| Abstract|| |
Transplant renal artery stenosis (TRAS) is a recognized and potentially curable cause of post transplant arterial hypertension, allograft dysfunction, and graft loss. It usually occurs 3 months to 2 years after transplantation, but early or later presentations are not uncommon. We present a case of renal artery narrowing due to intimal dissection that was managed medically.
Keywords: Kidney transplantation, Renal artery stenosis, Angiography
|How to cite this article:|
Khattab OS, Al-Taee K. Early post transplantation renal allograft perfusion failure due to intimal dissection of the renal artery. Saudi J Kidney Dis Transpl 2009;20:112-5
|How to cite this URL:|
Khattab OS, Al-Taee K. Early post transplantation renal allograft perfusion failure due to intimal dissection of the renal artery. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2019 Aug 21];20:112-5. Available from: http://www.sjkdt.org/text.asp?2009/20/1/112/44716
| Introduction|| |
Impairment of renal allograft perfusion in the early postoperative period is usually associated with acute transplant rejection. However, vascular complications such as transplant renal artery stenosis or graft venous thrombosis are rare, but critical causes. ,,,,
Sudden oliguria is often the initial symptom of decreased graft perfusion and indicates a need for immediate imaging evaluation. For this purpose, Doppler sonography is usually the first diagnostic procedure.  Although Doppler examination readily measures the organ perfusion itself and may identify flow levels in the main renal vessels including the anastomotic region, the exact anatomic cause of perfusion failure cannot necessarily be identified. Therefore, in such challenging cases, the necessity for angiography should be well recognized because it allows not only diagnosis but also the option of immediate correction of vascular complications. The role of interventional radiology in the early period after transplantation has rarely been discussed. ,,
We herewith report a case of acute allograft perfusion failure associated with transplant renal artery stenosis due to intimal dissection for which stent angioplasty was technically undesirable, and conservative management was successful.
| Case Report|| |
A 34-year-old Iraqi male was referred to the renal transplant center at the Medical City Teaching Hospital, Baghdad, Iraq for renal transplantation. His end-stage renal disease was due to chronic pyelonephritis and was on regular hemodialysis. He underwent renal transplantation from his brother in July 2006; the left kidney with double arteries was transplanted. One of the arteries was lower polar and both were anastomosed end to end (double barrel) to the internal iliac artery in the right iliac fossa. Four immunosuppressive drugs were used including Basiliximab 20 mg given 2 hours prior to transplantation with a repeated dose on the 4th post-operative day, Azathioprine 1.5 mg/kg/d, Tacrolimus 0.2mg/kg/d, and corticosteroid (intravenous methylprednisolone 1gm/d for three days, followed by oral prednisolone 30 mg/d). Diltiazem 240 mg/d and long-acting nifedipine 40 mg/d were given to control blood pressure. The postoperative period was uneventful, and the patient had brisk diuresis. His serum creatinine decreased from 7.8 to 1.1 mg/dL within 72 hours of surgery.
In the 14 th postoperative day the patient's serum creatinine increased suddenly to 2.3 mg/ dL, blood urea 185 mg/dL, and his urine output decreased significantly. Serum potassium, WBC, platelet count, and lipid profile were within normal. Color Doppler ultrasonography revealed very poor flow within the whole allograft, increased peak systolic velocity more than 200 cm/s within the renal artery, and resistive index < 0.50, indicating severe stenosis at the site of anastomosis. Arteriography was performed through a retrograde contralateral femoral artery puncture, and the renal artery origin was selectively catheterized [Figure 1]. A filling defect (intimal flap) inside the main renal artery near the anastomotic line was identified causing poor distal flow. Stenting was deferred to avoid jeopardizing the flow to the lower polar artery, since the problem was near the anastomotic line. Acetylsalicylic acid 100mg/d and nadroparine calcium (Fraxiparine) 2850 IU/0.3 mL subcutaneously were prescribed for 10 days. The patient's serum creatinine started to decrease gradually, and within 30 days it reached 1.1 mg/dL, and the blood urea decreased to 48 mg/dL. Color Doppler ultrasonography revealed good flow within the allograft and peak of systolic velocity within the renal artery, and the resistive index returned to normal. One year later the duplex ultrasonography and serum creatinine were within normal limits.
| Discussion|| |
Transplant renal artery stenosis occurs late in the post transplantation period, and presents with refractory hypertension, renal dysfunction, or both. The cause of transplant renal artery stenosis is multifactorial, including long cold ischemia time, type of allograft,  surgical technique,  immunologic factors,  and cytomegalovirus infection.  Theoretically, transplant renal artery stenosis associated with surgical techniques can also occur in the early postoperative days. An imperfect suturing technique of the anastomosis or kinking of the graft artery may cause early stenosis, requiring surgical correction. , On the other hand, excessive traction of the graft artery during the harvesting, cannulation for transplant perfusion, or a surgical clamp may cause endothelial injury or intimal tears, which can eventually result in vascular dissection.  Thin and unstable intimal flap may not necessarily be visualized with color doppler sonography, and delay in diagnosis may result in renal artery thrombosis and graft loss.  Sudden oliguria with doppler sonographic findings of decreased graft perfusion is nonspecific for arterial dissection or even for transplant renal artery stenosis, especially with delayed graft function and the differential diagnosis may include acute rejection, acute tubular necrosis, cyclosporine toxicity, and graft venous thrombosis.  Vascular complications in the early post transplant period, should be much higher on the list of differential diagnosis, and angiographic confirmation is indicated.
In our patient, doppler sonography revealed severe perfusion failure of allograft, but failed to identify the vascular changes. Thus, our use of the emergency catheter angiography was warranted with the high index of suspicion. Contrast use during angiography can expose the patient to the potential risk of nephrotoxicity and contrast-enhanced MR angiography may be an alternative. 
Stent angioplasty is accepted as the treatment of choice for vascular dissection nevertheless, carries a higher risk of complications for stenosis at the anastamosis line.  Surgical treatment of transplant renal artery stenosis is on the other hand often difficult, risking significant injury to renal hilar structures, and it is associated with a 15% graft loss and 5% mortality. 
In conclusion, transplant renal artery stenosis should be suspected in any renal transplant patient with worsening renal function unexplained by rejection or cyclosporin toxicity. High index of suspicion, and early use of non-invasive diagnostic procedures (e.g., doppler ultrasonography) may help in detecting significant stenosis. Timely use of interventional radiology for recognition and management can help achieve full recovery of allograft kidney function.[Figure 1]
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Omar Salem Khattab
General and Transplant Surgeon, College of Medicine, Baghdad University, P.O. Box: 19503, Baghdad