Renal transplant recipients (RTRs) are at high risk of urological complications. The most common of these is transplant ureteric stricture (TUS), accounting for approximately 50% of cases [1]. The overall incidence of TUS among RTRs has been estimated at between 0.6% and 12.5% [2]. We describe a case of TUS in a 37-year-old man.

Written informed consent for this report was obtained from the patient. Because this is a case report, the requirement for ethical approval was waived by the relevant institutional ethics board.

A 37-year-old man was diagnosed with chronic kidney disease in 2016, with a serum creatinine level of 2.3 mg/dL at that time. Kidney biopsy indicated the presence of immunoglobulin A (IgA) nephropathy. The patient began maintenance hemodialysis in 2021, at which point his blood urea nitrogen and serum creatinine levels were 120 mg/dL and 9.6 mg/dL, respectively.

The patient received ABO-incompatible living donor kidney transplantation (LDKT) on March 3, 2022. The donor, his wife, underwent laparoscopic left donor nephrectomy. Preoperative computerized tomography renal angiography of the donor revealed bilateral single renal arteries and renal veins (Fig. 1). The recipient’s blood type was O positive, while the donor had B positive blood. The initial anti-B IgG titers for the recipient are presented in Table 1. The immunosuppressive regimen included sodium mycophenolate, tacrolimus, and prednisolone. A single 200-mg dose of rituximab was given 15 days prior to the transplant, an anti-B immunosorbent column was applied 1 day before surgery, and induction therapy was administered with antithymocyte globulin.

Following transplant surgery, the patient exhibited good diuresis, and his serum creatinine levels decreased to 1.3 mg/dL by postoperative day (POD) 7. However, these levels then began to rise steadily, reaching 4.8 mg/dL by POD 11. Color Doppler ultrasound of the transplanted kidney (TK) revealed normal blood flow in the renal artery and vein. The posttransplant IgM titer, measured on POD 9, was 1:512. Biopsy of the TK, performed on POD 10, revealed the presence of antibody-mediated rejection (ABMR) along with borderline acute cellular rejection (Table 2). The patient was treated with methylprednisolone pulse therapy, plasmapheresis, and intravenous Ig (IVIg). The double J (DJ) stent was removed 2 weeks after the transplant. Response to treatment was suboptimal; the patient’s creatinine levels decreased to a nadir of 4.1 mg/dL on POD 21, and his urine output declined to 400 mL.

A second TK biopsy was performed, revealing chronic ABMR accompanied by acute tubular necrosis (Table 2). Throughout the previous IVIg therapy, the patient’s globulin levels had remained below 1.5 mg/dL. Consequently, IVIg and plasmapheresis therapy were resumed. Following this intervention, the patient’s serum creatinine levels decreased to 1.9 mg/dL, and his urine output increased to 6,300 mL/day. The patient was discharged on POD 39.

One week after discharge, the patient returned with a high-grade fever that had persisted for 1 day. Clinical examination was unremarkable; however, the patient exhibited pancytopenia and severe metabolic acidosis. Empirical treatment was initiated with broad-spectrum antibiotics and antifungals. Urinalysis showed a considerable presence of pus cells, and urine culture revealed Burkholderia cepacia. Bone marrow aspiration culture additionally indicated the presence of B. cepacia. The patient displayed clinical improvement, but his renal function deteriorated. Consequently, he was treated with two hemodialysis sessions. Repeat TK biopsy indicated ABMR and severe borderline cellular rejection. Treatment with plasmapheresis and low-dose IVIg was resumed; however, after only two sessions, the patient experienced recurrence of fever and pancytopenia. As a result, antirejection therapy was discontinued, antibiotic therapy was recommenced, and immunosuppression was reduced.

Ultrasonography revealed hydronephrosis of the TK (Fig. 2). During cystoscopy, placement of a DJ stent was unsuccessful because the guidewire could not be advanced into the transplant ureter. Consequently, percutaneous nephrostomy (PCN) was established, and antegrade DJ stenting was performed due to suspicion of TUS. Over the 3 days following DJ stent placement, the patient exhibited a urine output of 23 L. His serum creatinine levels decreased to a range of 1.6–1.7 mg/dL. The DJ stent was removed 3 months later, in August 2022. On the same day, the patient developed anuria, necessitating immediate cystoscopic stent reinsertion. Significant TUS was confirmed, and the patient was scheduled for definitive surgical intervention.

Seven months after the transplant, on October 6, 2022, the patient underwent exploratory surgery and was found to have extensive perinephric and periureteric adhesions, along with severe fibrosis throughout the entire length of the transplanted ureter (TU). Dissecting this structure was challenging, and the ureter was only identifiable by the presence of the indwelling DJ stent. A minimal portion of the intrarenal pelvis remained intact, which was then anastomosed to the native right ureter over the DJ stent, with considerable technical difficulty (Fig. 3). The patient experienced an uneventful recovery. However, due to the complexity of the anastomosis to the small remaining segment of the intrarenal pelvis, we opted to leave the DJ stent in place for an additional 3 months. Upon discharge, the patient’s serum creatinine level was 1.66 mg/dL.

On January 2, 2023, the DJ stent was removed, and the patient was able to pass urine for 24 hours before developing anuria. Due to ureteropelvic junction stenosis, cystoscopic DJ stenting could not be performed; instead, a PCN was once again placed, which led to improved urine output and renal function. With no alternative treatments available, we performed inferior polar nephrectomy (IPN) of the TK along with vesicocalicostomy on February 9, 2023. During the initial dissection, the presence of extensive perinephric adhesions led to an inadvertent tear in the TK parenchyma (Fig. 4A). The IPN was conducted by locating the tip of the inferior calyx under fluoroscopic guidance, using a nephrostogram performed through the PCN to preserve the maximum amount of functioning renal parenchyma (Fig. 4B). Due to the adhesions, the arterial supply to the TK could not be visualized and was not clamped; instead, bleeding was managed by an assistant’s application of pressure to the TK while the surgeon excised the inferior pole (Fig. 5A). Vesicocalicostomy was completed using 4-0 polyglactin 910 interrupted sutures beginning at the posterior aspect. This was followed by the placement of a DJ stent, then the creation of the anterior anastomosis. Finally, the site was wrapped in omentum after an incision was made in the peritoneum (Figs. 5B–D). Postoperatively, the patient experienced a temporary increase in serum creatinine levels, which subsequently normalized. He also developed a catheter-associated urinary tract infection and pyelonephritis of the TK, which was treated with culture-sensitive antibiotics. The patient was discharged on POD 21 following removal of the DJ stent. After 7 months of follow-up, he continued to show no signs of stricture recurrence and maintained stable renal function, with a serum creatinine level of 1.6 mg/dL.

The TU is highly vulnerable to ischemic damage because its blood supply is obtained entirely from the renal pelvic vessels, which traverse the periureteric adventitia. These vessels are prone to injury during the explantation process. Urine leakage represents the most frequent early urological complication following renal transplantation, with reported incidence rates ranging from 1.2% to 8.9% [3]. Beyond 3 months posttransplantation, strictures represent the leading cause of ureteric obstruction, affecting 1% to 9% of patients. Ischemia is the primary etiology of TUS. Additional factors contributing to TUS include urine leakage, graft rejection, chronic infection, and infections caused by BK virus and cytomegalovirus [4]. In the present case, TUS was attributed to graft rejection.

The decision to manage TUS with endourologic or surgical repair is influenced by a range of factors, including the patient’s overall health, existing comorbidities, and the stricture’s length and location. The options for open surgical reconstruction vary and similarly depend on the size and placement of the stricture. These options include allograft ureter reimplantation, anastomosis of the ipsilateral native ureter to the transplant ureter or renal pelvis, Boari flap repair, appendix or ileum interposition, or pyelovesicostomy [5]. In the present case, we initially attempted an anastomosis of the ipsilateral native ureter to the transplant renal pelvis, as this seemed to be the simplest and most feasible solution at the time. However, it is likely that the minimal remaining intrarenal pelvis was also compromised due to rejection, which may have led to the recurrence of the ureteric stricture.

To date, only three cases of vesicocalicostomy in TUS have been reported. The first involved a 13-year-old girl who underwent deceased donor KT (DDKT) in 1977. After experiencing three acute rejection episodes, she developed TUS in 1980. During surgery, the entire TU was found to be fibrosed, prompting a vesicocalicostomy. Unfortunately, the kidney was lost to chronic rejection 14 months later [6]. The second case concerned a 19-year-old girl with neurogenic bladder who underwent DDKT in 1983. She developed stenosis of the distal ureter following the removal of a DJ stent in the immediate postoperative period. A ureteroneovesicostomy using the donor ureter was performed 49 days later. One month following this procedure, the patient developed urosepsis and recurrent distal ureteric stricture, which ultimately necessitated vesicocalicostomy 6 months after the transplant. At 23 months of follow-up, the patient exhibited stable renal function [7]. The third case was a 59-year-old man who underwent LDKT in 1995 and was diagnosed with TUS in 2015. During surgery, the entire ureter was found to be fibrosed, and a vesicocalicostomy was performed. Entry into the collecting system was confirmed by injecting methylene blue through the PCN, and a peritoneal flap was harvested and sutured over the anastomosis for additional reinforcement. The patient remained free of recurrence at 6 months of follow-up [8]. Additionally, one report has been published on ureterocalicostomy in an RTR for a stricture at the pyeloureteral anastomosis. This patient initially underwent pyeloureterostomy using the native ureter, as the allograft ureter was too short for primary ureteroneocystostomy without tension due to an ischemic distal segment [9].

The present case represents the first reported instance in which vesicocalicostomy was performed for TUS arising from rejection in ABO-incompatible LDKT. We employed an innovative technique that utilized fluoroscopic guidance and a nephrostogram to identify the tip of the inferior calyx. This approach allowed us to efficiently determine the precise site for the IPN, minimizing time and blood loss. Additionally, we applied an omental wrap around the anastomosis to improve vascularity and promote healing.

Vesicocalicostomy, though infrequently discussed, represents an appropriate option for managing ureteric strictures in transplant kidneys when standard repair methods are unfeasible or have previously failed. All transplant surgeons and urologists should be cognizant of this viable alternative.