Mark, Patrick B.

Stoumpos, Sokratis

English

Sokratis Stoumpos

Patrick B. Mark

Crossref

Should We Ligate Arteriovenous Fistulas in Asymptomatic Patients After Kidney Transplantation?

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     Stoumpos, S. and Mark, P. B. (2019) Should we ligate arteriovenous fistulas in asymptomatic patients after kidney transplantation? Circulation, 139(25), pp. 2819-2821. (doi:10.1161/CIRCULATIONAHA.119.040361)  There may be differences between this version and the published version. You are advised to consult the publisher’s version if you wish to cite from it.    http://eprints.gla.ac.uk/182535/              Deposited on: 22 March 2019     Enlighten – Research publications by members of the University of Glasgow http://eprints.gla.ac.uk                 Should we ligate arteriovenous fistulas in asymptomatic patients after kidney transplantation?  Sokratis Stoumpos MD1, Patrick B Mark MB, ChB, PhD1  Running title: Cardiovascular effects of AVF ligation  1. BHF Glasgow Cardiovascular Research Centre, 126 University Place, Glasgow G12 8TA, United Kingdom  Corresponding author:  Patrick Mark, BHF Glasgow Cardiovascular Research Centre, 126 University Place, Glasgow G12 8TA, United Kingdom E: patrick.mark@glasgow.ac.uk T: +44 141 3308218  Total word count: 1341               When Brescia and Cimino first described a series of successful autogenous arteriovenous fistulas (AVF) creations for hemodialysis (HD) in 19661, they quickly recognized the ensuing increased cardiac output as the major disadvantage of the new technique. They considered it clinically insignificant and this was probably true in their cohort of young dialysis patients (mean age 43 years), none of which had end stage renal disease (ESRD) caused by diabetes or vascular disease. Over time, however, there have been significant changes in the demographics of the prevalent HD population, with trends toward increasing age and comorbidity, including impaired baseline cardiac function. Left ventricular hypertrophy (LVH) is primarily an adaptive remodelling process as a response to increased cardiac workload aiming to minimize ventricular wall stress and is almost universal in new dialysis patients. The development, severity, and persistence of LVH are strongly associated with cardiovascular (CV) events and mortality risk in chronic kidney disease (CKD), especially in patients in the highest tertiles of change in LV mass treated with conventional HD2. Despite its detrimental effects when present, the impact of LVH regression on mortality remains uncertain. An elegant multifactorial interventional study by London et al3 has demonstrated that a 10% decrease in LV mass translated into a 28% decrease in mortality risk from cardiovascular causes over a 5-year period. Contrary to these results, Foley et al4 found that improvements in LV mass over a 1-year period after initiation of dialysis were associated with a subsequent reduced likelihood of cardiac failure but not with mortality risk.  NATURAL HISTORY OF LV MASS CHANGE AFTER AVF CREATION AND AFTER KIDNEY TRANSPLANTATION  The hemodynamic effects following AVF creation include decreased peripheral resistance and thus increased cardiac output, which initially does not lead to symptoms of congestive (or high-output) cardiac failure. As the fistula increases in size, the increased blood volume results to increased right atrial, pulmonary artery, and LV end-diastolic volumes until the myocardium decompensates, the LV dilates, the ejection fraction declines, and the patient has symptoms of cardiac failure. Myocardial ischemia caused by an imbalance between subendocardial oxygen supply and increased oxygen demand as a result of increased cardiac output has also been implicated in the development of deleterious cardiac effects5. Using cardiac magnetic resonance (CMR) imaging, Dundon et al6 showed a mean increase of 25% in cardiac output, 12.7% in LV mass and 21% in LV end-systolic volumes 6 months after AVF creation. These changes add a significant burden to the pre-existing LV hypertrophy, dilatation and dysfunction caused by the underlying uremic cardiomyopathy as CKD progresses.  On the other hand, re-establishment of renal function following kidney transplantation and avoidance of the pronounced intravascular volume shifts occurring during thrice-weekly hemodialysis therapy consistently reduces LVH7. More interestingly, regression of LVH continues beyond the first year after renal transplantation, reaching a nadir at the second year and persisting thereafter8. Kidney transplant (KT) recipients have lower CV death risk compared with patients on the transplant waiting list9, suggesting that the progression of CV disease can be ameliorated by restoring renal function with a transplant.  AVF LIGATION IN KIDNEY TRANSPLANT RECIPIENTS  In this issue of Circulation, Rao and colleagues present a randomized controlled trial of 54 KT recipients equally randomized to AVF ligation or no intervention. All patients had a kidney transplant implanted at least 1 year prior (median 7.5-9 years), stable graft function, and underwent CMR at baseline and at 6 months (REFERENCE TO THE IN PRESS PAPER).  This was a well-conducted collaborative study with high standards in methodology. They have used CMR imaging which is widely considered to be the “gold standard” technique for the assessment of LV dimensions because it accurately defines mass, volume, and pattern of LVH (concentric, eccentric, or asymmetric) independently of geometric assumptions. The key primary finding was a 15% reduction in LV mass in the AVF ligation group associated with a decrease in cardiac output. There was approximately 20% decrease in LV and atrial sizes and also a reduction in NT-pro BNP levels. No significant changes were documented in LV ejection fraction, pulmonary artery velocity, blood pressure and estimated glomerular filtration rate (eGFR). Eight patients had minor complications following fistula ligation (6 had thrombosis and 2 had local infection). The authors advocate that these findings may have significant implications, given that a single intervention has the potential to provide substantial CV benefits.  The findings from Rao et al certainly are provocative, and they reflect the scarcity of knowledge and guidance in this particular field. They are hypothesis generating and, as the authors properly state, not definitive. Nevertheless, several important considerations must be addressed before widespread dissemination of the proposed approach. These data significantly expand previously reported observational studies investigating the cardiac effects of AVF closure post-KT. Studies of the renal transplant population10, 11 show that closure of the fistula results in significant reductions in both LV end-diastolic diameter and LV mass. Nevertheless, AVF closure does not restore a normal LV geometry and the reduction in LV mass is a result of the reduction in LV end-diastolic volume rather than a decrease in wall thickness12.  NOT ALL AVF ARE EQUAL Many unknowns remain and several of those key questions are highlighted by the authors. First, this study was not adequately powered to detect differences in cardiovascular and survival outcomes. Whether the decrease in LV mass and reversal of LVH following AVF closure imparts a protective effect and changes the trajectory of patient outcomes is still a matter to be resolved. Second, a risk stratification using surrogate markers such as fistula blood flow (Qa) measurements or the fistula site (i.e. upper arm compared with forearm AVF) has not be applied. Traditionally, patients with a Qa greater than 2L/min or an upper arm AVF are at increased risk for the development of cardiac failure13 and perhaps would benefit more from fistula closure. Third, thoughtful consideration of the benefit of AVF ligation against the risk of losing a dialysis access site, especially in patients that will potentially return to HD during their lifetime should be applied. No doubt, preservation of the AVF or a flow reduction procedure may be preferable to fistula closure for younger patients. And finally when is the best time to ligate an AVF following successful KT? It may be that the benefit on cardiovascular or even graft outcomes is greater if the fistula is ligated 3 to 6 months post-KT presuming stable graft function.   WHERE DO WE GO FROM HERE? The added CV risk following AVF creation in patients with CKD, who already have excessive CV disease burden, is difficult to quantify. Even more so, the CV risk reduction attributed to AVF closure after successful kidney transplantation, where both events have a perceived favourable effect in cardiac indices, is even harder to examine. Notably, current guidelines in post-operative care in the kidney transplant recipient make no recommendations on management of a redundant AVF14. Studies such as the one from Rao and colleagues are a necessary step in the right direction.  The interplay of various factors contributing to LVH during a renal patient’s timeline from the development of CKD to progression to ESRD requiring dialysis and transplantation dictates that a more holistic approach targeting all potential contributors starting early in CKD should be adopted. As part of this strategy fistula closure should be reserved for stable kidney transplant recipients with symptoms of overt cardiac failure or pulmonary hypertension and access-related complications (mainly aneurysm formation with risk of rupture, steal syndrome, infection or high Qa). For the rest, an individualized patient-centered approach which will include patients’ preferences and beliefs is deemed more appropriate. The pros and cons of AVF ligation are summarized in Figure 1.  In the wake of this admirable work from Rao and colleagues, AVF closure post-KT has a role for selected patients. The adoption of this approach must be weighed against its generalizability to diverse transplant populations, the lack of definitive hard clinical end-points, and potentially high implementation costs. Future longitudinal studies focused on cardiovascular and survival outcomes with appropriate stratification and long-term follow-up will shed more light in this important controversy.    Conflict of Interest Disclosures None  Legend  Figure 1 Theoretical advantages and disadvantages of AVF ligation  References 1. Brescia MJ, Cimino JE, Appel K and Hurwich BJ. Chronic hemodialysis using venipuncture and a surgically created arteriovenous fistula. N Engl J Med. 1966;275:1089-92. 2. Zoccali C, Benedetto FA, Mallamaci F, Tripepi G, Giacone G, Stancanelli B, Cataliotti A and Malatino LS. Left ventricular mass monitoring in the follow-up of dialysis patients: prognostic value of left ventricular hypertrophy progression. Kidney Int. 2004;65:1492-8. 3. London GM, Pannier B, Guerin AP, Blacher J, Marchais SJ, Darne B, Metivier F, Adda H and Safar ME. Alterations of left ventricular hypertrophy in and survival of patients receiving hemodialysis: follow-up of an interventional study. J Am Soc Nephrol. 2001;12:2759-67. 4. Foley RN, Parfrey PS, Kent GM, Harnett JD, Murray DC and Barre PE. Serial change in echocardiographic parameters and cardiac failure in end-stage renal disease. J Am Soc Nephrol. 2000;11:912-6. 5. Savage MT, Ferro CJ, Sassano A and Tomson CR. The impact of arteriovenous fistula formation on central hemodynamic pressures in chronic renal failure patients: a prospective study. Am J Kidney Dis. 2002;40:753-9. 6. Dundon BK, Torpey K, Nelson AJ, Wong DT, Duncan RF, Meredith IT, Faull RJ, Worthley SG and Worthley MI. The deleterious effects of arteriovenous fistula-creation on the cardiovascular system: a longitudinal magnetic resonance imaging study. Int J Nephrol Renovasc Dis. 2014;7:337-45. 7. Zolty R, Hynes PJ and Vittorio TJ. Severe left ventricular systolic dysfunction may reverse with renal transplantation: uremic cardiomyopathy and cardiorenal syndrome. Am J Transplant. 2008;8:2219-24. 8. Rigatto C, Foley RN, Kent GM, Guttmann R and Parfrey PS. Long-term changes in left ventricular hypertrophy after renal transplantation. Transplantation. 2000;70:570-5. 9. Meier-Kriesche HU, Schold JD, Srinivas TR, Reed A and Kaplan B. Kidney transplantation halts cardiovascular disease progression in patients with end-stage renal disease. Am J Transplant. 2004;4:1662-8. 10. Unger P, Wissing KM, de Pauw L, Neubauer J and van de Borne P. Reduction of left ventricular diameter and mass after surgical arteriovenous fistula closure in renal transplant recipients. Transplantation. 2002;74:73-9. 11. van Duijnhoven  EC, Cheriex EC, Tordoir JH, Kooman JP and van Hooff  JP. Effect of closure of the arteriovenous fistula on left ventricular dimensions in renal transplant patients. Nephrol Dial Transplant. 2001;16:368-72. 12. Unger P, Velez-Roa S, Wissing KM, Hoang AD and van de Borne P. Regression of left ventricular hypertrophy after arteriovenous fistula closure in renal transplant recipients: a long-term follow-up. Am J Transplant. 2004;4:2038-44. 13. Basile C, Lomonte C, Vernaglione L, Casucci F, Antonelli M and Losurdo N. The relationship between the flow of arteriovenous fistula and cardiac output in haemodialysis patients. Nephrol Dial Transplant. 2008;23:282-7. 14. Kasiske BL, Zeier MG, Chapman JR, Craig JC, Ekberg H, Garvey CA, Green MD, Jha V, Josephson MA, Kiberd BA, Kreis HA, McDonald RA, Newmann JM, Obrador GT, Vincenti FG, Cheung M, Earley A, Raman G, Abariga S, Wagner M, Balk EM and Kidney Disease: Improving Global O. KDIGO clinical practice guideline for the care of kidney transplant recipients: a summary. Kidney Int. 2010;77:299-311.  

Should we ligate arteriovenous fistulas in asymptomatic patients after kidney transplantation?

Enlighten: Publications

  
 
 
 
Stoumpos, S. and Mark, P. B. (2019) Should we ligate arteriovenous fistulas in 
asymptomatic patients after kidney transplantation? Circulation, 139(25), pp. 2819-
2821. (doi:10.1161/CIRCULATIONAHA.119.040361) 
 
There may be differences between this version and the published version. You are 
advised to consult the publisher’s version if you wish to cite from it. 
 
 
 
http://eprints.gla.ac.uk/182535/  
      
 
 
 
 
 
 
Deposited on: 22 March 2019 
 
 
 
 
Enlighten – Research publications by members of the University of Glasgow 
http://eprints.gla.ac.uk  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Should we ligate arteriovenous fistulas in asymptomatic patients after 
kidney transplantation? 
 
Sokratis Stoumpos MD1, Patrick B Mark MB, ChB, PhD1 
 
Running title: Cardiovascular effects of AVF ligation 
 
1. BHF Glasgow Cardiovascular Research Centre, 126 University Place, 
Glasgow G12 8TA, United Kingdom 
 
Corresponding author:  Patrick Mark, BHF Glasgow Cardiovascular 
Research Centre, 126 University Place, Glasgow G12 8TA, United Kingdom 
E: patrick.mark@glasgow.ac.uk 
T: +44 141 3308218 
 
Total word count: 1341 
 
 
 
 
 
 
 
 
 
 
  
  
When Brescia and Cimino first described a series of successful 
autogenous arteriovenous fistulas (AVF) creations for hemodialysis (HD) in 
19661, they quickly recognized the ensuing increased cardiac output as the 
major disadvantage of the new technique. They considered it clinically 
insignificant and this was probably true in their cohort of young dialysis patients 
(mean age 43 years), none of which had end stage renal disease (ESRD) 
caused by diabetes or vascular disease. Over time, however, there have been 
significant changes in the demographics of the prevalent HD population, with 
trends toward increasing age and comorbidity, including impaired baseline 
cardiac function. 
Left ventricular hypertrophy (LVH) is primarily an adaptive remodelling 
process as a response to increased cardiac workload aiming to minimize 
ventricular wall stress and is almost universal in new dialysis patients. The 
development, severity, and persistence of LVH are strongly associated with 
cardiovascular (CV) events and mortality risk in chronic kidney disease (CKD), 
especially in patients in the highest tertiles of change in LV mass treated with 
conventional HD2. Despite its detrimental effects when present, the impact of 
LVH regression on mortality remains uncertain. An elegant multifactorial 
interventional study by London et al3 has demonstrated that a 10% decrease in 
LV mass translated into a 28% decrease in mortality risk from cardiovascular 
causes over a 5-year period. Contrary to these results, Foley et al4 found that 
improvements in LV mass over a 1-year period after initiation of dialysis were 
associated with a subsequent reduced likelihood of cardiac failure but not with 
mortality risk. 
 
NATURAL HISTORY OF LV MASS CHANGE AFTER AVF CREATION AND 
AFTER KIDNEY TRANSPLANTATION 
 The hemodynamic effects following AVF creation include decreased 
peripheral resistance and thus increased cardiac output, which initially does not 
lead to symptoms of congestive (or high-output) cardiac failure. As the fistula 
increases in size, the increased blood volume results to increased right atrial, 
pulmonary artery, and LV end-diastolic volumes until the myocardium 
decompensates, the LV dilates, the ejection fraction declines, and the patient 
has symptoms of cardiac failure. Myocardial ischemia caused by an imbalance 
between subendocardial oxygen supply and increased oxygen demand as a 
result of increased cardiac output has also been implicated in the development 
of deleterious cardiac effects5. Using cardiac magnetic resonance (CMR) 
imaging, Dundon et al6 showed a mean increase of 25% in cardiac output, 
12.7% in LV mass and 21% in LV end-systolic volumes 6 months after AVF 
creation. These changes add a significant burden to the pre-existing LV 
hypertrophy, dilatation and dysfunction caused by the underlying uremic 
cardiomyopathy as CKD progresses. 
 On the other hand, re-establishment of renal function following kidney 
transplantation and avoidance of the pronounced intravascular volume shifts 
occurring during thrice-weekly hemodialysis therapy consistently reduces 
LVH7. More interestingly, regression of LVH continues beyond the first year 
after renal transplantation, reaching a nadir at the second year and persisting 
thereafter8. Kidney transplant (KT) recipients have lower CV death risk 
compared with patients on the transplant waiting list9, suggesting that the 
progression of CV disease can be ameliorated by restoring renal function with 
a transplant. 
 
AVF LIGATION IN KIDNEY TRANSPLANT RECIPIENTS  
In this issue of Circulation, Rao and colleagues present a randomized 
controlled trial of 54 KT recipients equally randomized to AVF ligation or no 
intervention. All patients had a kidney transplant implanted at least 1 year prior 
(median 7.5-9 years), stable graft function, and underwent CMR at baseline 
and at 6 months (REFERENCE TO THE IN PRESS PAPER).  
This was a well-conducted collaborative study with high standards in 
methodology. They have used CMR imaging which is widely considered to be 
the “gold standard” technique for the assessment of LV dimensions because it 
accurately defines mass, volume, and pattern of LVH (concentric, eccentric, or 
asymmetric) independently of geometric assumptions. 
The key primary finding was a 15% reduction in LV mass in the AVF 
ligation group associated with a decrease in cardiac output. There was 
approximately 20% decrease in LV and atrial sizes and also a reduction in NT-
pro BNP levels. No significant changes were documented in LV ejection 
fraction, pulmonary artery velocity, blood pressure and estimated glomerular 
filtration rate (eGFR). Eight patients had minor complications following fistula 
ligation (6 had thrombosis and 2 had local infection). The authors advocate that 
these findings may have significant implications, given that a single intervention 
has the potential to provide substantial CV benefits.  
The findings from Rao et al certainly are provocative, and they reflect 
the scarcity of knowledge and guidance in this particular field. They are 
hypothesis generating and, as the authors properly state, not definitive. 
Nevertheless, several important considerations must be addressed before 
widespread dissemination of the proposed approach. 
These data significantly expand previously reported observational 
studies investigating the cardiac effects of AVF closure post-KT. Studies of the 
renal transplant population10, 11 show that closure of the fistula results in 
significant reductions in both LV end-diastolic diameter and LV mass. 
Nevertheless, AVF closure does not restore a normal LV geometry and the 
reduction in LV mass is a result of the reduction in LV end-diastolic volume 
rather than a decrease in wall thickness12. 
 
NOT ALL AVF ARE EQUAL 
Many unknowns remain and several of those key questions are 
highlighted by the authors. First, this study was not adequately powered to 
detect differences in cardiovascular and survival outcomes. Whether the 
decrease in LV mass and reversal of LVH following AVF closure imparts a 
protective effect and changes the trajectory of patient outcomes is still a matter 
to be resolved. Second, a risk stratification using surrogate markers such as 
fistula blood flow (Qa) measurements or the fistula site (i.e. upper arm 
compared with forearm AVF) has not be applied. Traditionally, patients with a 
Qa greater than 2L/min or an upper arm AVF are at increased risk for the 
development of cardiac failure13 and perhaps would benefit more from fistula 
closure. Third, thoughtful consideration of the benefit of AVF ligation against 
the risk of losing a dialysis access site, especially in patients that will potentially 
return to HD during their lifetime should be applied. No doubt, preservation of 
the AVF or a flow reduction procedure may be preferable to fistula closure for 
younger patients. And finally when is the best time to ligate an AVF following 
successful KT? It may be that the benefit on cardiovascular or even graft 
outcomes is greater if the fistula is ligated 3 to 6 months post-KT presuming 
stable graft function.  
 
WHERE DO WE GO FROM HERE? 
The added CV risk following AVF creation in patients with CKD, who 
already have excessive CV disease burden, is difficult to quantify. Even more 
so, the CV risk reduction attributed to AVF closure after successful kidney 
transplantation, where both events have a perceived favourable effect in 
cardiac indices, is even harder to examine. Notably, current guidelines in post-
operative care in the kidney transplant recipient make no recommendations on 
management of a redundant AVF14. Studies such as the one from Rao and 
colleagues are a necessary step in the right direction.  
The interplay of various factors contributing to LVH during a renal 
patient’s timeline from the development of CKD to progression to ESRD 
requiring dialysis and transplantation dictates that a more holistic approach 
targeting all potential contributors starting early in CKD should be adopted. As 
part of this strategy fistula closure should be reserved for stable kidney 
transplant recipients with symptoms of overt cardiac failure or pulmonary 
hypertension and access-related complications (mainly aneurysm formation 
with risk of rupture, steal syndrome, infection or high Qa). For the rest, an 
individualized patient-centered approach which will include patients’ 
preferences and beliefs is deemed more appropriate. The pros and cons of AVF 
ligation are summarized in Figure 1. 
 In the wake of this admirable work from Rao and colleagues, AVF 
closure post-KT has a role for selected patients. The adoption of this approach 
must be weighed against its generalizability to diverse transplant populations, 
the lack of definitive hard clinical end-points, and potentially high 
implementation costs. Future longitudinal studies focused on cardiovascular 
and survival outcomes with appropriate stratification and long-term follow-up 
will shed more light in this important controversy. 
 
  
Conflict of Interest Disclosures 
None 
 
Legend 
 
Figure 1 
Theoretical advantages and disadvantages of AVF ligation 
 
References 1. Brescia MJ, Cimino JE, Appel K and Hurwich BJ. Chronic hemodialysis using venipuncture and a surgically created arteriovenous fistula. N Engl J Med. 1966;275:1089-92. 2. Zoccali C, Benedetto FA, Mallamaci F, Tripepi G, Giacone G, Stancanelli B, Cataliotti A and Malatino LS. Left ventricular mass monitoring in the follow-up of dialysis patients: prognostic value of left ventricular hypertrophy progression. 
Kidney Int. 2004;65:1492-8. 3. London GM, Pannier B, Guerin AP, Blacher J, Marchais SJ, Darne B, Metivier F, Adda H and Safar ME. Alterations of left ventricular hypertrophy in and survival of patients receiving hemodialysis: follow-up of an interventional study. J Am Soc 
Nephrol. 2001;12:2759-67. 4. Foley RN, Parfrey PS, Kent GM, Harnett JD, Murray DC and Barre PE. Serial change in echocardiographic parameters and cardiac failure in end-stage renal disease. J Am Soc Nephrol. 2000;11:912-6. 5. Savage MT, Ferro CJ, Sassano A and Tomson CR. The impact of arteriovenous fistula formation on central hemodynamic pressures in chronic renal failure patients: a prospective study. Am J Kidney Dis. 2002;40:753-9. 6. Dundon BK, Torpey K, Nelson AJ, Wong DT, Duncan RF, Meredith IT, Faull RJ, Worthley SG and Worthley MI. The deleterious effects of arteriovenous fistula-creation on the cardiovascular system: a longitudinal magnetic resonance imaging study. Int J Nephrol Renovasc Dis. 2014;7:337-45. 7. Zolty R, Hynes PJ and Vittorio TJ. Severe left ventricular systolic dysfunction may reverse with renal transplantation: uremic cardiomyopathy and cardiorenal syndrome. Am J Transplant. 2008;8:2219-24. 8. Rigatto C, Foley RN, Kent GM, Guttmann R and Parfrey PS. Long-term changes in left ventricular hypertrophy after renal transplantation. 
Transplantation. 2000;70:570-5. 9. Meier-Kriesche HU, Schold JD, Srinivas TR, Reed A and Kaplan B. Kidney transplantation halts cardiovascular disease progression in patients with end-stage renal disease. Am J Transplant. 2004;4:1662-8. 10. Unger P, Wissing KM, de Pauw L, Neubauer J and van de Borne P. Reduction of left ventricular diameter and mass after surgical arteriovenous fistula closure in renal transplant recipients. Transplantation. 2002;74:73-9. 11. van Duijnhoven  EC, Cheriex EC, Tordoir JH, Kooman JP and van Hooff  JP. Effect of closure of the arteriovenous fistula on left ventricular dimensions in renal transplant patients. Nephrol Dial Transplant. 2001;16:368-72. 
12. Unger P, Velez-Roa S, Wissing KM, Hoang AD and van de Borne P. Regression of left ventricular hypertrophy after arteriovenous fistula closure in renal transplant recipients: a long-term follow-up. Am J Transplant. 2004;4:2038-44. 13. Basile C, Lomonte C, Vernaglione L, Casucci F, Antonelli M and Losurdo N. The relationship between the flow of arteriovenous fistula and cardiac output in haemodialysis patients. Nephrol Dial Transplant. 2008;23:282-7. 14. Kasiske BL, Zeier MG, Chapman JR, Craig JC, Ekberg H, Garvey CA, Green MD, Jha V, Josephson MA, Kiberd BA, Kreis HA, McDonald RA, Newmann JM, Obrador GT, Vincenti FG, Cheung M, Earley A, Raman G, Abariga S, Wagner M, Balk EM and Kidney Disease: Improving Global O. KDIGO clinical practice guideline for the care of kidney transplant recipients: a summary. Kidney Int. 2010;77:299-311. 
 


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Should we ligate arteriovenous fistulas in asymptomatic patients after kidney transplantation?

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