The management of hemodialysis arteriovenous fistulas in well functioning renal transplanted patients: Many doubts, few certainties
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1.Department of Renal Pathology, Azienda Ospedaliera G. Brotzu, Cagliari - Italy
2.Servizio di Nefrologia e Dialisi, Distretto Sanitario Sorgono - Isili (NU) - Italy
3.Casa di cura Ospedale Internazionale, Naples - Italy
ABSTRACT
Vascular access (VA) for hemodialysis (HD) is one of the most important clinical problems in end-stage renal disease (ESRD) patients because it can limit a life support system and can influence long-term dialysis patient survival. Nevertheless, VA becomes useless after a successful renal transplant. Therefore, we wanted to evaluate the natural history of arteriovenous fistulas (AVF) in renal transplanted patients and the possibility of maintaining the fistula as patent or not.
Methods: A retrospective study was conducted to evaluate kidney transplant patients in our unit from April 1994 to April 2004. We studied 542 patients.
Results: There were 365 patients with a well functioning kidney. Eighty-six patients died. Ninety-one patients were put back on dialysis: 89 patients on HD and two patients on CAPD. Of the 365 patients with functioning kidney transplants, 198 patients demonstrated a patent fistula, while 167 patients had a closed fistula. One hundred and twenty-five patients had a spontaneous closure and 42 patients had a surgical closure. Of the 89 patients put back on dialysis, 49 patients used the previous AVF, while it was necessary to create a new VA in 40 patients.
Conclusions: As demonstrated by the results of our study, after renal transplantation the possibility of spontaneous
AVF closure caused by a thrombosis is not a rare event. The dilemma is whether to preserve a fistula that could be useful in case of restarting HD or to perform a systematic fistula closure because of cardiac output and cardiac failure risks. Concerning this question there is no consensus between different authors in the literature. In reviewing the literature and analyzing our data, we conclude that the definite indications for AVF closure in well functioning renal transplanted patients are heart failure, high flow fistula, VA complications and important aesthetic reasons. Routine AVF closure is not indicated until prospective and randomized studies can demonstrate the ability of this procedure to reduce the high incidence of cardiac morbidity and mortality that is present,
even after renal transplantation.
Key Words: Arterovenous fistula, Renal transplant, Heart failure
INTRODUCTION
Vascular access (VA) for hemodialysis (HD) is one of the most important clinical problems in endstage renal disease (ESRD) patients because an important relationship exists between dialytic dose and mortality (1-3). Good dialysis is possible only with good VA. Further, there is a negative impact on
patient survival in relation to the number of surgical interventions for VA (4). Therefore, VA is a crucial element that can limit a life support system and
can influence the long-term survival of dialysis patients. The DOQI guidelines (5) state that the arteriovenous fistula (AVF) is the best VA because of the lower incidence of infective complications, but the long-term consequences of AVF on hemodynamic and cardiac function are still debated.
Cardiovascular disease (CVD) is the principal cause of morbidity and mortality in dialysis patients (6). Silberberg (7) showed that left ventricular hypertrophy
(LVH) is an important cardiac death predictor in uremic patients, as well as in patients with primary hypertension. LVH has been largely documented in renal failure (8-11). By multivariate analysis, London et al (12) further identified cardiac output as an important contributor to LVH. Pressure overload causes an increased systolic pressure that leads to increased systolic stress, which is associated with a parallel addiction of new sarcomers
(Q parallel addiction correct? and is sarcomers correct or 憇arcoma?or 憇arcomeres?), finally leading to cardiac wall thickening and concentric hypertrophy. Volume overload causes an increased diastolic pressure. This is a very important stimulus to the series addiction of new sarcomers and the development of eccentric hypertrophy (13). Chronic volume overload is associated with three principal factors: sodium and water retention, AV shunts and anemia (14, 15). Studies on rats (16) have confirmed that an AV shunt is a cause of LV dilatation and high output state.
Other adverse effects on cardiac function have been described in a prospective study demonstrating that myocardial ischemia caused by an adverse imbalance between subendocardial oxygen supply and increased oxygen demand is a possible consequence of AVF creation (17).
It has been reported that occasionally VA creation for HD can lead to cardiac failure. The first two cases of cardiomegaly with high output cardiac failure
occurred as a complication of high flow shunts, reported in 1972 (18), but the majority of high output cardiac failure has been thought to be related to high flow AVF, especially in pre-existing heart disease (19-24). Meeus et al (6) pointed out that symptomatic cardiac failure due to AV shunt is uncommon
and usually occurs in patients with underlying cardiac disease.
However, significant changes in CV hemodynamics have also been reported in patients with radiocephalic fistulas (25, 26). Ori (27) investigated the long-term effects of HD AV access on cardiac hemodynamics in a prospective study of 12 predialysis patients who were studied before, 1 and 3 months after primary AVF creation. The LVH incidence increased from 67% at baseline to 83% and 90% at 1 and 3 months, respectively. On the contrary, an observational but non-randomized study (28) on 993 elderly patients, followed for 4 yrs after dialysis start, did not show a significant rise in the incidence of heart failure and acute coronary syndromes in relation to the VA type (natural AVF, prosthetic fistulas or catheters).
Arteriovenous fistula and kidney transplant
Patients with well functioning renal transplants are particularly important for studying the cardiac effects of persistent HD AV access. Increased LVH often
persists after renal transplantation, and a relationship between blood pressure and LVH is found even in normotensive renal graft recipients (29).
In transplant recipients, multivariate analysis (30) showed that the presence of an AVF is independently associated with arterial stiffness augmentation.
This finding is relevant, as the arterial stiffness augmentation is positively and independently associated with CV morbidity in dialysis patients (31).
Savage (25) found that the subendocardial perfusion index increased immediately in transplanted recipients who underwent AVF ligation, even in the
absence of arterial stiffness modification.
A prospective study (32) on well functioning renal transplantation patients showed no differences regarding LV mass and volume changes between patients with or without a patent fistula (follow-up 10 months after renal transplantation). Huting (33) evaluated the course of LVH and function in ESRD after renal transplantation in a prospective study on 24 well functioning renal transplantation patients (follow up 41 ?30 months after transplantation). Huting found a reduction in left atrial diameter in patients with an occluded AVF, but no differences in cardiac structure or function in patients with a patent fistula vs those with a non-patent fistula.
The cardiac effects of persistent HD AV access in renal allograft recipients were evaluated in a retrospective study (34) of 61 stable renal transplant patients (39 with functioning AVF and 22 with closed AVF). No differences in LV mass, cardiac index, ejection fraction and LVH were observed; only an increase in LV and diastolic dimensions were associated with the presence of an AVF. This study concluded that the persistence of a large, high flow AVF for prolonged periods has little impact on cardiac morphology and function.
Van Dujnhover (35) evaluated the effect of AVF closure on LV dimensions in renal transplant patients in a prospective study of 20 patients with stable kidney transplants and with a mean fistula flow of 1790 ?640 mL/min. Echocardiography performed 4 months after AVF closure showed a reduced LV
mass and a reduction in LV end diastolic diameter.
Unger (36) documented a reduction in LV diameter and LV mass after surgical AVF closure in renal transplant recipients in a prospective study of 17 patients.
OBJECTIVE
The aim of our study was to evaluate both the natural history of the AVF and the kind of surgical procedures performed because of fistula problems in
the transplanted patients. In particular, we evaluated whether the surgical closure of the fistula was necessary because of the potential LVH risk.
MATERIALS AND METHODS
A retrospective study was conducted to evaluate kidney transplanted patients in our unit from April 1994 to April 2004. We studied 542 patients with average age of 47 yrs old and with a prevalence of males over female (367/175).
RESULTS
At the time of our observations, 86 patients died (12 patients due to CVD and in particular, nine patients due to acute myocardial ischemia and three
patients due to heart failure). Ninety-one patients were put back on dialysis: 89 patients on HD and two patients on CAPD. There were 365 patients with a well functioning kidney and the kidney survival rate of our patients is 82% after 5 yrs, in keeping with the results of the best European transplant
centers. Of the 365 patients with a functioning kidney transplant, 198 patients showed a patent fistula, while 167 patients had a closed fistula.
Of the 89 patients put back on dialysis, 49 patients used the previous AVF, while it was necessary to create a new VA in 40 patients. The average survival of the transplanted kidney was 22.2 months in the first group (min 1 - max 109) and 95.4 in the second group (min 1 - max 175). Figures 1 and 2 report the VA outcomes in our patients.
DISCUSSION
VA management after kidney transplant is a matter of debate between nephrologists. After a successful renal transplant, the VA is forgotten because it is neither used nor useful. As demonstrated by the results of our study, after a renal transplantation the possibility of spontaneous AVF closure caused by a thrombosis is not a rare event. The dilemma is whether to preserve a fistula that could be useful in case of restarting HD or to perform a systematic fistula closure because of the cardiac output and cardiac failure risks. In the literature, there is no consensus on this issue: according to De Lima (34) available data does not support routine AVF closure, while Van Dujnhover (35) suggests that AVF closure should be considered in patients with well functioning allografts and persistent LV dilatation. Unger (36) questions whether the effects of surgical closure on LV diameter or LV mass can be translated in terms of clinical benefit, and Patard (37) assumes that it seems reasonable to have a conservative attitude in the case of a well-tolerated native AVF. The theoretical or documented suppositions that show an important role of AVF in LVH and in the increased CV risk (11, 16, 27, 30), as well as the effectiveness of AVF closure in renal transplant recipients in improving some cardiac mass indices (35, 36), are in favor of routine AVF ligation in renal transplanted patients. On the other hand, reports that do not show a relationship between CV risk and a patent AVF or a significant alteration in cardiac indices after AVF closure (32-34) are against routine ligation. Further clinical benefits on the prevention of long-term complications by AVF closure remain not well documented.
CONCLUSION
In answering the question as to whether surgical AVF closure in transplanted patients is a therapeutic option, we think that the definite indications for
AVF closure in well functioning renal transplanted patients are heart failure, high flow fistula (especially large proximal fistula), VA complications (aneurysm, ischemia and infections) and important aesthetic reasons.
Routine AVF closure is not indicated until prospective and randomized studies can demonstrate the ability of this procedure to reduce the high incidence
of cardiac morbidity and mortality that is present, even after a renal transplantation. Currently, we consider for each patient cardiac function parameters, age, survival of the transplanted kidney, as well as the possibility and the simplicity of creating a new VA. It is necessary to
remember that every patient is a unique case.
REFERENCES
1. Hakim RM, Depner TA, Parker TF. Adequacy of haemodialysis. Am J Kidney Dis 1992; 20: 107-23.
2. Held PJ, Port FK, Wolfe RA, et al. The dose of haemodialysis and patient mortality. Kidney Int 1996; 50: 550-6.
3. Bloembergen WE, Stannard DC, Port FK, et al. Relationship of dose of haemodialysis and cause-specific mortality. Kidney Int 1996; 50: 557-65.
4. De Almeida E, Dias L, de Sousa FT, Mil-Homens MC, Pataca I, Parata MM. Survival in hemodialysis: is there a role for vascular access? Nephrol Dial Trasplant 1997; 12: 852.
5. NKF-K/DOQI Clinical Practice Guidelines for Vascular Access: update 2000. Am J Kidney Dis 2001; 37 (suppl 1): S137-81.
6. Meeus F, Kourilsky O, Guerin AP, Gaudry C, Marchais SJ, London GM. Pathophysiology of cardiovascular disease in hemodialysis patients. Kidney Int 2000; 76 (suppl): S140-7.
7. Silberberg J, Barre PE, Prichard SS, Sniderman AD. Impact of left ventricular hypertrophy on survival in end stage renal disease. Kidney Int 1989; 36: 286-90.
8. Harnett JD, Parfrey PS, Griffiths SM, Gault MH, Barre PG, Uttmann RD. Left ventricular hypertrophy in end-stage renal disease. Nephron 1988; 48: 107-15.
9. Foley RN, Parfrey PS, Harnett JD. Left ventricular hypertrophy in dialysed patients. Semin Dial 1992; 5: 34-41.
10. Parfey PS, Foley RN. Hamett JD, Kent GM, Urray DC, Barre PE. Outcome and risk factors for left ventricular hypertrophy in chronic uraemia. Nephrol Dial Transplant 1996, 11: 1277-85.
11. London GM, Guerin AP, Marchais S. Pathophysiology of left ventricular hypertrophy in dialysed patients. Blood Purif 1994; 12: 277-83.
12. London GM, Marchais SJ, Guerin AP, Metivier F. Contributive factors to cardiovascular hypertrophy in renal failure. Am J Hypertens 1989; 2: 261-5.
13. Guerin AP, Adda H, London GM, Marchais SJ. Cardiovascular disease in renal failure. Minerva Urol Nefrol 2004; 56: 279-88.
14. Foley RN, Parfrey PS, Harnett JD, et al. Clinical and echocardiographic disease in patient starting endstage renal disease therapy. Prevalence, associations and prognosis. Kidney Int 1995; 47: 186-92.
15. London GM, Parfrey PS. Cardiac disease in chronic uremia: pathogenesis. Adv Ren Replace Ther 1997; 4: 194-211.
16. Noma K, Brandle M, Rupp H, Jacob R. Left ventricular performance in rats with chronic cardiac overload due to arterio-venous shunt. Heart Vessels 1990; 5: 65-70.
17. Savage MT, Ferro CJ, Sassano A, Tomson CR. The impact of arteriovenous fistula formation on central hemodynamic pressure in chronic renal failure patients. A prospective study. Am J Kidney Dis 2002; 40: 753-9.
18. Ahearn DJ, Mahler JF. Heart failure as a complication of hemodialysis arteriovenous fistula. Ann Intern Med 1972; 77: 201-4.
19. Anderson CB, Codd JR, Graft RA, Groce MA, Harter HR, Newton WT. Cardiac failure and upper extremity arteriovenous dialysis fistulas. Cases reports and a review of literature. Arch Intern Med 1976; 136: 292-7.
20. Isoda S, Kajiwara H, Kondo J, Matsumoto A. Banding a hemodialysis arteriovenous fistula to decrease blood venous and resolve high output cardiac failure. Report of a case. Surg Today 1994; 24: 734-6.
21. Engelbert I, Tordoir IHM, Boon ES, Schreij G. High output cardiac failure due to excessive shunting in a hemodialysis access fistula: an easily overlooked diagnosis. Am J Nephrol 1995; 15: 323-6.
22. Young PR Jr, Rohr MS, Marterre WF. High output cardiac failure secondary to a brachiocephalic areteriovenous fistula. Two cases. Am Surg 1998; 64: 239-41.
23. Tzanakis I, Hatziathanassiou A, Kagia S, Papadaki A, Karephyllakis N, Kallivretakis N. Banding of an overfunctioning fistula with a prosthetic graft segmental. Nephron 1999; 81: 351-2.
24. Bailey WB, Talley JD. High output cardiac failure related to hemodialysis arteriovenous fistula. J Ark Med Soc 2000; 96: 340-1.
25. Savage MT, Ferro CJ, Sassano A, Tomson CRV. The impact of arterio-venous fistula formation on central hemodynamic pressures in long term renal failure patients: a prospective study. Am J Kidney Dis 2002; 40: 753-9.
26. Iwashima Y, Horio T, Takami Y. Effects of the creation of arteriovenous fistula for hemodialysis on cardiac function and natriuretic peptide levels in CRF. Am J Kidney Dis 2002; 40: 974-82.
27. Ori Y, Korzets A, Katzz M, et al. The contribution of an arteriovenous access for hemodialysis to left ventricular hypertrophy. Am J Kidney Dis 2002; 40: 745-52.
28. Abbot KC, Trespalacios FC, Agodoa LY. Arteriovenous fistula use and heart disease in long-term elderly hemodialysis patients: analysis of United States Renal Data System Dialysis Morbidity and Mortality Wave II. J Nephrol 2003; 16: 822-30.
29. Lipkin GW Tucker B, Giles M, Raine AE. Ambulatory blood pressure and left ventricular mass in cyclosporin- and non-cyclosporin-treated renal transplant recipients. J Hypertens 1993, 11: 439-42.
30. Ferro CJ, Savage T, Plinder SJ, Omson CR. Central aortic pressure augmentation in stable renal transplant recipients. Kidney Int 2002; 62: 166-71.
31. London GM, Blacher J, Pannier B, Guerin AP, Marchais SSJ, Safar ME. Arterial wave reflections and survival in end-stage renal failure. Hypertension 2001; 38: 434-8.
32. Peteiro J, Alvarez N, Calvino R, Penas M, Ribera F, Castro-Beiras A. Changes in left ventricular mass and filling after renal transplantation are related to changes in blood pressure. An echocardiographic and pulsed doppler study. Cardiology 1994; 85: 273-83.
33. Huting J. Course of LVH and function in end stage renal disease after renal transplantation. Am J Cardiol 1992; 70: 1481-4.
34. De Lima JJ, Vieira MLC, Molnar LJ, Medeiros CJ, Ianhez LE, Krieger EM. Cardiac effects of persistent hemodialysis arteriovenous access in recipient of renal allograft. Cardiology 1999; 92: 236-9.
35. Van Dujnhover ECM, Cheriex ECM, Tordoir JHM, Kooman JP, 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.
36. Unger P, Wissing KM, De Pauw L, Neubauer J, Van De Born P. Reduction of left ventricular diameter and mass after surgical arteriovenous fistula closure in renal transplant recipients. Transplantation 2002; 74: 73-9.
37. Patard JJ, Bensalah K, Lucas A, et al. Management of vascular access for hemodialysis after successful kidney transplantation. Scan J Urol Nephrol 2002; 36: 373-6.(O. Manca, G.L. Pisano, P.)
2.Servizio di Nefrologia e Dialisi, Distretto Sanitario Sorgono - Isili (NU) - Italy
3.Casa di cura Ospedale Internazionale, Naples - Italy
ABSTRACT
Vascular access (VA) for hemodialysis (HD) is one of the most important clinical problems in end-stage renal disease (ESRD) patients because it can limit a life support system and can influence long-term dialysis patient survival. Nevertheless, VA becomes useless after a successful renal transplant. Therefore, we wanted to evaluate the natural history of arteriovenous fistulas (AVF) in renal transplanted patients and the possibility of maintaining the fistula as patent or not.
Methods: A retrospective study was conducted to evaluate kidney transplant patients in our unit from April 1994 to April 2004. We studied 542 patients.
Results: There were 365 patients with a well functioning kidney. Eighty-six patients died. Ninety-one patients were put back on dialysis: 89 patients on HD and two patients on CAPD. Of the 365 patients with functioning kidney transplants, 198 patients demonstrated a patent fistula, while 167 patients had a closed fistula. One hundred and twenty-five patients had a spontaneous closure and 42 patients had a surgical closure. Of the 89 patients put back on dialysis, 49 patients used the previous AVF, while it was necessary to create a new VA in 40 patients.
Conclusions: As demonstrated by the results of our study, after renal transplantation the possibility of spontaneous
AVF closure caused by a thrombosis is not a rare event. The dilemma is whether to preserve a fistula that could be useful in case of restarting HD or to perform a systematic fistula closure because of cardiac output and cardiac failure risks. Concerning this question there is no consensus between different authors in the literature. In reviewing the literature and analyzing our data, we conclude that the definite indications for AVF closure in well functioning renal transplanted patients are heart failure, high flow fistula, VA complications and important aesthetic reasons. Routine AVF closure is not indicated until prospective and randomized studies can demonstrate the ability of this procedure to reduce the high incidence of cardiac morbidity and mortality that is present,
even after renal transplantation.
Key Words: Arterovenous fistula, Renal transplant, Heart failure
INTRODUCTION
Vascular access (VA) for hemodialysis (HD) is one of the most important clinical problems in endstage renal disease (ESRD) patients because an important relationship exists between dialytic dose and mortality (1-3). Good dialysis is possible only with good VA. Further, there is a negative impact on
patient survival in relation to the number of surgical interventions for VA (4). Therefore, VA is a crucial element that can limit a life support system and
can influence the long-term survival of dialysis patients. The DOQI guidelines (5) state that the arteriovenous fistula (AVF) is the best VA because of the lower incidence of infective complications, but the long-term consequences of AVF on hemodynamic and cardiac function are still debated.
Cardiovascular disease (CVD) is the principal cause of morbidity and mortality in dialysis patients (6). Silberberg (7) showed that left ventricular hypertrophy
(LVH) is an important cardiac death predictor in uremic patients, as well as in patients with primary hypertension. LVH has been largely documented in renal failure (8-11). By multivariate analysis, London et al (12) further identified cardiac output as an important contributor to LVH. Pressure overload causes an increased systolic pressure that leads to increased systolic stress, which is associated with a parallel addiction of new sarcomers
(Q parallel addiction correct? and is sarcomers correct or 憇arcoma?or 憇arcomeres?), finally leading to cardiac wall thickening and concentric hypertrophy. Volume overload causes an increased diastolic pressure. This is a very important stimulus to the series addiction of new sarcomers and the development of eccentric hypertrophy (13). Chronic volume overload is associated with three principal factors: sodium and water retention, AV shunts and anemia (14, 15). Studies on rats (16) have confirmed that an AV shunt is a cause of LV dilatation and high output state.
Other adverse effects on cardiac function have been described in a prospective study demonstrating that myocardial ischemia caused by an adverse imbalance between subendocardial oxygen supply and increased oxygen demand is a possible consequence of AVF creation (17).
It has been reported that occasionally VA creation for HD can lead to cardiac failure. The first two cases of cardiomegaly with high output cardiac failure
occurred as a complication of high flow shunts, reported in 1972 (18), but the majority of high output cardiac failure has been thought to be related to high flow AVF, especially in pre-existing heart disease (19-24). Meeus et al (6) pointed out that symptomatic cardiac failure due to AV shunt is uncommon
and usually occurs in patients with underlying cardiac disease.
However, significant changes in CV hemodynamics have also been reported in patients with radiocephalic fistulas (25, 26). Ori (27) investigated the long-term effects of HD AV access on cardiac hemodynamics in a prospective study of 12 predialysis patients who were studied before, 1 and 3 months after primary AVF creation. The LVH incidence increased from 67% at baseline to 83% and 90% at 1 and 3 months, respectively. On the contrary, an observational but non-randomized study (28) on 993 elderly patients, followed for 4 yrs after dialysis start, did not show a significant rise in the incidence of heart failure and acute coronary syndromes in relation to the VA type (natural AVF, prosthetic fistulas or catheters).
Arteriovenous fistula and kidney transplant
Patients with well functioning renal transplants are particularly important for studying the cardiac effects of persistent HD AV access. Increased LVH often
persists after renal transplantation, and a relationship between blood pressure and LVH is found even in normotensive renal graft recipients (29).
In transplant recipients, multivariate analysis (30) showed that the presence of an AVF is independently associated with arterial stiffness augmentation.
This finding is relevant, as the arterial stiffness augmentation is positively and independently associated with CV morbidity in dialysis patients (31).
Savage (25) found that the subendocardial perfusion index increased immediately in transplanted recipients who underwent AVF ligation, even in the
absence of arterial stiffness modification.
A prospective study (32) on well functioning renal transplantation patients showed no differences regarding LV mass and volume changes between patients with or without a patent fistula (follow-up 10 months after renal transplantation). Huting (33) evaluated the course of LVH and function in ESRD after renal transplantation in a prospective study on 24 well functioning renal transplantation patients (follow up 41 ?30 months after transplantation). Huting found a reduction in left atrial diameter in patients with an occluded AVF, but no differences in cardiac structure or function in patients with a patent fistula vs those with a non-patent fistula.
The cardiac effects of persistent HD AV access in renal allograft recipients were evaluated in a retrospective study (34) of 61 stable renal transplant patients (39 with functioning AVF and 22 with closed AVF). No differences in LV mass, cardiac index, ejection fraction and LVH were observed; only an increase in LV and diastolic dimensions were associated with the presence of an AVF. This study concluded that the persistence of a large, high flow AVF for prolonged periods has little impact on cardiac morphology and function.
Van Dujnhover (35) evaluated the effect of AVF closure on LV dimensions in renal transplant patients in a prospective study of 20 patients with stable kidney transplants and with a mean fistula flow of 1790 ?640 mL/min. Echocardiography performed 4 months after AVF closure showed a reduced LV
mass and a reduction in LV end diastolic diameter.
Unger (36) documented a reduction in LV diameter and LV mass after surgical AVF closure in renal transplant recipients in a prospective study of 17 patients.
OBJECTIVE
The aim of our study was to evaluate both the natural history of the AVF and the kind of surgical procedures performed because of fistula problems in
the transplanted patients. In particular, we evaluated whether the surgical closure of the fistula was necessary because of the potential LVH risk.
MATERIALS AND METHODS
A retrospective study was conducted to evaluate kidney transplanted patients in our unit from April 1994 to April 2004. We studied 542 patients with average age of 47 yrs old and with a prevalence of males over female (367/175).
RESULTS
At the time of our observations, 86 patients died (12 patients due to CVD and in particular, nine patients due to acute myocardial ischemia and three
patients due to heart failure). Ninety-one patients were put back on dialysis: 89 patients on HD and two patients on CAPD. There were 365 patients with a well functioning kidney and the kidney survival rate of our patients is 82% after 5 yrs, in keeping with the results of the best European transplant
centers. Of the 365 patients with a functioning kidney transplant, 198 patients showed a patent fistula, while 167 patients had a closed fistula.
Of the 89 patients put back on dialysis, 49 patients used the previous AVF, while it was necessary to create a new VA in 40 patients. The average survival of the transplanted kidney was 22.2 months in the first group (min 1 - max 109) and 95.4 in the second group (min 1 - max 175). Figures 1 and 2 report the VA outcomes in our patients.
DISCUSSION
VA management after kidney transplant is a matter of debate between nephrologists. After a successful renal transplant, the VA is forgotten because it is neither used nor useful. As demonstrated by the results of our study, after a renal transplantation the possibility of spontaneous AVF closure caused by a thrombosis is not a rare event. The dilemma is whether to preserve a fistula that could be useful in case of restarting HD or to perform a systematic fistula closure because of the cardiac output and cardiac failure risks. In the literature, there is no consensus on this issue: according to De Lima (34) available data does not support routine AVF closure, while Van Dujnhover (35) suggests that AVF closure should be considered in patients with well functioning allografts and persistent LV dilatation. Unger (36) questions whether the effects of surgical closure on LV diameter or LV mass can be translated in terms of clinical benefit, and Patard (37) assumes that it seems reasonable to have a conservative attitude in the case of a well-tolerated native AVF. The theoretical or documented suppositions that show an important role of AVF in LVH and in the increased CV risk (11, 16, 27, 30), as well as the effectiveness of AVF closure in renal transplant recipients in improving some cardiac mass indices (35, 36), are in favor of routine AVF ligation in renal transplanted patients. On the other hand, reports that do not show a relationship between CV risk and a patent AVF or a significant alteration in cardiac indices after AVF closure (32-34) are against routine ligation. Further clinical benefits on the prevention of long-term complications by AVF closure remain not well documented.
CONCLUSION
In answering the question as to whether surgical AVF closure in transplanted patients is a therapeutic option, we think that the definite indications for
AVF closure in well functioning renal transplanted patients are heart failure, high flow fistula (especially large proximal fistula), VA complications (aneurysm, ischemia and infections) and important aesthetic reasons.
Routine AVF closure is not indicated until prospective and randomized studies can demonstrate the ability of this procedure to reduce the high incidence
of cardiac morbidity and mortality that is present, even after a renal transplantation. Currently, we consider for each patient cardiac function parameters, age, survival of the transplanted kidney, as well as the possibility and the simplicity of creating a new VA. It is necessary to
remember that every patient is a unique case.
REFERENCES
1. Hakim RM, Depner TA, Parker TF. Adequacy of haemodialysis. Am J Kidney Dis 1992; 20: 107-23.
2. Held PJ, Port FK, Wolfe RA, et al. The dose of haemodialysis and patient mortality. Kidney Int 1996; 50: 550-6.
3. Bloembergen WE, Stannard DC, Port FK, et al. Relationship of dose of haemodialysis and cause-specific mortality. Kidney Int 1996; 50: 557-65.
4. De Almeida E, Dias L, de Sousa FT, Mil-Homens MC, Pataca I, Parata MM. Survival in hemodialysis: is there a role for vascular access? Nephrol Dial Trasplant 1997; 12: 852.
5. NKF-K/DOQI Clinical Practice Guidelines for Vascular Access: update 2000. Am J Kidney Dis 2001; 37 (suppl 1): S137-81.
6. Meeus F, Kourilsky O, Guerin AP, Gaudry C, Marchais SJ, London GM. Pathophysiology of cardiovascular disease in hemodialysis patients. Kidney Int 2000; 76 (suppl): S140-7.
7. Silberberg J, Barre PE, Prichard SS, Sniderman AD. Impact of left ventricular hypertrophy on survival in end stage renal disease. Kidney Int 1989; 36: 286-90.
8. Harnett JD, Parfrey PS, Griffiths SM, Gault MH, Barre PG, Uttmann RD. Left ventricular hypertrophy in end-stage renal disease. Nephron 1988; 48: 107-15.
9. Foley RN, Parfrey PS, Harnett JD. Left ventricular hypertrophy in dialysed patients. Semin Dial 1992; 5: 34-41.
10. Parfey PS, Foley RN. Hamett JD, Kent GM, Urray DC, Barre PE. Outcome and risk factors for left ventricular hypertrophy in chronic uraemia. Nephrol Dial Transplant 1996, 11: 1277-85.
11. London GM, Guerin AP, Marchais S. Pathophysiology of left ventricular hypertrophy in dialysed patients. Blood Purif 1994; 12: 277-83.
12. London GM, Marchais SJ, Guerin AP, Metivier F. Contributive factors to cardiovascular hypertrophy in renal failure. Am J Hypertens 1989; 2: 261-5.
13. Guerin AP, Adda H, London GM, Marchais SJ. Cardiovascular disease in renal failure. Minerva Urol Nefrol 2004; 56: 279-88.
14. Foley RN, Parfrey PS, Harnett JD, et al. Clinical and echocardiographic disease in patient starting endstage renal disease therapy. Prevalence, associations and prognosis. Kidney Int 1995; 47: 186-92.
15. London GM, Parfrey PS. Cardiac disease in chronic uremia: pathogenesis. Adv Ren Replace Ther 1997; 4: 194-211.
16. Noma K, Brandle M, Rupp H, Jacob R. Left ventricular performance in rats with chronic cardiac overload due to arterio-venous shunt. Heart Vessels 1990; 5: 65-70.
17. Savage MT, Ferro CJ, Sassano A, Tomson CR. The impact of arteriovenous fistula formation on central hemodynamic pressure in chronic renal failure patients. A prospective study. Am J Kidney Dis 2002; 40: 753-9.
18. Ahearn DJ, Mahler JF. Heart failure as a complication of hemodialysis arteriovenous fistula. Ann Intern Med 1972; 77: 201-4.
19. Anderson CB, Codd JR, Graft RA, Groce MA, Harter HR, Newton WT. Cardiac failure and upper extremity arteriovenous dialysis fistulas. Cases reports and a review of literature. Arch Intern Med 1976; 136: 292-7.
20. Isoda S, Kajiwara H, Kondo J, Matsumoto A. Banding a hemodialysis arteriovenous fistula to decrease blood venous and resolve high output cardiac failure. Report of a case. Surg Today 1994; 24: 734-6.
21. Engelbert I, Tordoir IHM, Boon ES, Schreij G. High output cardiac failure due to excessive shunting in a hemodialysis access fistula: an easily overlooked diagnosis. Am J Nephrol 1995; 15: 323-6.
22. Young PR Jr, Rohr MS, Marterre WF. High output cardiac failure secondary to a brachiocephalic areteriovenous fistula. Two cases. Am Surg 1998; 64: 239-41.
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