Delayed renal transplant failure secondary to renal vein thrombosis in a patient with a permanent IVC filter

  1. Kristyn L Lewis 1,
  2. Payal Patel 2,
  3. Hani M Wadei 3 and
  4. Pramod K Guru 4
  1. 1 Pulmonary and Critical Care, Mayo Clinic, Jacksonville, Florida, USA
  2. 2 Endocrinology, Mayo Clinic, Jacksonville, Florida, USA
  3. 3 Transplant, Mayo Clinic, Jacksonville, Florida, USA
  4. 4 Critical Care Medicine, Mayo Clinic, Jacksonville, Florida, USA
  1. Correspondence to Dr Pramod K Guru; Guru.Pramod@Mayo.edu

Publication history

Accepted:17 Mar 2021
First published:29 Mar 2021
Online issue publication:29 Mar 2021

Case reports

Case reports are not necessarily evidence-based in the same way that the other content on BMJ Best Practice is. They should not be relied on to guide clinical practice. Please check the date of publication.

Abstract

Renal vein thrombosis is a rare, but potentially serious complication in patients with renal transplantation as it can lead to non-reversible graft injury and failure. Often this clinical entity is found in the early transplantation period, and the available management strategies are associated with favourable patient outcomes. The incidence, pathophysiology and outcomes for the delayed occurrence of renal vein thrombosis are unknown. The case here describes a unique situation with an excellent clinical outcome related to early diagnosis and appropriate care.

Background

Renal vein thrombosis in kidney transplant recipients can lead to irreversible graft failure. This relatively rare complication is reported in only 0.1%–4.2% of renal transplant recipients, predominantly in the first 30 days of the post-transplant period.1 The case presented here is not one of these common presentations.

Case presentation

A 53-year-old man, with history of anaemia, obesity resolved after gastric bypass, placement of an inferior vena cava (IVC) filter for a questionable pulmonary embolism at the time of bypass 15 years prior, end-stage renal disease secondary to glomerulonephritis who had received a deceased donor renal transplant in the right lower quadrant almost 10 years ago presented with progressively worsening generalised weakness and bilateral lower extremity pain for 2 weeks. The patient also noticed shortness of breath, and progressively decreasing and dark-coloured urine. His renal graft function has been stable over the years with baseline creatinine of 1.2–1.4 mg/dL on the immunosuppressive regimen of tacrolimus and mycophenolic acid. The patient had no history of previous graft rejection. Other significant medical history includes chronic anaemia, obesity and non-alcoholic steatohepatitis. He was diagnosed and managed with antibiotics for presumed urinary tract infection on basis of urinalysis and culture about a week prior to presentation at an outside facility. Blood tests performed at the outside facility were not available for review. The only other significant symptom included a recent involuntary weight gain of 20 pounds. He denied fevers, chills, nausea, vomiting, headache, blurred vision, chest pain, dysuria or changes in bowel habits. No history of any travel, trauma or other interventions. No prior history of thromboembolic episodes. On physical examination, the patient was found to be afebrile, blood pressure of 152/75 mm Hg, heart rate of 85/min, respiratory rate of 24/min and saturating 100% on room air. His systemic examination was significant for bilateral pedal oedema, tenderness overlying the renal allograft in the right lower quadrant and pallor.

Initial lab tests were significant for anaemia with a haemoglobin of 93 g/L (135–175 g/L), white cell count of 12.7×109/L (3.5–10.5×109/L), serum bicarbonate level of 21 mmol/L (22–29 mmol/L), blood urea nitrogen (BUN) of 28 mg/dL (8–24 md/dL), creatinine of 2 mg/dL (0.8–1.3 mg/dL), estimated glomerular filtration rate of 35 mL/min/body surface area (BSA) (>60 mL/min/BSA), lactate level of 3.4 mmol/L (0.6–2.3 mmol/L), serum albumin of 3.9 g/dL (3.5–5.0 g/dL) and a tacrolimus level of 4.1 ng/mL (5–15 ng/mL trough). Urinalysis was positive for proteinuria and granular casts. The 24-hour urine protein level was 658 mg/24 hours (0–150 mg/24 hours) on the day of admission, and increased to 1600 mg/24 hours (0–150 mg/24 hours) on day 10 of admission.

Investigations

Ultrasound of the lower extremity veins demonstrated bilateral occlusive thrombus from the popliteal veins through the femoral veins with extension to the external iliac veins. Ultrasound of the renal transplant demonstrated occlusive thrombus of the transplant renal vein through the iliac vein with borderline elevated resistive indices demonstrating possibly patent venous collaterals with mild hydronephrosis. CT with intravenous contrast demonstrated suboptimal contrast-enhanced CT venogram with distention of the lower IVC and renal vein suggesting thrombus, as well as a retained IVC filter (figure 1). Biopsy of the transplanted kidney was deferred given the urgent need for thrombolysis and the antecedent risk of bleeding in relation to the invasive nature of the procedure.

Figure 1

Abdominal subtractions angiography, coronal view, showing extensive ileocaval thrombosis (black arrows) and the associated inferior vena cava filter (blue arrow).

Differential diagnosis

The initial differential entertained for his graft dysfunction and leg swelling include acute graft rejection with fluid retention, lower extremity deep venous thrombosis (DVT) with extension into the renal vein, pyelonephritis and cardiorenal syndrome. Pyelonephritis would be prudent to consider in this patient as he was recently diagnosed with a urinary tract infection at an outside facility and undertreatment could lead to pyelonephritis. Cardiorenal syndrome could additionally cause renal dysfunction and was considered in this patient as he has obesity and cardiac disease. Nephrotic syndrome, either due to reoccurrence of the primary glomerulonephritis or due to other causes, and the resultant hypercoagulable states leading to thrombosis was also considered in the differential. However, it was deemed an unlikely cause given the absence of significant proteinuria and hypoalbuminaemia at admission. Renal biopsy was not performed due to perceived high risk for procedural complications in a patient on systemic anticoagulation.

Treatment

The patient was started on systemic heparin therapy and subsequently had an AngioJet pharmacomechanical thrombectomy (Boston Scientific, Marlborough, Massachusetts, USA), which is a catheter that provides direct thrombolysis using localised tissue plasminogen activator (tPA) infusion (0.5 mg/hour) and direct mechanical disruption of the clot using the force of the tPA jet, which is followed by thrombus aspiration (thrombectomy mode). All this happens while systemic heparin therapy is being infused. This was performed on the bilateral popliteal, femoral and iliac vein thrombosis and through bilateral popliteal vein access up through the IVC filter. Initially, bilateral lower extremity thrombosis demonstrated improvement with therapy and the right-sided catheter was successfully advanced through the right femoral and external iliac veins to the transplanted renal vein where additional TPA and thrombectomy were performed. No systemic TPA was used.

The patient had worsening graft function leading to renal replacement therapy 2 days after admission. His hospitalisation was also complicated by the development of rectus sheath haematoma possibly related to anticoagulation use.

Outcome and follow-up

A venogram was obtained before (figure 2), and after administration of tPA using the AngioJet (figure 3) showing that there was improvement in the clot burden. The patient’s renal function improved over the 2 weeks during the hospitalisation and was back to near baseline by discharge. He was bridged to warfarin therapy with a goal international normalized ratio (INR) of 2.5–3.5 for thrombosis. Due to the patients’ medical history as well as the in vivo IVC filter, the patient will be kept on lifelong anticoagulation with warfarin. Risks were thought to outweigh benefits of IVC filter removal on multidisciplinary evaluation and the IVC filter was not able to be removed. Haemolysis, a potential side effect of the AngioJet system, did not occur in our case.

Figure 2

View of the clot at the origin of the transplanted renal vein and the external iliac vein (black arrow).

Figure 3

Improvements can be seen in the blood vessel lumen in the iliac vein (black arrow) and the transplanted renal vein (blue arrows) after the use of AngioJet pharmacomechanical thrombectomy.

Discussion

Transplant renal vein thrombosis is extremely rare after the initial few weeks post transplant.2 3 Clinically, the patient’s presentation of this disease process includes pain, swelling of the affected allograft, oedema in the ipsilateral extremity and fever.3 Our patient’s presentation is consistent with this description.

Patient, donor and procedure-related factors were responsible for heightened risk of renal vein thrombosis in the immediate post-transplant period. Presence of diabetic nephropathy and prior history of venous thromboembolism in the recipient, and haemodynamic instability as well as technical difficulties during the transplantation are the major risk factors for early renal vein thrombosis. Donation of right kidney is also described as a risk factor.2 4 The patient described above did not have any of these well-known risk factors and is out of the window period of early risk. The possible factors, which might have played a role in the development and extension of the thrombus in this patient include a retained IVC filter, proteinuria or a possible undiagnosed hypercoagulable disorder given the prior history of DVT. On literature search of this topic, there was one other case report by Senitko et al 5 reporting similar findings. As such, renal transplant patients may be more vulnerable to thrombosis of their transplanted renal vein in the setting of IVC filter use. The exact roles played by these entities in the transplanted renal vein thrombosis are not clear and certainly shows the need for vigilance and future research.

There are two main treatment options for patients who present with transplant renal vein thrombosis: thrombolytic therapy and/or a surgical thrombectomy.

Learning points

  • In patients with extensive thrombosis of the lower extremities, further evaluation of transplanted kidney should be pursued if delayed graft failure is also present.

  • Early detection and treatment of renal allograft dysfunction from renal vein thrombosis can enable salvaging of the graft.

  • Renal vein thrombosis can lead to significant morbidity and mortality if left untreated.

  • Patient’s with inferior vena cava filter placements or found on imaging incidentally should be removed as soon as deemed appropriate.

Footnotes

  • Twitter @pkguru10

  • Contributors KLL contributed to concept and design, drafting of the article and final approval. PP, HMW and PKG contributed to concept and design, critical revision of the article for important intellectual content and final approval.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer-reviewed.

References

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