Last updated: Lupus Nephritis…
on 26 Aug 2016

September 2014

Transplant Renal Artery Stenosis - A complication of intervention

K Nettleton MBCHB and Y Aggarwal MRCP MA

The case:  A 30 year old man with end stage renal failure received a pre-emptive ABO incompatible (ABOi) from his father 6 weeks prior to admission.  He had required immunoabsorption in preparation for ABOi transplant.  The immediate transplant operative period was uncomplicated and the patient was discharged home within 5 days of his operation with a creatinine that had fallen from 450mmol/l to 280mmol/l.  A transplant ureteric stent had been placed with a plan to remove it in 6 weeks’ time[1].

Post-transplantation, the patient was initially treated with a standard regime of Prednisolone, Mycophenolate Mofetil and Prograf (Tacrolimus). Asides anti-fungal, CMV and PCP prophylaxis, the patient was not on any other medication.

At 4 weeks post transplantation:  After an initial improvement in the patient’s renal function, the creatinine had started to plateau at 150mmol/l and then started to rise to 200mmol/l by 6 weeks post.  The Tacrolimus levels were in range.

The patient was admitted and had the following urgent investigations:

  1. BK (polioma virus) PCR:  Negative
  2. MSU: No evidence of infection
  3. Urine albumin:creatinine:  normal range
  4. Transplant kidney ultrasound with doppler:  Normal architecture with no evidence of hydronephrosis.  Patent perfusion of graft.  Normal resistive indices.
  5. Donor Specific Antibodies (DSAs)and non-HLA antibodies: Nil detected
  6. ABO antibodies:  Low tires
  7. Transplant renal biopsy: No evidence of rejection or de novo disease.  Essentially normal looking kidney tissue with virtually no chronic damage.
  8. MAG3: Delayed perfusion of graft with a normal excretory phase suggestive of transplant renal artery stenosis.

 Hypertension post transplantation:  It was noted that his blood pressure post-transplant had started to become poorly controlled.  He had not been on any anti-hypertensives pre-transplantation.  Amlodipine and Doxazosin were started.  ACEi and ARBs were avoided due to the need to avoid potential concurrent renal insults.

Transplant dysfunction secondary to probable transplant renal artery stenosis TRAS:  An MRA demonstrated a moderate to severe renal transplant stenosis on MRA and a catheter angiogram +/- intervention was suggested.

At this stage the creatinine was 190mmol/l and the patient had pre-procedure hydration in order to reduce the risk on contrast induced nephropathy and proceeded to angiography 24 hours later.

A catheter angiogram demonstrated stenosis in proximal transplant artery of 60% severity, with pressure measurements demonstrated a gradient of 38 mmHg systolic.

Balloon dilatation was undertaken and an expandable metal stent, visible on image below, was placed which improved patency of the artery.

The patient was reviewed within two hours of his procedure and within an hour of his return to the ward.  The patient felt well and his graft was non-tender.  His post procedure observations were normal and however his blood pressure remained elevated at 160/90mmol/l.

Post procedure bloods which were taken four hours after the procedure showed that the creatinine had risen to 210mmol/l but as the patient felt well no further intervention was required overnight.

Overnight the patient was reviewed to ensure his fluid balance was optimal given the risk of post-obstructive diuresis.  It was noted that the patient had a reduced urine output of around 0-5ml/hour.  He remained asymptomatic.

Repeat blood tests, taken 12-hours after the procedure, showed the following, and an acute stent occlusion was suspected.  Na 141, K 7.2, Ur 26, Cr 335, Hb 129, WBC 9.3, Plats 206, Lactate 3, Bicarbonate 14.


Subsequent management:

1.  As the patient had an anuric stage 3 acute kidney injury with hyperkalaemia and acidosis, he had emergency haemodialysis through a temporary femoral dialysis line.

2.  The serum potassium was temporarily corrected with insulin and dextrose infusion pre haemodialysis.

3.  An urgent bedside ultrasound showed very poor flow into the transplant kidney.

4.  Angiography demonstrated no flow into the transplant renal artery as it was occluded by thrombus.

5.  The patient was counselled for intra-arterial alteplase & systemic heparin therapy.

6.  The patient was transferred to a high-dependency setting for close renal and cardiovascular monitoring.

7.  A post thrombolysis check angiogram 5 hours later demonstrated a patent transplant renal artery, and absent venous filling.  The intra-arterial thrombolytic therapy and heparin were continued overnight.

8.  Overnight the patient became unwell and complained of pain over the graft.  Observations were as follows:  Temp 38.1,  HR 134, BP 162/100,  O2 sats 99% RA and RR 28 bpm.  The venous lactate elevated to 8.  Antibiotics were given for suspected transplant-related sepsis/necrosis.

9.  A further check angiogram, completed 12 hours after the first angio (4.) showed no arterial or venous flow.

10.  The patient proceeded to a urgent transplant nephrectomy to reduce his risk of further immune-sensitisation (the consequence being for future transplantation) and because he was clinically deteriorating.

Outcome:  Post nephrectomy the patient clincally imporved.  He was established on chronic haemodialysis (having previosuly being pre-emptive) through a tunnelled line and re-entered work up for an ABOc renal transplantation.  His subsequent ABOc transplant which occurred 14 months later has been successful and 18 months post-transplant the patient's creatinine is 95mmol/l.



a) ABOi transplantations

ABOi transplantations are blood group incompatible transplants.  The chance of the transplant failing soon after the transplant is increased compared to ABO compatible (ABOc) transplants.  Normally 1 in 20 transplants will fail in the first year after the transplant. The risk of transplant failure is about 1 in 10 with this procedure.  Rejection, antibody-mediated and cellular, being a common cause with rates immediately post op being as high as 1 in 3 compared to 1 in 4 for an ABOc transplant.  Other important factors are the immunosuppressive drugs given at induction, the ABO tires post plasmaphoresis (usually aim for less than 1:8), the presence of post-operative titres (association) and treatment compliance. The clinical relevance of this is that there is a lower threshold to proceed to a renal biopsy.


b) Transplant renal artery stenosis (TRAS)

- Incidence:  Transplant renal artery stenosis (TRAS) is the most frequent vascular complication in renal transplantation with an incidence varying between 1 and 25%. The aetiology and management of TRAS vary by location relative to the anastomosis.

- Site:  TRAS can occur proximal to the anastomosis (pre-anastomotic), at the anastomosis, or within the donor artery (post-anastomotic).  Pre-anastomotic TRAS is usually due to atherosclerosis or a clamp injury.  Anastomotic site TRAS is usually due to a technical problem related to surgery.  Post anastomotic TRAS is usually due to immune reactions or haemodynamic turbulence from the anastomosis causing an intimal hyperplasia; or intrarenal due to chronic rejection.  Post-anastomotic TRAS tend to be more severe and associated with end-to-side anastomoses as compared with end-to-end anastomoses, which tend to be at the anastomosis.

- Clinical presentation:  Patients can present early or late in the post-transplantation period with either no symptoms, poorly controlled/refractory hypertension, compromised function of the allograft which may be exacerbated by excess diuresis or occur after use of angiotensin-converting enzyme (ACE) inhibitors, or rejection refractory to immunotherapy.  Occasionally, a bruit in the iliac fossa can be heard.

- Aetiology:  Mechanical or technical mechanisms of TRAS include atherosclerosis of the donor renal arteries or recipient iliac arteries, or both. In addition, trauma to the vessels during harvesting and transplantation, clamp injury, cannulation for organ perfusion, excess traction on the vessels, and suture techniques are other potential causes. Small subintimal flaps or dissections are thought to occur, leading to intimal scarring and hyperplasia and eventual anastomotic stenosis.

Early (within a few months of surgery) TRAS is likely to be caused by mechanical or technical trauma, whereas TRAS developing remote (more than 6 months) from the time of transplantation cannot be explained and may be associated with progression of underlying atherosclerotic disease.

- Imaging evaluation: 

Non-invasive screening tests:  Color flow duplex ultrasound (CFDU) or MRA.  * MRA - 100% sensitivity and 75–98% specificity for greater than 50% stenosis BUT if there is a strong clinical suspicion of TRAS despite negative noninvasive imaging studies, proceeding to angiography should be considered.

Invasive confirmatory tests:  Renal transplant angiography (ass. with a risk of contrast-induced nephropathy) or CO2 angiography:  CO2 is not nephrotoxic.

- Management of TRAS:

Three different treatment methods are available:

1.  Medical management to control hypertension with unknown effect on kidney function. This approach is indicated if the degree of stenosis is not considered hemodynamically significant or the risk of percutaneous intervention is considered high for graft loss, or both.

2. Surgical intervention with revascularization. This is considered a major operation with graft loss following vascular reconstruction approaching 30% with a recurrence rate of ~12%.

3.  Percutaneous endovascular management using transluminal angioplasty (PTA) or metallic stent placement, or both.

PTA is the initial treatment of choice for TRAS and does not preclude subsequent surgical correction.  Serious complications, which may lead to graft loss, include acute thrombosis, arterial dissection, renal artery rupture, branch occlusion, distal embolization, and contrast-induced renal failure. As with any renal artery angioplasty, complications are reduced by utilising adequate heparinization, vasodilators, minimal wire manipulations, proper balloon sizing, and inflation pressures.

Metallic stents have been inserted for treatment of recurrent or ostial stenosis and have been associated with high initial technical success and a good patency rate with minimal complications.  Complications related to stent insertion include thrombosis, peripheral embolization, transient renal failure, subintimal dissection, stent misplacement or migration, and restenosis related to myointimal hyperplasia from the normal healing process.  With improved equipment and the use of antispasmodics and heparin, more serious complications, such as arterial dissection, rupture, or thrombosis, occur in less than 4% of cases.



  1. Benoit G, Moukarzel M, Hiesse C et al. Transplant renal artery stenosis: experience and comparative results between surgery and angioplasty. Transpl Int 3: 137–140, 1990
  2. BTS.  Guidelines for Antibody Incompatible Transplantation 2011, BTS found at
  3. Clements R, Evans C, Salaman JR.  Percutaneous transluminal angioplasty of renal transplant artery stenosis. Clin Radiol 50: 245–250, 1995
  4. **Rajan DK, Stavropoulos SW, Shlansky-Goldberg RD.  Management of Transplant Renal Artery Stenosis. Semin Intervent Radiol. 21(4): 259–269, 2004.

** Excellent review article


[1] Transplant ureteric stents are not routinely placed in all transplant centres in the UK.  In those centres where it is not routine practice, a ureteric stent is placed if there are concerns about the integrity of the ureteric anastomosis, and it I usually removed at 4-8 weeks post operatively


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