Uterine artery embolization for fibroid-induced hydronephrosis in a renal transplant recipient

Abstract

Obstructive uropathy from uterine fibroids is recognized in the general population but is rare in renal transplant recipients. We report the first case, to our knowledge, of uterine artery embolization successfully treating fibroid-induced hydronephrosis of a transplanted kidney. A woman with a prior renal transplant presented with urinary symptoms and anemia due to menorrhagia from uterine fibroids. Imaging revealed a markedly leiomyomatous uterus causing transplant ureteral compression with hydronephrosis. Uterine artery embolization was performed without traversing the transplant arterial anastomosis. At 4 weeks postintervention, hemoglobin levels improved from 7.1 to 11.4 g/dL. Subsequent magnetic resonance imaging performed 6 months after therapy confirmed a 34% reduction in uterine volume and resolution of hydronephrosis. Renal function remained stable. Uterine artery embolization may be a feasible treatment option for fibroid-induced hydronephrosis in selected renal transplant patients, with symptom resolution and preservation of allograft function.

Introduction

Uterine fibroids are common benign tumors and can cause compressive symptoms, including obstructive uropathy. ¹ While fibroid-associated hydronephrosis affects approximately 9% of women in the general population, ² such obstruction is rare in renal transplant recipients. ³ These patients present unique management challenges, including the need to protect allograft function and manage comorbidities such as anemia, while simultaneously controlling debilitating gynecological symptoms.^4,5 Previous reports have described fibroid-induced hydronephrosis in renal transplant recipients, but these were managed surgically rather than by embolization.^3,6 Uterine artery embolization has emerged as an effective minimally invasive treatment for symptomatic fibroids, with systematic reviews demonstrating comparable outcomes to surgical myomectomy.^7,8 Resolution of hydronephrosis following uterine artery embolization has been documented in the general population,^9,10 but no prior cases have documented uterine artery embolization for hydronephrosis of a transplanted kidney caused by uterine fibroid compression. This case, therefore, represents a novel contribution, demonstrating a successful, minimally invasive, organ-preserving treatment in this rare scenario.

Case presentation

The patient was a woman in her late 30s with advanced chronic kidney disease from fibrillary glomerulonephritis who had undergone renal transplantation 8 years before presentation and was maintained on tacrolimus-based immunosuppression. She had recurrent unprovoked deep vein thrombosis in the lower extremities treated with apixaban as well as iron deficiency anemia attributed to menorrhagia from multiple uterine fibroids. The patient also reported increased urinary frequency. Magnetic resonance imaging (MRI) demonstrated large uterine fibroids measuring up to 8.1 cm compressing the right lower quadrant renal transplant ureter and resulting in moderate obstructive hydronephrosis.

Considering her transplant status, the need for anticoagulation, and surgical risk, our multidisciplinary team recommended uterine artery embolization. The procedure was performed in the interventional radiology suite using ultrasound and angiographic imaging guidance. Apixaban and tacrolimus were not held for the procedure. The left common femoral artery was accessed using a 19-gauge needle, which was exchanged over an 0.035-inch wire for a 5 French sheath. Through the sheath, a 5 French catheter was advanced into the right common iliac artery; coaxially, a 2.8 French microcatheter and a 0.016-inch microwire were used to select the right uterine artery, with meticulous attention to avoid traversing the arterial anastomosis of the right lower quadrant transplanted kidney as shown in Figure 1. Embolization of the right uterine artery was performed using calibrated microspheres measuring 500–700 and 700–900 microns in diameter until complete stasis of flow was obtained. The above procedural steps were repeated for the left uterine artery which was also embolized to complete stasis using microspheres. Hemostasis of the left common femoral artery was achieved using a vascular closure device.

Figure 1.

(a) Right common iliac angiography demonstrates the origin of the renal allograft arterial anastomosis (white arrow). (b) During embolization therapy, the right uterine artery (black arrow) was selectively catheterized using a microcatheter while avoiding the transplant arterial anastomosis.

The patient’s recovery was uncomplicated. At 4 weeks postintervention, hemoglobin levels had increased from 7.1 to 11.4 g/dL, coinciding with the resolution of anemia symptoms. Structural success was confirmed by MRI at 6 months, which showed the fibroids had become avascular and the uterine volume decreased from 1041 to 687 cm³ (34% reduction) as shown in Figure 2. Consequently, the anatomical compression on the transplanted kidney resolved, and hydronephrosis was eliminated as shown in Figure 3, with preservation of renal transplant function (serum creatinine was 0.77 mg/dL pre-procedure, 0.69 mg/dL 4 weeks postprocedure, and 0.73 mg/dL 6 months postprocedure).

Figure 2.

Coronal T2-weighted abdominopelvic MRI. (a) Preembolization imaging shows multiple large uterine fibroids (arrow) exerting mass effect on the transplant ureter and urinary bladder. (b) Six months after uterine artery embolization, the fibroids are markedly decreased in size (arrowhead) with resolution of hydronephrosis in the renal transplant.

Figure 3.

Axial T2-weighted MRI focused on the renal transplant. (a) Preembolization imaging demonstrates hydronephrosis of the transplanted kidney with proximal transplant ureter (arrow) compression by uterine fibroids. (b) After uterine artery embolization, the fibroids are decreased in size with resolution of hydronephrosis (arrowhead).

Discussion

Obstructive uropathy due to uterine fibroids is not unusual in the general population but is rare in women with renal transplantation.^1–3 A literature review found only a few reports of transplant hydronephrosis caused by fibroid compression, all of which were managed surgically.^3,6 To our knowledge, this is the first published case documenting the successful use of uterine artery embolization for hydronephrosis involving a transplanted kidney caused by fibroid compression.

This case highlights several important points. First, it expands the differential diagnosis for new-onset hydronephrosis in transplant recipients to include benign gynecologic disease. ¹¹ Second, it demonstrates that uterine artery embolization can be a technically feasible, safe, and effective organ-preserving procedure in the high-risk posttransplant population, even in the context of chronic anticoagulation.^12,13 Expert guidelines support uterine artery embolization as an effective treatment for symptomatic fibroids, ¹⁴ and recent meta-analyses confirm comparable efficacy to surgical approaches.^7,8 A recent case report further supports this minimally invasive strategy, describing a successful outcome using uterine artery embolization combined with a GnRH antagonist in a patient with inoperable uterine fibroids. ¹⁵ Lastly, the choice of microsphere size (500–900 microns) aligns with current technical recommendations for optimal fibroid devascularization while minimizing complications.^14,16

Our experience adds to the growing evidence that uterine artery embolization can effectively resolve fibroid-induced hydronephrosis.^9,10 The 34% reduction in uterine volume achieved in our case is consistent with published outcomes, where volume reductions of 30%–50% are typically reported.^7,17 Importantly, this volume reduction was sufficient to relieve the mechanical compression on the transplanted kidney, resulting in complete resolution of hydronephrosis and preservation of allograft function. Beyond these mechanical benefits, the rapid improvement of hemoglobin underscores the procedure’s efficacy in controlling symptoms even in anticoagulated patients.

Conclusion

This case underscores the critical role of multidisciplinary decision-making in complex clinical situations involving nephrology, gynecology, hematology, and interventional radiology. Managing transplant recipients requires careful procedural planning, given the unique need to preserve allograft function and the potential impact of immunosuppression on fibroid growth. Given the rarity of this condition in the transplant population and the absence of prior reports using uterine artery embolization in this exact setting, our findings may guide clinicians in considering this minimally invasive treatment as an alternative to surgery in similar high-risk patients.