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. Author manuscript; available in PMC: 2022 Sep 1.
Published in final edited form as: Clin Imaging. 2021 Feb 26;77:142–146. doi: 10.1016/j.clinimag.2021.02.022

Transplant Renal Artery and Vein Occlusion Evaluated with Ferumoxytol-Enhanced Magnetic Resonance Angiography

Ayaz Aghayev 1, Aliza Anwar Memon 2, Sijie Zheng 3, Matthew Menard 4, Andrew M Siedlecki 2
PMCID: PMC8550796  NIHMSID: NIHMS1680881  PMID: 33684787

Abstract

Background:

Compromise of the transplanted vasculature accompanying a kidney allograft can lead to graft failure if not diagnosed and treated expeditiously. Location of the vascular defect in the transplant renal artery or vein is difficult to anticipate, given the variety of etiologies. However, early diagnosis can anticipate further progression of kidney allograft dysfunction. Ferumoxytol-enhanced magnetic resonance angiography (FeMRA) can precisely localize lesions in both the transplant renal artery and vein and provide a comprehensive survey of the vascular conduits of concern. It avoids complications of kidney injury associated with intravenous iodinated contrast that may amplify a diagnosis of delayed graft function or further impair an allograft already compromised by donor-derived vascular disease.

Methods:

We report a case of concomitant and irreversible proximal transplant renal artery and vein stenosis diagnosed by FeMRA and treated with surgical intervention.

Results and Conclusions:

FeMRA offers a rapid, non-invasive approach to simultaneously diagnose compromised blood flow through the transplant artery and or vein in preparation for definitive correction of the defect.

Keywords: ferumoxytol-enhanced magnetic resonance angiography, transplant renal artery stenosis, transplant renal vein stenosis

Introduction

Vascular compromise of the kidney allograft can result in devastating sequelae, including graft failure and patient death. Current techniques to evaluate allograft vasculature include Doppler ultrasonography (US) followed by non-invasive angiography and invasive arteriography. While Doppler US is readily available and can provide serial assessments, accuracy in identifying discrete lesions is limited [1]. Concern for the effect of gadolinium-based imaging remains despite more quantified risk [2,3] Ferumoxytol enhanced magnetic resonance angiography (FeMRA) is a clinically relevant diagnostic tool that offers an alternate technique to identify allograft-threatening defects to the arterial and/or venous conduits without the added risk of acute tubular necrosis associated with iodinated imaging contrast [4]. FeMRA has been used successfully to diagnose transplant renal artery stenosis (TRAS), but confidence in the resultant diagnoses to justify surgical intervention is seldom described [5]. In this report, we characterize the utility of FeMRA for the precise localization of proximal lesions occurring simultaneously in the transplant renal artery and vein. Using this diagnostic approach, the clinical team was given essential data that guided successful surgical repair of proximal transplant renal artery and vein compression.

Materials/Methods

The patient gave written consent to participate in an institutional review board-approved protocol investigating the clinical utility of FeMRA. Ferumoxytol was infused as an intravenous contrast agent (3mg/kg) over 10 minutes. MRA sequences of the abdomen and pelvis were obtained after intravenous ferumoxytol infusion, as previously described [6,7]. Maximum intensity projection (MIP) reconstruction and three-dimensional angiographic reformatting was performed. Invasive angiography was performed by an interventional radiologist.

Results

A 30-year-old man with end-stage kidney disease (ESKD) due to lupus nephritis received a living unrelated kidney transplant. He was admitted 16 days after transplant with new hypertension and acute kidney injury. An MRA of the pelvis was obtained following an 8 mL (240 mg) infusion of intravenous ferumoxytol. An apparent constriction of the transplant renal artery 3mm from the surgical anastomosis was identified. Transplant renal vein stenosis at the proximal segment of the vessel 7mm from the surgical anastomosis was also identified (Figure 1A,B, 2A,B). A diagnosis of transplant renal artery and vein stenosis was made based on the MRA findings. Invasive arteriography was performed showing transplant renal artery stenosis but could not clarify the extent of the transplant renal vein occlusion for concern of additional exposure to iodinated contrast. Due to concern for transplant renal vein stenosis in addition to transplant renal artery stenosis, surgical intervention was selected to correct the vascular defects. The patient was taken to the operating room. The surgical team removed the transplanted kidney and reconstructed the renal artery on the back table. On opening the renal artery, there was no clear constriction, although the area of the distal main trunk of the renal artery was narrowed. Similarly, the main trunk of the renal vein was also narrowed without evidence of clear constriction. The main trunk the renal artery was amputated, and the two distal renal artery branches were opened to complete a new fish mouth re-anastomosis of the two branches. The kidney was then brought back onto the field, and a primary end-to-side anastomosis was made to the external iliac artery. The transplant renal vein was then transposed to the external iliac vein. The flow was initially sluggish but improved after a few minutes. It appeared that the flow was dependent on position of the allograft, with the kidney kinking the transplant renal vein when placed anteriorly in the iliac fossa. The decision was made to place the allograft in a retroperitoneal position to prevent kinking. Blood flow was restored to the allograft, and repeat FeMRA was performed, demonstrating a resolution of the stenoses (Figure 3A,B, 4A,B). Serum creatinine decreased to 2.3mg/dL seven days afterward and 2.11 mg/dL 60 days after re-implantation.

Figure 1.

Figure 1.

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MRA demonstrating severe stenosis at the proximal segment of the transplanted renal artery. (A) Multiplanar reformatted (MPR) and Maximum Intensity Projection (MIP) MRA image of the transplanted renal artery shows severe stenosis (blue arrow) at the proximal segment 3mm from the surgical anastomosis, which bifurcates immediately afterward. (B) MPR and MIP image of severe stenosis (blue arrow) in the transplanted renal vein 7mm from the surgical anastomosis with the external iliac vein (S=superior, I=inferior, L=left, R=Right).

Figure 2.

Figure 2.

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3D reformatted MRA images demonstrate severe stenosis at the proximal segment of the transplanted renal artery and vein (A) Transplant renal artery stenosis (yellow arrow) 3mm from external iliac artery anastomosis and (B) transplant renal vein stenosis (yellow arrowhead) 7mm from the external iliac vein anastomosis. (C) Invasive arteriography and catheter injection of iodinated contrast to the transplanted renal artery confirms severe stenosis at the proximal segment of the transplant artery (A= anterior, P=posterior).

Figure 3.

Figure 3.

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Multiplanar reformatted (MPR) and Maximum Intensity Projection (MIP) MRA image of the transplanted renal artery (A) and vein (B) show patent vessels following surgical intervention.

Figure 4.

Figure 4.

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3D reformatted MRA images confirm patent (A) transplant renal vein and (B) transplant renal artery following surgical intervention.

Discussion:

We previously reported the use of FeMRA for the assessment of arterial and venous vasculature in the context of kidney transplantation [8–10]. Here we utilize the same resolution afforded by FeMRA to more precisely characterize the behavior of transplant renal artery and renal vein stenoses adjacent to the surgical anastomosis in preparation for surgical intervention. Herein we also describe the feasibility of FeMRA as a diagnostic tool to assess the patency of the transplant renal artery and vein after surgical repair without the potential side effects of iodinated or gadolinium-based radiologic contrast agents.

Transplant renal artery stenosis (TRAS) has been reported in up to 23% of kidney transplant recipients at some institutions [11]. TRAS can be caused by anastomotic stricture, thrombosis, a kinking of the renal artery, or a combination of these scenarios [8] [9]. Irreversible kinking of the transplant renal artery is uncommon, but intermittent kinking may occur in 10% of patients with suspected TRAS [9] [12,13]. TRAS leads to decreased allograft perfusion and activates the renin-angiotensin-aldosterone pathway. A majority of TRAS occurs within six months of implantation.

Compromised blood flow in the transplant renal artery (TRA) can present throughout the length of the arterial conduit. It is more likely reversible when involving the middle segment compared to a location adjacent to the surgical anastomosis. This is consistent with the mechanical attributes of a vessel articulating about the fixed point of the surgical anastomosis. Conservative management is a viable option if serum creatinine approaches an anticipated nadir. If this does not occur, the risk of recurrent kinking and subsequent procedures such as invasive arteriography with iodinated contrast can lead to successive kidney injury and potentially allograft failure. Compromise of the transplant renal vein (TRV) is most often due to thrombosis and less likely due to stenosis. Incidence of TRV thrombosis (TRVT) during the early post-operative weeks is 0.1–4%[14]. TRV stenosis (TRVS) is a less common event making an estimation of incidence challenging [15]. Various factors contribute include hypovolemia, vessel friability, and external compression of renal vein by adjacent structures. It is critical to diagnose transplant renal vein lesions promptly. Doppler ultrasonography may not be able to identify characteristic changes in the diastolic waveform due to the location of the anastomosis with the external iliac vein deep in the pelvis [16]. Early detection of a lesion should be accompanied by treatment in the form of anticoagulation, renal vein stenting, thrombectomy, or exploration if external compression is suspected[17].

Simultaneous transplant renal artery and renal vein compromise has not been clearly delineated with radiologic imaging in the past. May-Thurner syndrome (MTS) involving occlusion of the native common iliac vein by the common iliac artery is known to impact the function of the transplant renal vein but is not the appropriate term for the compression of the transplant renal vein in the case we report since MTS is due to an anomaly of the recipient during development [18]. Because FeMRA offers a modality to simultaneously evaluate the full length of the TRA and TRV with relatively low risk to the patient, it is anticipated that this rare finding will be identified more frequently. In the current report, the most likely cause for simultaneous compromise of both the TRA and TRV remains unknown.

Our findings were consistent with previous reports of renal artery stenosis evaluated by FeMRA. Fananapazir and colleagues demonstrated the accuracy of FeMRA to identify stenosis of >50% in 33 patients with clinical suspicion or sonographic findings consistent with TRAS [4]. Building on this previous work, we further demonstrate that FeMRA can be used to precisely characterize severe proximal TRAS and concomitant renal vein occlusion.

In conclusion, our findings describe the utility of FeMRA to identify the precise location of lesions in the transplant renal artery and vein of transplant patients with compromised kidney function who are at risk of complications associated with conventional radiologic contrast agents.

Highlights.

  • Transplant Renal artery and vein stenosis leads to compromise of kidney allograft

  • There are various etiologies underlying the development of transplant renal artery and vein stenosis

  • Early diagnosis and intervention of the renal artery and vein stenosis is crucial in preventing graft failure

  • Ferumoxytol enhanced Magnetic Resonance Angiography (FeMRA) provides safe and precise modality for the localization of stenotic lesions in the renal artery and vein.

Acknowledgments

Grant Funding: K08DK089002, NIH/NIDDK (Bethesda, MD)(A.M.S.); AMAG Pharmaceuticals, Inc (Waltham, MA), Investigator-sponsored research grant # 2016D004506 (A.M.S.).

Footnotes

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