a low- In the non-transplant population with CKD, the creation of an resistance, high-compliance venous segment in parallel to the AVF for the purpose of HD initiation has been reported to slow systemic arterial circulation reduces overall systemic vascular down CKD progression [15, 16]. Golper et al.  retrospectively resistance (SVR), similar to Ohm’s law of electrical resistance observed in a series of 123 CKD patients that AVF surgery was . Cardiac afterload is further reduced by the reduction of ef- associated with a significant deceleration of estimated glom- fective arterial volume and arterial stress, and the slowing of re- erular filtration rate (eGFR) slope decline from 5.9 to 0.5 mL/ flected pressure waves . Reduction of distending BP in the min/year. These intriguing observations were confirmed in a aorta may also improve arterial compliance, thereby generating nationwide cohort of 3026 CKD US veterans: a significant reduc- a feed-forward loop based on reduced SVR, improved compli- tion of eGFR loss was observed following AVF creation (from ance and reduced BP and the long-term beneficial cardiac and 5.6 to 4.1 mL/min/1.73 m /year) . These clinical findings aortic remodelling. Finally, AVF-mediated venous return neces- may be partly explained by the pathophysiological cascades of sarily favours pulmonary flow, which may in turn recruit larger remote ischaemic preconditioning . AVF causes brief, but re- lung areas and increase arterial oxygen content . One may peated, periods of local ischaemia, thereby inducing systemic thus advocate that AVF favourably influence CKD progression protection against tissue hypoperfusion. AVF also adds a low- by improving oxygen delivery to the kidney, thereby attenuating resistance, high-compliance venous compartment to the arter- the vasoconstrictive renal chemo-reflex [18, 27] (Figure 1). ial system, which may attenuate both arterial stiffness and These encouraging data may be challenged by the adverse pressure load . In animals, experimental AVF acutely de- impact of AVF on the balance between poorer subendocardial creases BP and increases pulse pressure, whereas fistula closure oxygen supply and increased oxygen demand consequent to a restores BP to normal levels by modulating sodium excretion greater CO [28, 29] (Figure 1). [19–21]. Similar observations were made in humans . Within 14 days following AVF creation, the secretion of the atrial natri- uretic peptide is induced by volume loading, whereas the re- Haemodynamic impacts of high-flow AVF in lease of brain natriuretic peptide is stimulated by progressive patients under chronic HD left ventricle (LV) diastolic dysfunction . In an open-label, multicentre, prospective, randomized, controlled trial, Lobo AVF has been associated with various haemodynamic compli- et al. [22, 24] demonstrated that implanting a central iliac ar- cations in patients under chronic HD, including arterial steal, teriovenous coupler in patients with uncontrolled hypertension PH and high-output cardiac failure. The first clinical manifest- produced a marked reduction in average 24-h ambulatory BP at ation of arterial ‘steal’ was reported in 1969 [30, 31]. Patients 6 months and significantly reduced hypertensive complications. with steal progressively develop mild paraesthesia, persistent Downloaded from https://academic.oup.com/ckj/article-abstract/11/3/406/4557542 by Ed 'DeepDyve' Gillespie user on 20 June 2018 408 | P. Vanderweckene et al. pain, motor dysfunction and ulcerations, which correspond to associated with increased risk of death . Buchanan et al.  ischaemic neuropathy . Risk factors for the development of recently performed a comprehensive study of the cardiovascu- arterial steal include diabetes mellitus, tobacco use, female gen- lar impact of HD sessions using intradialytic cardiac MRI in 12 der, advanced age, prior ipsilateral arteriovenous access place- stable patients. Cardiac MRI measurements included cardiac ment and peripheral arterial disease . HD-related steal index, stroke volume index, global and regional contractile seems to occur more frequently with brachial AVF than with ra- function (myocardial strain), coronary artery flow and myocar- dial or ulnar fistulas. In a systematic review of the Medline lit- dial perfusion. All measures of systolic contractile function erature (from 2000 to 2014, including 43 English-written reports dropped during HD, with partial recovery after dialysis. All pa- of prospective trials), Al-Jaishi et al.  concluded that the me- tients experienced some degree of segmental LV dysfunction, dian complication rate of steal events per 1000 patient days was with severity proportional to ultrafiltration rate and BP reduc- 0.05. The authors acknowledged that the risk of bias was high tion. Myocardial perfusion decreased significantly during HD and event rates were highly variable, partly due to poor quality session . In a single centre between 2003 and 2006, Movilli studies, significant heterogeneity of study populations and in- et al.  enrolled 25 consecutive HD patients who underwent consistent definitions of ‘steal syndrome’. AVF ligation and conversion to a tunnelled central venous PH secondary to high-flow AVF has been reported . PH is catheter, and compared them with 36 controls with a well- defined as a mean pulmonary artery pressure 25 mmHg at rest functioning AVF. Outcomes were changes in echocardiographic and concerns 40–48% of the population receiving long-term HD parameters obtained before and 6 months after AVF closure for via surgical AVF [35–37]. Both ESRD and AVF are thought to partici- patients in the AVF-closure group, and at baseline and 6 months pate in PH development . Hormonal and metabolic perturb- later for controls. Closure of the AVF caused a significant de- ations caused by ESRD induce pulmonary arterial vasoconstriction crease in LV internal diastolic diameter, interventricular septum and elevated pulmonary vascular resistance. Pulmonary arterial thickness and diastolic posterior wall thickness. This was asso- pressure may be further increased by the AVF-associated high CO, ciated with a significant decrease in LV mass and a more anaemia and fluid overload. Mortality among PH patients is three favourable shift of cardiac geometry towards normality. times higher compared with those without PH . To date, there is no consensus as to the threshold flow val- High-output cardiac failure is characterized by signs and ues in the management of steal syndrome, PH and cardiac fail- symptoms (i.e. dyspnoea, orthopnoea, paroxysmal dyspnoea ure in patients under chronic HD [48, 49]. The causal link and pulmonary and/or peripheral oedema) of systemic conges- between access flow and increased morbi-mortality probably tion in combination with a CO >8.0 L/min and/or a cardiac index exists, but still needs to be directly proven [8, 50]. >4.0 L/min/m [39, 40]. LV ejection fraction is usually preserved. In such a typical case of chronic volume overload, normal sys- tolic function and low mass-to-volume ratio, the clinical out- Haemodynamic impacts of AVF in patients come appears more dependent on LV dilatation than LV following KTx hypertrophy . Still, LV hypertrophy is highly prevalent among patients with ESRD, and is an independent predictor of The impact of patent AVF after successful KTx on cardiac morbi-mortality in patients under chronic HD [42, 43]. LV hyper- morphology and function remains largely controversial. On one trophy results from combined effects of chronic haemodynamic hand, the persistence of large high-flow AVF for prolonged peri- overload, including increased flow and pressure, and non-hae- ods of time has been reported to have little influence on heart modynamic biochemical and neurohumoral factors, including parameters in 61 stable KTRs with adequate renal function (i.e. anaemia, chronically elevated fibroblast growth factor 23, hypo- serum creatinine level <2 mg/dL) . On the other hand, the albuminaemia and uraemic toxins [43, 44]. Age and diabetes maintenance of long-lasting AVF has been independently asso- also participate in LV hypertrophy. The HD-associated LV ciated with LV hypertrophy in a monocentric cohort of 162 KTRs hypertrophy is mostly eccentric, with increased LV mass and . LV hypertrophy, with uncontrolled hypertension and per- relatively normal wall thickness. Early observations estimated sistent anaemia, contributes to the increased cardiac mortality that when >20% of the CO is shunted through the AVF, it predis- observed among KTRs [51, 52]. Furthermore, high-output car- poses to cardiac failure . Reddy et al.  retrospectively char- diac failure secondary to high-flow AVF might be a frequent acterized the long-term changes in cardiac structure and condition in the KTR population. In a retrospective study function in 137 patients undergoing AVF creation for chronic including 113 KTRs with a functioning AVF, 25.7% required AVF HD. Of important note, the monocentric observational design of ligation for clinical suspicion of cardiac failure. The mean shunt this study, with no control group, does not allow separation of flow in the intervention group was 2197.2 mL/min, whereas the the beneficial effects of chronic HD (including volume removal) mean shunt flow in the non-intervention group was only from the deleterious haemodynamic effects of the AVF. Still, 850.9 mL/min . after a median follow-up of 2.6 years post-AVF and HD initi- The impact of surgical ligation of the AVF on cardiovascular ation, Reddy et al. observed reductions in BP, body weight and parameters has been studied in both observational cohorts and estimated plasma volume coupled with modest reverse LV prospective studies including a limited number of transplant remodelling, which may reflect decreased LV pressure load patients [12, 19, 47, 54–58] (Figure 1). In a retrospective mono- from efficient renal replacement therapy. In contrast, AVF cre- centric cohort, Soleimani et al.  showed that spontaneous ation was associated with significant right ventricle (RV) dilata- AVF thrombosis in 17 KTRs does not cause significant LV struc- tion and deterioration in RV function. Similar observations were tural modifications compared with 23 control KTRs with a func- reported in a longitudinal series including 24 ESRD patients . tioning AVF. Similarly, Glowinski et al.  reported in a Sequential cardiac magnetic resonance imaging (MRI) showed prospective series of nine KTRs with normal-flow AVF that AVF significant increases in LV and RV end-systolic volumes, left ligation (n¼ 5) or thrombosis (n¼ 4) does not significantly im- and right atrial area and LV mass following AVF creation. No pact cardiac function after a 3-month follow-up, in comparison significant change in aortic distensibility was identified. Note with nine age- and gender-matched controls with a functioning that such AVF-induced RV dilation has been independently AVF. By strong contrast, Unger et al.  demonstrated that AVF Downloaded from https://academic.oup.com/ckj/article-abstract/11/3/406/4557542 by Ed 'DeepDyve' Gillespie user on 20 June 2018 AVF management post-kidney transplantation | 409 surgical ligation reduced LV end-diastolic diameter and mass monitoring (ABPM) showed a significant increase of diastolic BP, indexes within 10 weeks post-surgery, in a prospective series of with no systolic changes, at 1 month after surgical AVF closure 17 stable KTRs. Note that the interventricular septum thickness . BP remained unchanged within a similar time frame in 14 remained unchanged, and a slight but significant increase in KTRs with a functioning fistula. It is important to remember posterior wall thickness was observed. Diastolic and mean ar- that 24-h ABPM better assesses BP load, better correlates with terial BP slightly, but significantly, increased following AVF liga- target organ lesions and has superior prognostic significance tion . These observations were confirmed after a long-term compared with single BP measurement . Since hypertension follow-up of 21 months . Interestingly enough, post-opera- negatively influences long-term outcomes after KTx, the clinical tive reductions in LV hypertrophy could be predicted by the dy- benefits of LV mass reduction after AVF ligation may be unbal- namic increase in total peripheral resistance (TPR) and BP anced by BP increase . Moreover, in hypertensive CKD pa- observed during an acute occlusion of the AVF by pneumatic tients, the concentric pattern of LV hypertrophy, which compression. Hence, an increase in TPR of more than a third of corresponds to the predominant geometry after AVF ligation, baseline value predicted a 5% reduction in LV end-diastolic represents an independent prognostic factor of cardiovascular diameter index with positive predictive value of 80%. Similarly, events [60, 61]. Finally, Ferro et al.  reported in 250 stable an increase in BP during pneumatic compression of >10% of KTRs that the presence of a functioning AVF independently cor- baseline predicted a 5% reduction in LV end-diastolic diameter related with an increased aortic augmentation index (calculated index with a positive predictive value of 88% . van by non-invasive pulse wave exploration) on the basis of a multi- Duijnhoven et al.  found a correlation between pre-operative variate analysis (Table 1). LV mass and LV end-diastolic diameter and the reduction in LV Concerning the evolution of renal graft function, Vajdic et al. mass as determined 4–5 months following AVF ligation. retrospectively showed in a historical cohort including 311 KTRs Such a beneficial flow-dependent impact of AVF ligation on that patients with a functioning AVF at 1 year post-KTx LV mass reduction may be partly blunted by the concurrent in- (696 21 mL/min/1.73 m , n¼ 239) had significantly lower crease of arterial BP and TPR, as well as by the persisting abnor- Modification of Diet in Renal Disease (MDRD) eGFR values than malities in LV geometry . In a well-designed prospective those with spontaneously closed AVF (746 19 mL/min/1.73 m , study including 16 KTRs, the 24-h ambulatory blood pressure n¼ 72). Adjusted analyses suggested that AVF persistence was Table 1. Summary of the main observations post ligation of functioning AVF in KTRs Study Year KTRs (n) Techniques Main findings Retrospective De Lima et al.  1999 61 Echocardiography AVF patency Little impact on cardiac morphology and function Soleimani et al.  2012 40 Echocardiography AVF thrombosis No impact on LV morphology Schier et al.  2013 113 AVF ligation in 25.7% of KTRs for suspected cardiac failure Kolonko et al.  2014 162 Echocardiography AVF patency LV hypertrophy Weekers et al.  2017 99 eGFR slope AVF ligation Accelerated eGFR decline Prospective van Duijnhoven et al.  2001 20 Echocardiography (12–16 weeks) AVF ligation Improvement in LV hypertrophy Reduction in LV end-diastolic diameter Unger et al.  2002 17 Echocardiography (10 weeks) AVF ligation Reduction in LV end-diastolic diameter Reduction in LV mass index Increase of diastolic arterial BP Unger et al.  2004 17 Echocardiography (21 weeks) AVF ligation Reduction in LV end-diastolic diameter Reduction in LV mass index Increase of diastolic arterial BP Unger et al.  2008 16 24 h ABPM (4 weeks) AVF ligation Increase of diastolic arterial BP Movilli et al.  2010 61 Echocardiography (24 weeks) AVF ligation LV normal or concentric remodelling Glowinski et al.  2012 18 Echocardiography (12 weeks) AVF ligation No impact on cardiac function Transversal Ferro et al.  2002 250 Pulse wave AVF patency Increased arterial stiffness Vajdic et al.  2010 311 eGFR AVF ligation Better renal function at 1-year AVF patency Increased risk of graft loss Downloaded from https://academic.oup.com/ckj/article-abstract/11/3/406/4557542 by Ed 'DeepDyve' Gillespie user on 20 June 2018 410 | P. Vanderweckene et al. associated with an increased risk allograft loss . Note that this Hospital in Lie ` ge, Belgium. F.J. is a Fellow of the Fonds retrospective cohort only considered patients with AVF at the National de la Recherche Scientiﬁque. time of KTx, and excluded 91 KTRs because of early graft loss, non-functioning kidneys, technical failures or deaths during the Conflict of interest statement first year post-KTx. Kidney graft function was transversally com- pared at 1 year post-KTx, with no consideration for eGFR slopes. None declared. Consequently, the main limitation of this observational retro- spective cohort concerns the complete identification of inequities References between groups. Ultimately, the physicians in charge may bias- edly decide not to close the functioning AVF in patients at higher risk for CKD progression and ESRD. In a retrospective monocen- tric study including 285 KTRs, we investigated whether the clos- 1. NKF-DOQI Clinical Practice Guidelines for Vascular Access. ure of a functioning AVF significantly influenced eGFR slope National Kidney Foundation-Dialysis Outcomes Quality (calculated using linear mixed models based on MDRD equation) Initiative. Am J Kidney Dis 1997; 30: S150–S191 post-KTx. AVF closure occurred at 6536 441 days post-KTx, with 2. Sequeira A, Naljayan M, Vachharajani TJ. Vascular access a thrombosis/ligation ratio of 19/95. In order to limit the unavoid- guidelines: summary, rationale, and controversies. Tech Vasc able influence of transplantation vintage on eGFR slope, we first Interv Radiol 2017; 20: 2–8 matched the follow-up periods before versus after AVF closure 3. Perera GB, Mueller MP, Kubaska SM et al. Superiority of au- for every single patient. Hence, we found that the closure of a togenous arteriovenous hemodialysis access: maintenance functioning AVF significantly accelerates eGFR decline over the of function with fewer secondary interventions. Ann Vasc consecutive 12-month period . Surg 2004; 18: 66–73 4. Lok CE, Foley R. Vascular access morbidity and mortality: trends of the last decade. Clin J Am Soc Nephrol 2013; 8: Conclusions and perspectives 1213–1219 The present review highlights that the current management of 5. Lok CE, Sontrop JM, Tomlinson G et al. Cumulative patency functioning AVF following KTx remains largely controversial of contemporary ﬁstulas versus grafts (2000–2010). Clin J Am (Figure 1). Surgical ligation is usually performed in patients with Soc Nephrol 2013; 8: 810–818 specific indications, like high-flow fistula with arterial steal, LV 6. Shechter SM, Skandari MR, Zalunardo N. Timing of arterio- dilation, high-risk cardiovascular status or cosmetic reasons. venous ﬁstula creation in patients With CKD: a decision ana- The possible threat of graft dysfunction and a return to chronic lysis. Am J Kidney Dis 2014; 63: 95–103 HD also need to be discussed with the patient. The creation of a 7. Jemcov TK, Van Biesen W. Optimal timing for vascular ac- novel efficient AVF in case of ESRD may be extremely difficult in cess creation. J Vasc Access 2017; 18: 29–33 KTRs and not always feasible when peripheral veins are 8. Basile C, Vernaglione L, Casucci F et al. The impact of haemo- exhausted. dialysis arteriovenous ﬁstula on haemodynamic parameters Small prospective series suggest that AVF ligation causes of the cardiovascular system. Clin Kidney J 2016; 9: 729–734 rapid and sustained reduction in LV hypertrophy [55, 56]. Still, 9. Reddy YN, Obokata M, Dean PG et al. Long-term cardiovascu- the benefits of such a cardiac remodelling in long terms lar changes following creation of arteriovenous ﬁstula in pa- of cardiovascular morbi-mortality still need to be proven. tients with end stage renal disease. Eur Heart J 2017; 38: Furthermore, as emphasized by Unger and Wissing , 1913–1923 the subsequent elevation of diastolic BP and evolution toward 10. Sequeira A, Tan TW. Complications of a high-ﬂow access LV concentric geometry (with increased wall thickness) may and its management. Semin Dial 2015; 28: 533–543 blunt the cardio-protection expected from AVF closure . 11. Kolonko A, Kujawa-Szewieczek A, Szotowska M et al. The as- Furthermore, the closure of a functioning AVF may accelerate sociation of long-functioning hemodialysis vascular access the decline of kidney graft function . Therefore, careful with prevalence of left ventricular hypertrophy in kidney pre-operative functional assessments, including the dynamic transplant recipients. BioMed Res Int 2014; 2014: 603459 response of TPR and BP to a transient pneumatic occlusion of 12. De Lima JJ, Vieira ML, Molnar LJ et al. Cardiac effects of per- the AVF  and the calculation of MDRD-eGFR slope , may sistent hemodialysis arteriovenous access in recipients of help better selection of KTRs who might benefit the most from renal allograft. Cardiology 1999; 92: 236–239 AVF closure. Additionally, BP levels should be systematically 13. Weekers L, Vanderweckene P, Pottel H et al. The closure of monitored following AVF surgery, a fortiori when pre-operative arteriovenous ﬁstula in kidney transplant recipients is asso- diastolic BP is >90 mmHg. These assumptions do not rely on ciated with an acceleration of kidney function decline. strong evidence-based data, and definitely need to be tested in Nephrol Dial Transplant 2017; 32: 196–200 large-scale prospective, ideally multi-centric, populations. 14. Korsheed S, Eldehni MT, John SG et al. Effects of arterioven- ous ﬁstula formation on arterial stiffness and cardiovascular performance and function. Nephrol Dial Transplant 2011; 26: Acknowledgements 3296–3302 The authors cordially thank the surgeons (M. Meurisse, C. 15. Golper TA, Hartle PM, Bian A. Arteriovenous ﬁstula creation Coimbra Marques, O. Detry, E. Hamoir, P. Honore ´ , L. Kohnen, may slow estimated glomerular ﬁltration rate trajectory. S. Maweja, N. Meurisse and J.-P. Squifﬂet), the physicians (A. Nephrol Dial Transplant 2015; 30: 2014–2018 Bouquegneau, C. Bonvoisin, L. Collard, S. Grosch, JM. 16. Sumida K, Molnar MZ, Potukuchi PK et al. Association be- Krzesinski, L. Vanovermeire and P. Xhignesse) and the tween vascular access creation and deceleration of esti- members of the local transplant coordination centre (Mme mated glomerular ﬁltration rate decline in late-stage M.-H. Delbouille, M.-H. Hans, J. Mornard) for their commit- chronic kidney disease patients transitioning to end-stage ment to kidney transplantation at the University of Lie `ge renal disease. Nephrol Dial Transplant 2017; 32: 1330–1337 Downloaded from https://academic.oup.com/ckj/article-abstract/11/3/406/4557542 by Ed 'DeepDyve' Gillespie user on 20 June 2018 AVF management post-kidney transplantation | 411 36. Yigla M, Nakhoul F, Sabag A et al. Pulmonary hypertension 17. Einollahi B, Sadeghi Ghahrodi M. Hemodialysis arterioven- ous ﬁstula after transplant: to keep or not to keep? Iran J in patients with end-stage renal disease. Chest 2003; 123: Kidney Dis 2012; 6: 159–161 1577–1582 18. Locatelli F, Zoccali C. Arteriovenous ﬁstula as a nephropro- 37. Nakhoul F, Yigla M, Gilman R et al. The pathogenesis of pul- tective intervention in advanced CKD: scientiﬁc discovery monary hypertension in haemodialysis patients via arterio- and explanation, and the evaluation of interventions. venous access. Nephrol Dial Transplant 2005; 20: 1686–1692 Nephrol Dial Transplant 2015; 30: 1939–1941 38. Abassi Z, Nakhoul F, Khankin E et al. Pulmonary hyperten- 19. Unger P, Xhaet O, Wissing KM et al. Arteriovenous ﬁstula closure sion in chronic dialysis patients with arteriovenous ﬁstula: after renal transplantation: a prospective study with 24-hour pathogenesis and therapeutic prospective. Curr Opin Nephrol ambulatory blood pressure monitoring. Transplantation 2008; 85: Hypertens 2006; 15: 353–360 482–485 39. Anand IS, Florea VG. High output cardiac failure. Curr Treat 20. Baumbach GL. Effects of increased pulse pressure on cere- Options Cardiovasc Med 2001; 3: 151–159 bral arterioles. Hypertension 1996; 27: 159–167 40. MacRae JM, Pandeya S, Humen DP et al. Arteriovenous 21. Abassi ZA, Brodsky S, Karram T et al. Temporal changes in ﬁstula-associated high-output cardiac failure: a review of natriuretic and antinatriuretic systems after closure of a mechanisms. Am J Kidney Dis 2004; 43: e17–e22 large arteriovenous ﬁstula. Cardiovasc Res 2001; 51: 567–576 41. Parfrey PS, Harnett JD, Foley RN et al. Impact of renal trans- 22. Lobo MD, Sobotka PA, Stanton A et al. Central arteriovenous plantation on uremic cardiomyopathy. Transplantation 1995; anastomosis for the treatment of patients with uncontrolled 60: 908–914 hypertension (the ROX CONTROL HTN study): a randomised 42. Harnett JD, Kent GM, Barre PE et al. Risk factors for the devel- controlled trial. Lancet 2015; 385: 1634–1641 opment of left ventricular hypertrophy in a prospectively 23. Iwashima Y, Horio T, Takami Y et al. Effects of the creation of followed cohort of dialysis patients. J Am Soc Nephrol 1994; 4: arteriovenous ﬁstula for hemodialysis on cardiac function 1486–1490 and natriuretic peptide levels in CRF. Am J Kidney Dis 2002; 43. Meeus F, Kourilsky O, Guerin AP et al. Pathophysiology of 40: 974–982 cardiovascular disease in hemodialysis patients. Kidney Int 24. Ott C, Lobo MD, Sobotka PA et al. Effect of arteriovenous Suppl 2000; 76: S140–S147 anastomosis on blood pressure reduction in patients with 44. Faul C, Amaral AP, Oskouei B et al. FGF23 induces left ven- isolated systolic hypertension compared with combined tricular hypertrophy. J Clin Invest 2011; 121: 4393–4408 hypertension. J Am Heart Assoc 2016; 5: e004234 45. Dundon BK, Torpey K, Nelson AJ et al. The deleterious effects 25. Kapil V, Sobotka PA, Saxena M et al. Central iliac arteriovenous of arteriovenous ﬁstula-creation on the cardiovascular sys- anastomosis for hypertension: targeting mechanical aspects tem: a longitudinal magnetic resonance imaging study. Int J of the circulation. Curr Hypertens Rep 2015; 17: 585 Nephrol Renovasc Dis 2014; 7: 337–345 26. Burchell AE, Lobo MD, Sulke N et al. Arteriovenous anasto- 46. Buchanan C, Mohammed A, Cox E et al. Intradialytic cardiac mosis: is this the way to control hypertension? Hypertension magnetic resonance imaging to assess cardiovascular re- 2014; 64: 6–12 sponses in a short-term trial of hemodiaﬁltration and hemo- 27. Korsheed S, Crowley LE, Fluck RJ et al. Creation of an arterio- dialysis. J Am Soc Nephrol 2017; 28: 1269–1277 venous ﬁstula is associated with signiﬁcant acute local and 47. Movilli E, Viola BF, Brunori G et al. Long-term effects of ar- systemic changes in microvascular function. Nephron Clin teriovenous ﬁstula closure on echocardiographic functional Pract 2013; 123: 173–179 and structural ﬁndings in hemodialysis patients: a prospect- 28. Bos WJ, Zietse R, Wesseling KH et al. Effects of arteriovenous ive study. Am J Kidney Dis 2010; 55: 682–689 ﬁstulas on cardiac oxygen supply and demand. Kidney Int 48. Tellioglu G, Berber I, Kilicoglu G et al. Doppler 1999; 55: 2049–2053 ultrasonography-guided surgery for high-ﬂow hemodialysis 29. Unger P, Wissing KM. Arteriovenous ﬁstula after renal trans- vascular access: preliminary results. Transplant Proc 2008; 40: plantation: utility, futility or threat? Nephrol Dial Transplant 87–89 2006; 21: 254–257 49. Basile C, Lomonte C, Vernaglione L et al. The relationship be- 30. Storey BG, George CR, Stewart JH et al. Embolic and ischemic tween the ﬂow of arteriovenous ﬁstula and cardiac output in complications after anastomosis of radial artery to cephalic haemodialysis patients. Nephrol Dial Transplant 2008; 23: vein. Surgery 1969; 66: 325–327 282–287 31. Anderson CB, Codd JR, Graff RA et al. Cardiac failure and 50. Engelberts I, Tordoir JH, Boon ES et al. High-output cardiac upper extremity arteriovenous dialysis ﬁstulas. Case reports failure due to excessive shunting in a hemodialysis access and a review of the literature. Arch Intern Med 1976; 136: ﬁstula: an easily overlooked diagnosis. Am J Nephrol 1995; 15: 292–297 323–326 32. Gupta N, Yuo TH, Konig G et al. Treatment strategies of arter- 51. Middleton RJ, Parfrey PS, Foley RN. Left ventricular hypertro- ial steal after arteriovenous access. J Vasc Surg 2011; 54: phy in the renal patient. J Am Soc Nephrol 2001; 12: 1079–1084 162–167 52. Rigatto C, Foley R, Jeffery J et al. Electrocardiographic left ven- 33. Padberg FT Jr, Calligaro KD, Sidawy AN. Complications of ar- tricular hypertrophy in renal transplant recipients: prognos- teriovenous hemodialysis access: recognition and manage- tic value and impact of blood pressure and anemia. J Am Soc ment. J Vasc Surg 2008; 48: 55S–80S Nephrol 2003; 14: 462–468 34. Al-Jaishi AA, Liu AR, Lok CE et al. Complications of the ar- 53. Schier T, Gobel G, Bosmuller C et al. Incidence of arterioven- teriovenous ﬁstula: a systematic review. J Am Soc Nephrol ous ﬁstula closure due to high-output cardiac failure in 2016; 28: 1839–1850 kidney-transplanted patients. Clin Transplant 2013; 27: 35. Clarkson MR, Giblin L, Brown A et al. Reversal of pulmonary 858–865 hypertension after ligation of a brachiocephalic arterioven- 54. van Duijnhoven EC, Cheriex EC, Tordoir JH et al. Effect of closure of the arteriovenous ﬁstula on left ventricular ous ﬁstula. Am J Kidney Dis 2002; 40: E8 Downloaded from https://academic.oup.com/ckj/article-abstract/11/3/406/4557542 by Ed 'DeepDyve' Gillespie user on 20 June 2018 412 | P. Vanderweckene et al. 60. Salvetti M, Muiesan ML, Paini A et al. Left ven- dimensions in renal transplant patients. Nephrol Dial Transplant 2001; 16: 368–372 tricular hypertrophy and renal dysfunction during antihy- 55. Unger P, Wissing KM, de Pauw L et al. Reduction of left ven- pertensive treatment adversely affect cardiovascular tricular diameter and mass after surgical arteriovenous ﬁs- prognosis in hypertensive patients. JHypertens 2012; 30: tula closure in renal transplant recipients. Transplantation 411–420 2002; 74: 73–79 61. Oktay AA, Lavie CJ, Milani RV et al. Current perspectives on 56. Unger P, Velez-Roa S, Wissing KM et al. Regression of left left ventricular geometry in systemic hypertension. Prog ventricular hypertrophy after arteriovenous ﬁstula closure Cardiovasc Dis 2016; 59: 235–246 in renal transplant recipients: a long-term follow-up. Am J 62. Ferro CJ, Savage T, Pinder SJ et al. Central aortic pressure aug- Transplant 2004; 4: 2038–2044 mentation in stable renal transplant recipients. Kidney Int 57. Soleimani MJ, Shahrokh H, Shadpour P et al. Impact of dialy- 2002; 62: 166–171 sis access ﬁstula on cardiac function after kidney trans- 63. Vajdic B, Arnol M, Ponikvar R et al. Functional status of plantation. Iran J Kidney Dis 2012; 6: 198–202 hemodialysis arteriovenous ﬁstula in kidney transplant re- 58. Glowinski J, Malyszko J, Glowinska I et al. To close or not to cipients as a predictor of allograft function and survival. Transplant Proc 2010; 42: 4006–4009 close: ﬁstula ligation and cardiac function in kidney allograft recipients. Pol Arch Med Wewn 2012; 122: 348–352 64. Masson I, Flamant M, Maillard N et al.MDRDversusCKD- 59. O’Brien E, Parati G, Stergiou G et al. European society of EPI equation to estimate glomerular ﬁltration rate in hypertension position paper on ambulatory blood pressure kidney transplant recipients. Transplantation 2013; 95: monitoring. J Hypertens 2013; 31: 1731–1768 1211–1217 Downloaded from https://academic.oup.com/ckj/article-abstract/11/3/406/4557542 by Ed 'DeepDyve' Gillespie user on 20 June 2018
Clinical Kidney Journal – Oxford University Press
Published: Oct 18, 2017
It’s your single place to instantly
discover and read the research
that matters to you.
Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.
All for just $49/month
Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly
Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.
Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.
Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.
All the latest content is available, no embargo periods.
“Hi guys, I cannot tell you how much I love this resource. Incredible. I really believe you've hit the nail on the head with this site in regards to solving the research-purchase issue.”Daniel C.
“Whoa! It’s like Spotify but for academic articles.”@Phil_Robichaud
“I must say, @deepdyve is a fabulous solution to the independent researcher's problem of #access to #information.”@deepthiw
“My last article couldn't be possible without the platform @deepdyve that makes journal papers cheaper.”@JoseServera