Open bypass revascularisation for endovascular-resistant transplant renal artery stenosis secondary to mechanical renal artery kinking

Abstract

Transplant renal artery stenosis (TRAS) represents a significant vascular complication subsequent to renal transplantation. This pathology is associated with grave implications including graft dysfunction and mortality. Early identification and therapeutical intervention are imperative for preserving graft longevity and achieving optimal clinical outcomes. We detail the case of a male in his 20s, following renal transplantation, who encountered recurrent TRAS, aetiologically linked to mechanical arterial kinking. Initial management using endovascular techniques yielded insufficient resolution. Consequently, the persistence of endovascular-resistant stenosis necessitated a surgical bypass intervention using the great saphenous vein, granting a 2-year period devoid of restenosis. The existing literature emphasises the indispensability of discerning the appropriate juncture for transitioning from endovascular to surgical management in TRAS cases. The robustness and durability of bypass grafts present an efficacious therapeutical strategy in contemporaneous practice.

Background

Transplant renal artery stenosis (TRAS), with prevalence rates between 1% and 23%, is a pivotal vascular complication after renal transplantation. While various factors contribute to the development of TRAS, mechanical arterial kinking poses unique challenges.¹ Endovascular techniques, though commonly employed in modern surgical practices, may not provide lasting resolution for stenosis due to kinking. Open revascularisation, specifically bypass grafting, emerges as a compelling solution in such scenarios. This technique, which has reported 1-year patency rates of approximately 80%–95%, offers an effective approach to address TRAS resulting from mechanical kinking, ensuring graft longevity and optimal patient outcomes.²

Case presentation

A male patient in his 20s, with a known history of end-stage renal failure secondary to Prune Belly syndrome, bilateral indirect inguinal hernia, hypertension and gout, underwent renal transplantation. The graft was obtained from a deceased donor in their 50s post-circulatory death, characterised by duplicated renal arteries and veins. Ex-vivo surgical reconstruction was performed to join the small accessory transplant renal artery (TRA) onto the main TRA using an aortic patch, forming a common stem. Both TRAs were anastomosed to the external iliac artery (EIA). Immediate graft function postoperatively was evidenced by a marked reduction in serum creatinine levels from 540 umol/L preoperatively to 263 umol/L on discharge. The patient’s immunosuppressive regimen consisted of maintenance tacrolimus, mycophenolate and prednisolone. Nine weeks post-transplantation, clinical concerns arose with elevated blood pressures, raised serum creatinine of 210 umol/L (baseline 110–130 umol/L) and pronounced proteinuria (albumin/creatinine ratio: 119.1 mg/mmol).

Investigations

Duplex ultrasonography highlighted haemodynamic abnormalities, notably a peak systolic velocity (PSV) of 729 cm/s in the proximal TRA, a marked increase from the 151 cm/s observed immediately post-transplant, while intraparenchymal resistive indices remained unchanged (figure 1). Subsequent digital subtraction angiography (DSA) confirmed TRAS, attributed to mechanical kinking in the proximal segment, and thrombosis of the accessory TRA.

Figure 1.

Ultrasonographic features of transplant renal artery stenosis (A) at the proximal renal artery with a duplex study showing increased peak systolic velocities (PSVs), (B) prior ultrasound with normal PSVs and (C) preserved PSVs at external iliac artery.

Differential diagnosis

In the post-transplant setting, a rise in creatinine and blood pressure prompts an extensive differential diagnosis.¹ Excluding acute and chronic graft rejection via transplant renal biopsy, attention turned to glomerular pathologies, which were not substantiated by the clinical findings. Attention then focused on TRAS, a critical diagnosis substantiated by Doppler ultrasonography and DSA, indicating compromised arterial flow as a plausible cause of graft dysfunction. Calcineurin inhibitor toxicity, another differential, was rendered improbable by normative tacrolimus levels. This systematic diagnostic approach ensures targeted management to preserve graft function and enhance patient prognosis.

Treatment

Initially, the TRAS was treated with plain balloon angioplasty, resulting in reduced serum creatinine (from preoperative creatinine of 180 to 142 umol/L postoperatively) and improved blood pressure (figure 2). Despite initial improvements, restenosis occurred and the patient re-presented with elevated serum creatinine level (160 umol/L), confirmed by DSA. A second intervention with a drug-eluting balloon was attempted, but ultrasound findings continued to indicate TRAS, as evidenced by a PSV of 770 cm/s (figure 2). His creatinine level remained elevated between 160 and 180 umol/L.

Figure 2.

Invasive angiography demonstrating (A) a sharp bend at the proximal transplant renal artery, (B) postangioplasty image with guidewire across the lesion and (C) follow-up ultrasound following second angioplasty with persistently raised peak systolic velocity of 770 cm/s.

In light of the recurrent, endovascular-resistant nature of the stenosis and ongoing clinical concerns, a surgical intervention was deemed imperative. The patient underwent a right EIA to mid-TRA bypass using a reversed great saphenous vein (GSV) 5 months post-initial transplantation. The procedure involved incision along the previous scar, identification and dissection of the EIA to the anastomosis site and exploration of the TRA to locate the stenosis. The proximal and distal EIA, and distal TRA were clamped. The GSV was harvested, reversed and anastomosed end-to-side to the distal EIA and distally to the mid-TRA. Total renal ischaemic time was 13 min, with optimal perfusion postoperatively (figure 3). The patient’s serum creatinine levels improved to 121 µmol/L post surgery, with blood pressure well-controlled on a single antihypertensive agent.

Figure 3.

Reversed great saphenous vein graft from the mid-external iliac artery to the mid-transplant renal artery (TRA) that allows bypass of the lesion in the proximal TRA. (Figure illustrated by Mei Ping Melody Koo.)

Outcome and follow-up

Over a 2-year follow-up period, serial duplex ultrasounds consistently demonstrated a patent bypass graft with normalised PSVs. The bypassed segment of the TRA was observed to be occluded, affirming the procedural success and sustained graft function.

Discussion

TRAS is an acknowledged vascular complication following renal transplantation, with incidence rates between 1% and 23%. It primarily manifests within the 1-year post-transplant and is a leading factor behind graft dysfunction and refractory hypertension.¹ Its clinical ramifications, such as the escalation of blood pressure, increase in serum creatinine and pronounced proteinuria, can compromise graft longevity if not addressed promptly. Early detection and intervention are crucial for graft survival and function.³

The aetiology of TRAS encompasses surgical, anatomical and immunological factors. Surgical techniques, including the number and type of anastomoses, can influence the onset of TRAS, particularly in the early post-transplant period. The incidence of renal artery kinking, while rare, can be attributed to various factors.⁴ In the discussed case, the intricate anatomy of the accessory TRA of small calibre necessitating reconstruction, and potential complexities during anastomosis might have predisposed to stenosis.

Endovascular techniques, notably percutaneous transluminal angioplasty (PTA), have become the first-line therapy for TRAS. While PTAs offer benefits including minimal invasiveness and shorter hospital stays, recurrence is not uncommon, with a 1-year restenosis rate postangioplasty reported to be approximately 20%–40%.² And in specific cases where arterial kinking is likely the cause of stenosis, only 15% of cases were successfully treated with endovascular repair according to the current literature. The stenting procedure was not opted in our case due to concerns of distal propagation of the lesion.²

Conversely, open surgical techniques, although more invasive, tend to offer better long-term patency rates. Techniques vary between localised endarterectomy, patch angioplasty and bypass grafting. The 1-year patency rates following open revascularisation is approximately 80%–95%, with a 10-year patency rates between 75%–85%.⁵

Described therapeutical options for TRAS secondary to mechanical kinking include nephropexy, re-anastomosis, shortening of TRA and bypass surgery.^{5 6} In this case, considering the patient’s age and likely establishment of fibrosis being 3 months down the track, a bypass was deemed the most viable long-term solution. The durability of GSV bypass grafts remains advantageous, especially in young patients where the graft’s long-term viability becomes paramount. The consistent findings of a patent bypass graft over 2 years in our patient further attest to the viability and efficacy of this approach in such cases.

In conclusion, while endovascular techniques are indispensable in managing TRAS, discerning when to opt for a surgical approach is paramount. The individualisation of treatment strategies, especially in cases with donor anatomical intricacies, is crucial for graft preservation and optimal patient outcomes.

Learning points.

• Anatomical complexity in donor kidney may necessitate arterial reconstruction that could introduce risks for complications like transplant renal artery stenosis (TRAS)

• Although percutaneous transluminal angioplasty serves as a first-line therapy for TRAS in contemporary practice, its efficacy can be limited in cases where mechanical kinking is the primary cause, necessitating alternate interventions.

• In scenarios where TRAS arises from mechanical kinking and is resistant to endovascular techniques, open surgical bypass, using the great saphenous vein, provides a durable solution. This approach ensures graft longevity, especially vital for young recipients.

• Each case of TRAS is unique, and the optimal treatment strategy should factor in both the donor’s anatomical intricacies and the recipient’s specific medical history. Tailored interventions can significantly improve graft preservation and overall patient outcomes.

Ethics statements

Patient consent for publication

Consent obtained directly from patient(s).