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Saudi Journal of Kidney Diseases and Transplantation
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Year : 1998  |  Volume : 9  |  Issue : 1  |  Page : 22-26
Renal Artery Stenosis in Renal Transplantation Presentation and Management


Department of Nephrology, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia

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   Abstract 

A review of the angioplasty records between 1990 and 1995 at the King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia revealed ten cases of transplant renal artery stenosis (RAS). The diagnosis in these cases was confirmed by renal angiography and all were treated by angioplasty. All study patients presented with uncontrolled hypertension in spite of multiple medications; eight had renal functional impairment and two patients had recurrent unexplained pulmonary edema in addition. Six patients had undergone end-to-end anastomosis, while four had end-to-side anastomosis of the artery during transplantation. Four had cadaveric renal transplants and six had living donor renal transplants. Eight of these patients responded well to angioplasty with marked improvement in their renal function and reduction in the number of anti-hypertensive medications. In one patient, it was not possible to pass the catheter through the stenosis and the patient underwent surgical reconstruction, while in another patient there were multiple stenotic lesions involving the external iliac and the transplant renal arteries suggesting atherosclerotic changes. We conclude that renal artery stenosis should be suspected in patients after renal transplant if they have uncontrolled or worsening hypertension, unexplained renal impairment or presentation with unexplained recurrent pulmonary edema. Renal angiography should be considered as part of the investigation of hypertension in renal transplant patients, and if the RAS is confirmed, angioplasty should be the procedure of choice.

Keywords: Renal impairment, Pulmonary edema, Hypertension, Angiography, Angioplasty.

How to cite this article:
Al-Harbi A, Chaudry T, Linjawi T, Alfarayh O, Al-Sohaibani H, Al-Shaibani K, Al-Meshari K, Minhas M, Abutaleb N. Renal Artery Stenosis in Renal Transplantation Presentation and Management. Saudi J Kidney Dis Transpl 1998;9:22-6

How to cite this URL:
Al-Harbi A, Chaudry T, Linjawi T, Alfarayh O, Al-Sohaibani H, Al-Shaibani K, Al-Meshari K, Minhas M, Abutaleb N. Renal Artery Stenosis in Renal Transplantation Presentation and Management. Saudi J Kidney Dis Transpl [serial online] 1998 [cited 2019 Dec 14];9:22-6. Available from: http://www.sjkdt.org/text.asp?1998/9/1/22/39297

   Introduction Top


The prevalence of hypertension in established renal transplant recipients is about 50% [1] . Only 40% of hypertensive patients have been shown to normalize their blood pressure following successful renal transplant, moreover, up to 16% of normotensive patients prior to transplantation became hypertensive afterwards [1] . The presence of hypertension may be a risk factor for graft survival as well as for other cardiovascular complications. Effective treatment of hypertension is important for long-term survival of both the graft and the recipient [2] . Various factors play a role in the pathogenesis of hypertension in renal transplant recipients [1],[2] . Identification of such factors, particularly those amenable to cure is essential for proper management of these patients [3] . The development of resistant hypertension after renal transplantation, particularly in normotensive recipients should always raise the possibility of renal artery stenosis (RAS) of transplanted kidney, the reported incidence of which ranges from 3­-12% [4],[5],[6] . Certain clinical features that should raise the suspicion of RAS include recent onset hypertension, a new bruit over the transplanted kidney, a marked change in the character of a pre-existing bruit, unexplained deterioration of allograft function and recurrent unexplained pulmonary edema. In this paper, we describe the clinical features and management of 10 patients who had transplant RAS.


   Clinical Data Top


During the period between 1990 to 1995, a total of 10 cases of transplant RAS were seen at our center. Of them, three had been transplanted at our center and follow-up records pre-transplant were available. The remaining patients were referred to us for angioplasty of RAS detected elsewhere or were on follow-up in our hospital after undergoing transplantation at a different center. The cause of renal failure in the native kidneys was not known in any of these patients. All the patients were on triple immunosuppression (azathioprine, cyclosporixi A and prednisone). All the patients received more than two anti­hypertensive drugs despite which their blood pressure remained uncontrolled (diastolic blood pressure > 100 rnmHg). Only two patients had normal renal function; one patient had a bruit documented in the past but the character had changed recently (systolic and diastolic phase), while one patient developed a new harsh bruit. Two patients presented with recurrent unexplained pulmonary edema and their myocardial function study by echocardiography was within normal limits. One patient was hemodialysis dependent for almost a month before the angioplasty. The details of the study patients are given in [Table - 1].


   Results and Management Top


All the study patients had confirmed transplant RAS by angiography and the stenosis was considered significant if the narrowing was more than 60% of the arterial lumen. None of these patients were subjected to captopril challenge test. There were seven males and three females, and their age ranged from 18 to 62 years (mean age 35 ± 1.9 years). RAS was diagnosed as early as two months and as late as seven years after transplantation (mean time 20.9 ± 6.66 months). Four patients had undergone living non-related renal transplantation (India), four other patients had cadaveric renal transplantation, while two patients had living related renal transplantation. The angiographic findings showed predominance of patients who had undergone end-to-end anastomosis as compared with end-to-side anastomosis at the time of transplantation [Table - 1].

All patients were subjected to percutaneous transluminal angioplasty of the transplanted renal artery. Angioplasty failed in one patient because of severe stenosis and it was not possible to pass the catheter through the stenotic area. The stenosis was successfully repaired surgically. In one patient, angiography showed multiple stenotic areas involving the renal artery as well as the native external iliac artery, and the picture was clearly of atherosclerotic nature. This patient had a transient improvement of renal function and blood pressure control following angioplasty but four weeks later the serum creatinine rose again to the previous level and his blood pressure control required more drugs. With the exception of this patient, all the other patients including the patient with surgical reconstruction had remarkable improvement after angioplasty with the blood pressure becoming more amenable to control with less medications. The patient who was on hemodialysis developed brisk diuresis post angioplasty, and renal functions improved. None of the patients developed any complications post-angioplasty and none had a follow-up angiography. The initial presentation, anti-hypertensive medications and serum creatinine levels pre- and post­angioplasty in the study patients are shown in [Table - 2].


   Discussion Top


The presence of hypertension after renal transplant is a risk factor for graft survival as well as for cardiovascular complications in the recipient, and effective treatment improves long-term graft and recipient survival [2] . Potentially curable factors contributing to hypertension post-transplant should be looked for carefully and managed appropriately [1],[3] . Transplant RAS is considered a curable cause of hypertension and the reported incidence which ranges from 3-12% probably reflects the use of renal angiography in different centers [3],[5] . The occurrence of transplant RAS may be more than was thought at one stage and it has been suggested that one should perform renal arteriography routinely after transplant [7] . A bruit over the transplanted kidney is commonly found and has limited significance, but when the character of an existing bruit changes (systolic and diastolic), or when a new one develops, it may indicate RAS which may or may not be a clinically significant stenosis. Renal impairment in kidney transplant patients might be the consequence of ischemia to the kidney which might be worsened by anti-hypertensive medications or by the direct effect of hypertension [2] . Pulmonary edema has been reported in hypertensive patients with unilateral or bilateral RAS in native kidneys [8],[9] , pulmonary edema that resolves quickly and is out of proportion to the degree of myocardial functional impairment might be considered as a manifestation of transplant RAS and is possibly volume related [10],[11] . Several factors have been blamed as a cause of transplant RAS which include atheroma, faulty surgical technique, trauma to the renal artery during surgery, disturbed hemodynamics and possibly immune related damage [2],[7],[12] .

The diagnosis of transplant RAS is mainly based on renal angiography and is considered significant if the stenosis is more than 60% [6],[7] , Non-invasive tests including color Doppler ultrasound remain operator dependent and cannot exclude the diagnosis of RAS [13] . Once the diagnosis of transplanted RAS is made, percutaneous transluminal angioplasty should be considered the procedure of choice, as compared to surgical reconstruction which carries a higher morbidity [4],[6],[14],[15],[16] .

In our series, most of the patients presented within the first 12 months after transplantation and we noticed a predominance of stenosis in those with end­to-end anastomosis. Theoretically intimate proliferation might be a result of rejection and may lead to narrowing and stenosis of renal artery, or the stenosis might trigger rejection [12] . Atherosclerotic changes can cause RAS in transplanted patients, especially in the elderly. Angioplasty may not be beneficial in such patients. All our study patients had remarkable improvement in their renal function and their blood pressure became easily controlled with less medications. They have remained well during follow-up which has ranged from four months up to four years without worsening of their renal function or blood pressure.

In summary, transplant RAS should be suspected in patients presenting with the above mentioned signs and symptoms. To confirm the diagnosis, renal angiography is mandatory and we recommend it strongly to be part of the investigation of hypertensive patients after transplantation. Percutaneous transplant angioplasty is the procedure of choice in experienced hands, and surgical reconstruction should be considered when angioplasty fails.

 
   References Top

1.Feinstein El, Campese VM, Finck E, Silberman H, Chandrasoma P. Hypertension in arenal transplant recipient. Am J Nephrol 1984;4:262-71.  Back to cited text no. 1    
2.Wakzer WC, Turners, Frohnert P, Rapaport FT.Etiology and pathogenesis of hypertension following renal transplantation. Nephron 1986;42:102-9.  Back to cited text no. 2    
3.Dubousky EV, Charles R. Diagnosis of renovascular hypertension after renal transplantation.Am J Hypertens 1991;4(12):724S-30S.  Back to cited text no. 3    
4.Tilney NL, Rocha A, Strom TB, Kirkman RL.Renal artery stenosis in transplant patients. Ann Surg 1984;199(4):454.  Back to cited text no. 4    
5.Fabrega AJ, Lopez-Boado M, Gonzalez S.Problems in the long-term renal allograft recipient. Crit Care Clin 1990; 6(4):979-1005.  Back to cited text no. 5    
6.Grossman RA, Dafoe DC, Shoenfeld RB.Percutaneous transluminal angioplasty treatment of renal transplant artery stenosis. Transplantation1982;34(6):339-43.  Back to cited text no. 6    
7.Lacombe M. Arterial stenosis complicating renal allo transplantation in man, a study of 38 cases. Ann Surg 1975;181(3):283-8.  Back to cited text no. 7    
8.Diamond JR. Flash pulmonary edema and the diagnostic suspicion of occult renal artery stenosis. Am J Kidney Dis 1993;21(3):328-30.  Back to cited text no. 8    
9.Pickering TG, Herman L, Devereux RB,et al. Recurrent pulmonary edema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. Lancet 1988;3:551.  Back to cited text no. 9    
10.Lye WC, Leong SO, Lee EJC. Transplant renal artery stenosis presenting with recurrentacute pubnonaiy edema. Nephron 1996;72:302-4.  Back to cited text no. 10    
11.Mansy H, Al-Harbi A. Recurrent pulmonary edema as a presentation of renal artery stenosis in renal transplant patient. Clin Nephrol - pending publication.  Back to cited text no. 11    
12.Simmons RL, Tallent MB, KjellstrandCM, Najarian JS. Renal allograft rejection simulated by arterial stenosis. Surgery 1970;68(5):800-4.  Back to cited text no. 12    
13.Erley CM, Duda SH, Wakat RJ, et al. Non-invasive procedures for diagnosis of renovascular hypertension in renal transplant recipients - a prospective analysis. Transplantation 1992;54(5):863.  Back to cited text no. 13    
14.Raynaud A, et al. Percutaneous transluminal angjoplasty of renal transplant arterystenosis. Am J Radiol 1986;146:853.  Back to cited text no. 14    
15.Spipse Aoer AM, Mali WP,Donckerwolcke RA Renal transplant artery stenosis in children :treatment with percutaneous transluminal angioplasty. Pediatr Radiol 1992;22:519-21.  Back to cited text no. 15    
16.Tegtmeyer CJ, KeUum CD, Ayers C.Percutaneous transluminal angioplasty of the renal artery. Results and long-term follow-up. Radiology 1984;153:77-84.  Back to cited text no. 16    

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Correspondence Address:
Ali Al-Harbi
Department of Internal Medicine, North West Armed Forces Hospital, P.O. Box 100, Tabuk
Saudi Arabia
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PMID: 18408278

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