Transplant renal artery stenosis (TRAS) is a common vascular complication after kidney transplant (reported incidence 1-23%), which can cause resistant hypertension, allograft dysfunction, and even graft loss. [1,2] Endovascular management, Percutaneous Transluminal Angioplasty (PTA)/stenting is the main management although repeat treatment may be necessary. [1,3] The overall safety of this approach is established. [1,4,5,6] We present a rare complication of stent insertion, with a discussion of possible mechanism and management.
A 19-year-old man with end-stage renal failure (Ig-A nephropathy) underwent living related kidney transplantation. The graft was a left kidney with one artery, one vein and one ureter, which were anastomosed to the right external iliac artery (EIA), right external iliac vein and the bladder respectively. Immediately after the operation, Doppler Ultrasound Scan (DUS) showed good perfusion throughout the graft. His Serum Creatinine (SCr) fell from 861 µmol/l on pre-operation measurement to 212 µmol/l 4 days post operation.
Nine days post operation, the SCr level was 234 µmol/lit and DUS showed dampened flow in the transplant renal artery (TRA), with Resistance Indices (RI) measuring only 0.33-0.48. Measurement of flow indices in TRA showed a decreased Acceleration Flow of 65 cm/sec2 (Normal Range [NR] > 300 cm/sec2) and elevated Peak Systolic Velocity (PSV) of 455-535 cm/sec (NR < 250 cm/sec). There was a focal narrowing at the site of anastomosis of TRA to EIA and the findings were consistent with TRAS. It was planned to have serial follow-up DUS as his SCr level was stable and it was too soon after surgery to undergo any intervention.
Three weeks post transplantation and following a rise in his SCr from 208 to 226 µmol/l, he was reviewed in the hospital. As the histopathology on-call service was not available over the weekend, he was given a single dose of Methyl-Prednisolone (Aventis Phrma. Ltd., UK) before undergoing transplant kidney biopsy (Bx) the next day which showed areas of chronic inflammatory cell infiltrate accompanied by moderate tubulitis, representing borderline features suspicious of acute T-Cell-Mediated Rejection. Following anti-rejection treatment, his SCr came down from 226 to 170 µmol/l.
One month post transplantation, DUS demonstrated persistently elevated blood flow velocity within TRA, with a PSV measurement of 520 cm/sec compared with a PSV of 150 cm/sec in EIA. Incidental note was made of a one centimetre arterio-venous fistula (AVF) at the Bx site arising from an upper pole segmental vessel. At this stage the patient was referred for angiography and endovascular therapy.
Arteriography confirmed a significant stenosis of TRA just distal to it's anastomosis with the right EIA. There was a pressure gradient of 60-80mmHg across the stenosis. Angioplasty was performed using a 6mm diameter balloon. There was a residual systolic arterial pressure gradient (25-30 mmHg) across the stenotic area after the procedure. However, no further intervention was performed in view of the improved angiographic appearance and the short time interval since surgery. DUS one week later showed that flow velocities were still elevated. Furthermore there had been no improvement in SCr levels, therefore repeat angiography was performed. This confirmed residual stenosis at the site of recent angioplasty (pressure gradient of 40mmHg) so we proceeded with endovascular stenting. Stent positioning was difficult due to angulation at the arterial anastomosis. Therefore 3 separate (6 mm, 1.5 cm long) balloon-expandable stents (Palmaz® Genesis â„¢, Cordis Europa, The Netherlands) were required for a satisfactory result (Figure-1). At the end of the procedure, the pressure gradient was lowered to 10 mmHg. Post procedure angiography showed satisfactory stent position with no evidence of any complications and an entirely normal intra-renal arterial tree. Finally, a vascular closure device (Angio-Seal, St. Jude Medical Europe Inc., Belgium) was used without complications.
However, 6 hours post procedure, urine output decreased significantly. DUS showed a large sub-capsular haematoma (10 cm x 3.1 cm x 6cm), which was surrounding the anterior aspect of the transplant kidney, opposite to the renal hilum (Figure-2). Good blood flow was seen throughout the transplant but RI values were increased to around 0.69-0.73.
The haematoma was seen to significantly compress the kidney. The diagnosis APK was made and this was felt to account for the decreased urine output. His SCr was raised to 512 µmol/l. Following discussion, he underwent ultrasound guided drainage of the sub-capsular haematoma. Following aspiration, a 10 Fr (3.3mm) drainage pigtail catheter (Flexitimeâ„¢ regular APDL, Boston Scientific Co., USA) was inserted into this collection.
Examination with DUS showed improved blood flow within the transplant kidney. The drain was kept in for 4 days. Serial follow-up DUS showed reducing pressure effect of haematoma on the kidney and good vascular perfusion with RI values of 0.57-0.64. The PSV at the transplant artery anastomosis site was measured between 340-440 cm/sec, with a PSV in the EIA of 380 cm/sec. His SCr level started to decrease, following the successful stent insertion. Six months after stenting his SCr has decreased to 189 µmol/l. Figure-3 shows the change in his SCr level since the time of transplant. Most recent SCr 2 years after Tx is 164, eGFR 45.
DISCUSSION: TRAS is a common vascular complication after renal transplantation which can present months to years postoperatively. [7] TRAS can be caused by trauma to donor/recipient artery, poor suturing technique, kinking/damage to the iliac/renal artery during transplantation and atherosclerotic plaque. The first report of successfully using expandable metal stents for management of resistant TRAS comes from St Mary's Hospital in London, UK. [8]
In the last 2 years in our centre, we have seen 2 other cases of TRAS in 131 living donor kidney transplants (incidence rate of 2.3%). Both cases were stented successfully, without complications. In a retrospective study on 32 interventions in 30 allografts, the stenting technical success rate was 100% with a single major complication, "puncture site pseudo-aneurysm". [1]
Major complications are rare but are associated with severe morbidity. The most feared complication after percutaneous intervention for TRAS is immediate arterial rupture, requiring either immediate surgical repair or the insertion of a covered stent. Delayed haemorrhage, as seen in our case, is much less common. Even then, one would expect it to be related to bleeding from the puncture site. To our knowledge, there has been only one previous report of major haemorrhage post stenting (not related to the main arterial rupture). [9] This was thought to be due to "trans-cortical position of the guide wire". Attempted renal artery embolization failed to control the haemorrhage.[9]
External compression of the kidney causing subsequent ischemia and hypertension has been described as APK. [10] It can happen in native and allograft kidneys. Trauma, spontaneous bleeding in patients with predisposing factors (anticoagulation), bleeding post interventions (operation, Bx, lithotripsy) have been proposed as the aetiological factors. [11]
In our case, there are a few possible mechanisms for APK. Spontaneous bleeding, trans-cortical position of the guide wire during procedure, arterial rupture, bleeding from the low resistance paranchymal tract from the previous Bx sites, sudden increase in blood flow and pressure after relieving the stenotic area of the TRA post procedure and subsequent rupture of the previous AVF are the possible mechanisms.
In this case, the patient was not anti-coagulated, angiographic review did not show any acute arterial bleeding and there was no evidence of guide-wire perforation. The exact cause of the sub-capsular haematoma is not known. Whether the previous AVF or the Bx tract was a factor, can only be a matter of speculation.
In a report on 518 ultrasound-guided renal allograft biopsies, 4 recipients developed APK.[10] Surgical exploration (allograft capsulotomy) was successfully performed in all cases as the first measure to rescue the graft. [10] In our centre, between January 1996 and November 2008, there have been 774 kidney transplant operations (212 living donors, 562 deceased donors) and we have done 969 ultrasound guided renal allograft biopsies (including protocol biopsies more recently). None of these resulted in APK.
Spontaneous native-kidney APK in a young lady taking Warfarin for dilated cardiomyopathy has been previously reported from our centre. [12] After reversing her anticoagulation, she was treated successfully with percutaneous drainage. The current case is the first renal allograft APK we have seen.
In the past, the management of allograft APK has always been surgical. [10,13] Although there have been recent reports using laparoscopic and radiological methods for the treating native-kidney APK, [14,12] percutaneous drainage of the APK in a renal allograft using DUS has not been reported before. We have shown that such an approach is safe and effective. We therefore, propose considering this alternative option before proceeding with surgical exploration and renal capsulotomy in such cases.
CONCLUSION: APK is a rare but serious complication of TRA stenting. Early diagnosis is invaluable as immediate decompression can rescue the allograft. As radiological assisted decompression can be successful, we propose considering this alternative option before proceeding with surgical exploration.
