The Cologne team, led by T. Wagner and colleagues, reviewed 471 adult single-kidney transplant recipients operated between January 2012 and December 2022, after excluding pediatric recipients, combined organ transplants and cases with insufficient follow-up. Roughly half the grafts came from living donors and half from deceased donors. Urinary tract reconstruction was performed either by the intravesical Politano–Leadbetter technique, used in 432 patients (91.7%), or the extravesical Lich–Gregoir technique, used in 33 patients (7.0%), with a double-J ureteral stent routinely inserted and removed after 30 days. The diagnosis of ureteral stenosis required hydronephrosis on ultrasound combined with rising serum creatinine, after excluding other causes of graft dysfunction such as acute rejection, hematoma or lymphocele, and was confirmed by pyelography where clinically indicated.

The headline number: ureteral stenosis occurred in 6.37% of recipients — 30 of 471 patients — a figure that sits comfortably within the broad 0.5% to over 20% range reported in the literature. What makes the study genuinely valuable, however, is not the incidence but the risk-factor profile it uncovered. Recipient characteristics were remarkably well balanced between the stenosis and non-stenosis groups: median recipient age was 53 years in both, sex distribution, BMI and implantation side were statistically indistinguishable. The story lay entirely on the donor side of the equation.

Donors whose kidneys later developed strictures were significantly older, with a median age of 65 years compared to 56 years in the non-stenosis group (p = 0.006), and were also of shorter stature (1.70 vs. 1.73 m, p = 0.016). Even more striking was the vascular anatomy: multiple renal arteries were present in 33.3% of the stenosis group versus just 10.2% of the non-stenosis group (p < 0.001). This echoes a mechanistic picture that transplant surgeons have long suspected — the transplant ureter depends on a single ureteral artery branching from the renal artery, so complex vascular anatomy means compromised ureteral blood supply, and compromised blood supply means ischemic injury and fibrotic stricture formation. Older grafts, with impaired ureteral perfusion and reduced healing capacity, act synergistically with ischemic susceptibility to promote ureteral injury.

But the Cologne data also point to a second, viral mechanism — and this is where the study gets genuinely provocative. BK virus, a latent polyomavirus present in up to 90% of the adult population, reactivates under immunosuppression and is well established as a cause of ureteral inflammation and epithelial damage. In the Cologne cohort, clinically relevant BKV replication was dramatically more frequent in the stenosis group: BK viruria was present in 26.7% of stenosis patients versus 7.0% of non-stenosis patients (p = 0.002), and BK viraemia in 26.7% versus 8.6% (p = 0.005). Among patients with detectable replication, median urinary BKV load was 1.36 × 10⁷ copies/mL and median plasma load 3.75 × 10³ copies/mL. The temporal distribution of stenosis onset reinforces this biphasic etiology: early strictures, at a median of 61 days, predominantly reflect ischemic injury, surgical factors and periureteral fibrosis, whereas late strictures, at a median of 181 days, are more commonly attributed to viral-mediated urothelial damage. Among deceased donors, all early stenosis cases involved donors aged ≥60 years, fulfilling a primary extended-criteria donor criterion, compared to 50.0% in the late stenosis group (p = 0.085) — while BK viruria and viraemia were numerically more prevalent in the late stenosis group (50.0% vs. 20.0% and 42.9% vs. 13.3%), consistent with a viral mechanism predominating in late-onset disease, though these subgroup differences did not reach statistical significance given the limited sample size.

The clinical consequences were sobering. Patient survival did not differ significantly between groups (p = 0.833), and overall graft survival was likewise comparable (p = 0.2). But death-censored graft survival — graft survival independent of patient mortality — was significantly lower in the stenosis group at three years: 79.7% versus 93.3% (p = 0.01). Renal function told the same story. Median creatinine was comparable at discharge (1.660 vs. 1.865 mg/dL, p = 0.809), but became persistently elevated in the stenosis group at six months (1.540 vs. 1.890 mg/dL, p = 0.006), one year (1.5 vs. 1.96 mg/dL, p = 0.004) and two years (1.5 vs. 1.85 mg/dL, p = 0.017), with the difference at three years narrowly failing to reach significance (p = 0.079), possibly due to loss of follow-up and restricted sample size. In other words, even when the stricture is surgically corrected, the graft carries a lasting functional scar.

On the surgical side, the Cologne team compared two revision strategies in 29 patients: 17 underwent transposition — restoring the urinary tract to the ipsilateral native ureter, either from the graft renal pelvis (pyeloureterostomy) or from the graft ureter (ureteroureterostomy) — and 12 underwent ureteroneocystostomy, reimplanting the donor ureter directly into the recipient bladder, most commonly by the extravesical Lich–Gregoir technique in which the detrusor is incised, the spatulated ureter is anastomosed to the exposed bladder mucosa and the muscle layer is closed over it to create an antireflux tunnel. The two revision groups were comparable in age, donor type, sex, comorbidities and stenosis characteristics. Operative duration (105 vs. 85 minutes, p = 0.078) and time from diagnosis to intervention (35 vs. 58 days, p = 0.066) showed numerical trends toward longer values in the transposition group without reaching significance. Creatinine levels measured prior to revision and at discharge, six months, one, two and three years postoperatively showed no significant differences between the two approaches, and graft failure occurred in 3 of 17 (17.6%) transposition and 1 of 12 (8.3%) ureteroneocystostomy patients (p = 0.622).

The authors are careful about what this comparability does and does not mean. Given the small subgroup sizes, these findings should not be interpreted as evidence of equivalence, they write. Rather, the data support individualization of surgical technique based on anatomical and patient-specific factors — distal stenoses, which accounted for 77.8% of cases overall, are natural candidates for reimplantation into the bladder, whose rich vascular supply supports optimal healing of the ureterovesical anastomosis, while proximal or mid-ureteral lesions may favor transposition procedures, provided the integrity of the native ureter is confirmed. Notably, all 29 revision cases followed initial Politano–Leadbetter reconstruction, and no patient initially reconstructed with Lich–Gregoir developed a stenosis — a difference that did not reach statistical significance (p = 0.154) but that the authors attribute to a historical institutional preference for the Politano–Leadbetter technique during the early study period rather than inherent inferiority, as contemporary practice has shifted toward Lich–Gregoir in line with current European Association of Urology guidelines.

The study has limitations the authors acknowledge openly: its retrospective, single-center design may limit generalizability; viral screening protocols evolved technically over the extended study period, potentially underestimating BK virus incidence in earlier cases; and the relatively small stenosis subgroup limits statistical power for certain analyses. The diagnostic dilemma is real — pelvicalyceal dilatation of the denervated graft may represent a normal post-transplant finding rather than true obstruction, meaning asymptomatic or subclinical strictures may go undetected and intervention delayed, so the true incidence of 6.37% may well be an underestimate. Extrinsic factors also warrant consideration: periureteral lymphoceles, which were numerically more frequent in the stenosis group (20.0% vs. 8.8%, p = 0.055), may cause ureteral compression clinically similar to intrinsic strictures, though cases attributable exclusively to lymphoceles were excluded from the analysis.

Still, the message for transplant clinicians is clear and actionable. Ureteral stenosis, occurring in roughly one in sixteen recipients, is significantly associated with extended-criteria donor characteristics — older donor age, multiple renal arteries — and with BK virus infection. Although overall patient and graft survival were unaffected, death-censored graft survival was significantly reduced and kidney transplant function impaired, highlighting the need for early detection and timely intervention. Surgical revision effectively stabilized renal function regardless of the technique employed. The Cologne findings reinforce the clinical relevance of BK virus monitoring in post-transplant surveillance and suggest that vigilance should be highest for recipients of older grafts with complex vascular anatomy — precisely the donor population that organ shortage is pushing centers to accept. Prospective multicenter studies are now needed to validate these findings and further optimize surveillance and surgical strategies in the post-transplant setting.

Subject of Research: Post-transplant ureteral stenosis

Article Title: Post-transplant ureteral stenosis: donor-related risk factors, graft outcome and surgical management

Article References: Wagner, T., Heinrich, H., Schober, E., Ischebeck, L., Schleussner, N., Hummels, M., Koehler, F. C., Kurschat, C., Kann, M., Bruns, C., Stippel, D. L., & Thomas, M. N. (2026). Post-transplant ureteral stenosis: donor-related risk factors, graft outcome and surgical management. Frontiers in Nephrology, 6, Article 1943229. https://doi.org/10.3389/fneph.2026.1943229

Image Credits: AI Generated

DOI: 10.3389/fneph.2026.1943229

Keywords: kidney transplantation, ureteral stenosis, extended-criteria donors, BK virus, graft survival, surgical revision, ureteroneocystostomy, ureteral transposition, renal function, donor age, multiple renal arteries, transplant complications