This case report presents a patient with AKI due to urinary tract obstruction caused by bleeding from a renal transplant AVF, which was successfully treated by embolization. Notably, the bleeding occurred 9 years after a renal allograft biopsy, with no history of microscopic hematuria, stable blood pressure and renal function, and no changes in the renal transplant AVF until the patient’s presentation.

Although renal allograft biopsy is widely considered the best method for evaluating a transplanted kidney, one of the vascular complications associated with the procedure is the formation of an AVF, which occurs in 8.3–16.7% of patients undergoing renal allograft biopsy [4,5,6,7,8]. In most patients, the AVF resolves spontaneously, although they remain symptomatic in 30% of patients [6]. Hematuria is the most common symptom of renal transplant AVF [4,5,6], causing renal dysfunction, hypertension, and hemorrhagic shock due to bleeding from the AVF [13, 14]. AVF often occurs early to 1 year after renal allograft biopsy [4, 5, 9, 13, 14], and a history of multiple renal allograft biopsies has been reported as a high-risk factor for AVF development [16, 17].

The patient in this report underwent living-donor KT at 3 years using an intraperitoneal approach, followed by seven surveillance biopsies. As the intraperitoneal approach was used, the peritoneum and intestinal tract covered the anterior surface of the transplanted kidney, which may have resulted in a biopsy of a localized area of the lower pole of the allograft. A renal transplant AVF was detected during surveillance biopsy 10 years after KT in this patient, although approximately 9 years had passed before the onset of gross hematuria. The patient was not prescribed antihypertensive medication, her blood pressure was maintained at near 120/70 mmHg, and her serum creatinine level was stable at approximately 1.5 mg/dL. Furthermore, no microscopic hematuria was observed during the outpatient course. During a routine visit 20 days before the disease onset, the patient’s blood pressure was elevated at 147/107 mmHg, although no microscopic hematuria, worsening renal function, or fluid retention was observed. Renal AVFs lead to abnormal venous and arterial traffic. Further, the reduction in venous vascular resistance reduces blood flow through the renal parenchyma, causing renal ischemia, activation of the renin-angiotensin system, hypertension, and renal failure [18]. In addition, the vascular steal phenomenon caused by AVF increases venous return and may play a role in high-output heart failure [19]. Therefore, the elevated blood pressure before the disease onset in this patient may have been a predictor of symptomatic changes in renal transplant AVF.

Voiculescu et al. [13] reported a case of renal transplant AVF hemorrhage with gross hematuria similar to the present case. In this case, a kidney transplant biopsy was performed due to suspected rejection after KT, and a subsequent ultrasound scan revealed an AVF. During follow-up, the patient had multiple urinary tract infections and was treated in the hospital. Eight months later, she suddenly developed massive hematuria, bladder tamponade, hemorrhagic shock, and urinary tract sepsis. The bleeding from the renal transplant AVF was stopped by embolization. The authors noted that multiple urinary tract infections under immunosuppressive therapy after KT may have caused the AVF tissue to become fragile and hemorrhagic. In our experience, there was no history of urinary tract infection after KT. There was also no concurrent urinary tract infection at the disease onset, making it unlikely that the AVF tissue was fragile due to infection. Furthermore, 9 years had passed from the last kidney transplant biopsy to the disease onset, and the renal transplant AVF had not increased. However, the patient had mildly elevated blood pressure at the outpatient visit, suggesting that the transient increase in blood pressure may have caused the renal transplant AVF to rupture.

Few studies have reported the efficacy and safety of embolization for treating renal transplant AVF [10, 20]. In contrast, the management of asymptomatic renal transplant AVF is controversial, with proposed treatment methods not always improving renal function [12, 20]. Furthermore, endovascular therapy is associated with complications that may require emergency surgery [11]. Contrast media use in interventional radiology may lead to worse renal function and unexpected enlargement of the renal infarction after embolization. However, embolization is recommended for symptomatic renal transplant AVF due to the associated risk of bleeding, renal ischemia, and heart failure [20]. We monitored the patient for a large asymptomatic renal transplant AVF. In addition, no symptomatic changes were noted during the treatment course, and it was difficult to predict the rupture of the renal transplant AVF. After the rupture of the renal transplant AVF, anemia and renal function worsened, but there was no persistent bleeding. However, given the risk of rebleeding, angiographic embolization was performed on the renal transplant AVF. As a result, hemodialysis for AKI could be performed safely, and the renal allograft was salvaged.

In conclusion, unexpected bleeding from the renal transplant AVF leads to renal dysfunction and reduced quality of life. Angiographic embolization against the rupture of the renal transplant AVF may prevent rebleeding and rescue the renal allograft.