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CLINICAL CASE
Delayed ureteral metastasis from prostate cancer mimicking urothelial carcinoma
1 Kuban State Medical University, Krasnodar, Russia
2 Rostov State Medical University, Rostov-on-Don, Russia
Correspondence should be addressed: Polina Evgenievna Vorobyeva
ul. Sadovaya, 159, Krasnodar, 350002, Russia; ur.liam@ve_anilopaveiborov
Author contribution: Vorobyeva PE, Kirsanova PV, Tkachenko VV, Mosnaya AI — literature analysis, article authoring; Khachatryan KA, Chnavayan DV, Zaynullina RF — data processing, literature analysis, article authoring; Chikun SV, Moiseeva AD — article editing.
Compliance with ethical standards: all participants or their legal representatives provided written informed consent to participate in the study.
Prostate cancer (PC) is one of the most common malignant neoplasms in men. According to the International Agency for Research on Cancer (IARC), in 2020 the standardized incidence and mortality rates for prostate cancer were 30.7 and 7.7 per 100000 men, respectively [1, 2]. In the Russian Federation, there is also a marked trend towards an increase in the prevalence of this disease: from 2012 to 2022, the indicator more than doubled, from 93.6 to 198.9 cases per 100000 men. With the introduction of screening programs aimed at early detection of the disease, the number of diagnosed PC cases has been going up [3, 4]. In approximately 20% of patients, the disease progresses to the metastatic stage [5].
The most common metastatic sites in prostate cancer are regional lymph nodes, bone, lungs, distant lymph nodes, and the liver. Often, metastases result from hematogenous spread of tumor cells. However, it is not fully understood how metastases reach the ureter: both lymphogenic and hematogenic pathways of spread are assumed [6].
Ureteral metastasis from prostate cancer is an exceptionally rare manifestation of disease progression. The limited number of reported cases underscores both the uniqueness of this localization and the substantial diagnostic challenges it presents [7, 8]. One of the first papers about PC-associated ureteral metastasis was a case report published by French authors in 1978 [9]. Given the scarcity of works dedicated to this variant of PC progression, it is necessary to further investigate this path of metastatic spread, since the lack of clear understanding of its clinical features may handicap selection of the optimal diagnostic and treatment strategy.
This report presents a rare case of late progression of PC with metastatic involvement of the ureter long after radical surgical treatment and achievement of disease control. The case expands understanding of the possible patterns of metastatic spread of prostate cancer (PC) and highlights the need for oncological vigilance when diagnosing the causes of upper urinary tract obstruction in patients with urodynamic disorders and a history of PC. It also underscores the diagnostic difficulty of differentiating secondary ureteral lesions from primary tumors of the upper urinary tract, which necessitates comprehensive morphological and immunohistochemical (IHC) evaluation. In addition, the report illustrates the specifics of choosing therapeutic tactics for uncommon metastatic localizations, including relief of urinary tract obstruction, surgical intervention for local control, and subsequent adjustment of systemic antitumor therapy based on observed signs of disease progression.
Case description
In 2012, patient A. was diagnosed with prostate cancer. He underwent radical prostatectomy with pelvic lymphadenectomy for the localized neoplasm. Pathomorphological examination of surgical material (conducted on 07.12.2012) confirmed a large acinar adenocarcinoma of the prostate, pathomorphological stage pT2cN0M0, with a Gleason score of 5 (3 + 2). These findings were consistent with a localized tumor of low malignant potential. After surgery, the patient's condition was constantly monitored.
In August 2020, a follow-up examination with computed tomography of the pelvic organs (CT PO) revealed the progression of the disease in the form of a metastatic lesion of the left obturator lymph node without signs of local recurrence and distant metastasis. Given the oligometastatic nature of the process, the patient underwent a course of radiotherapy targeting the affected lymph node in combination with androgen deprivation therapy (ADT): buserelin 3.6 mg, administered long term. The available medical documentation does not offer information on the total dose or dose per fraction, which prevents specifying radiation dose parameters in this report. The combined treatment yielded a pronounced clinical and biochemical effect.
Subsequently, ¹⁸F-PSMA PET-CT (Biograph Horizon 4R; Siemens, Germany) and MRI of the abdominal cavity and pelvic organs (Brivo MR355 1.5 T; General Electric, USA) performed between 2022 and 2025 showed no evidence of local recurrence or other metastatic foci, confirming the disease was under control. Laboratory testing showed that the level of prostate-specific antigen (PSA) remained at 0.03 ng/ml and the testosterone level was at 1.27 nmol/L, which indicated a persistent pronounced biochemical response supported by the androgen deprivation therapy. Later, a ureteral tumor lesion was detected; following its surgical resection, new PSMA-positive metastatic lymph nodes were identified, indicating possible disease progression despite low PSA levels.
As shown by ¹⁸F-PSMA PET-CT (Biograph Horizon 4R; Siemens, Germany) of 28.01.2026, the kidneys were positioned typically, their size not increased. Imaging showed hydronephrotic transformation of the left kidney, with diffuse ureteral dilation up to 16 mm and enlargement of the pelvicalyceal system to 47 mm (previously 43 mm). The right kidney and the right ureter showed no signs of dilation. Urinary tract calculi were not visualized. The lymph nodes of the abdominal cavity, retroperitoneal space, pelvis, and peripheral lymph nodes were not enlarged and did not show abnormal accumulation of PSMA. After radical prostatectomy, no pathological neoplasms were identified in the prostate gland or seminal vesicles. There was no free fluid in the abdominal and pelvic cavities. No signs of local recurrence, regional or distant metastases with overexpression of PSMA were found. Compared to the examination of 29.11.2024, the overall trend was not negative. Left-sided hydronephrosis was the only significant finding.
In February 2026, helical computed tomography of the abdomen and pelvis, performed for urodynamic disorders, revealed a neoplasm involving the lower third of the left ureter, accompanied by severe left-sided calicopyeloureterectasia and impaired function of the left kidney (figure).
On 21 February 2026, the patient underwent left-sided percutaneous nephrostomy with placement of a 9 Ch pigtail nephrostomy catheter, indicated for evolving obstruction of the lower third of the left ureter and impaired left renal function.
Antegrade pyelography (EvolutionE+1) findings: no radiopaque calculi are seen in the projection of the kidneys or urinary tract on the review urogram; the nephrostomy catheter is visualized on the left. Following antegrade administration of contrast, there is opacification of a dilated pelvicalyceal system of the left kidney (renal pelvis up to 4.7 × 4.7 cm; calyces up to 2.8 cm). The upper third of the left ureter is not significantly dilated; the middle and lower thirds are dilated to 1.5 cm. Following contrast administration, the ureter is opacified down to the level of the S4 vertebra, where a blind-ending segment with a well-defined concave contour is visualized. The distal ureter and urinary bladder are not opacified, indicating impaired patency of the lower third of the left ureter. Conclusion: post-procedural changes following left percutaneous nephrostomy as evidenced by radiological signs. Left-sided pyelocalicoureterectasis. Obstruction of the lower third of the left ureter.
On 02.03.2026, left-sided ureteroscopy was performed, and a biopsy of a tumor in the left ureter was obtained to morphologically verify the neoplasm's classification. Approximately 2 cm from the left ureteral orifice, an obstruction preventing advancement of the catheter along the guidewire was encountered. Subsequent ureteroscopy revealed a bulky tumor in the distal left ureter, 2–3 cm from the ureteral orifice, almost completely occluding its lumen. A biopsy of the neoplasm was taken. Histological examination showed highgrade (HG) urothelial carcinoma; accordingly, the lesion was initially considered a primary tumor of the upper urinary tract.
Subsequently, on 02.04.2026, the patient underwent open radical left-sided nephroureterectomy with en bloc removal of the kidney and ureter, including the intramural ureter and ureteral orifice. The bladder defect was closed, and retroperitoneal drainage was established.
According to the final pathomorphological examination of the surgical specimen of 07.04.2026, which included IHC, the left ureteral neoplasm was identified as a metastasis from prostate adenocarcinoma. On IHC, the tumor cells were negative for cytokeratins CK7 and CK20, and showed strong PSA expression, confirming prostatic origin. The neoplasm infiltrated the ureteral wall and periureteral tissue. No tumor was present at the ureteral resection margin (R0).
In addition, the removed kidney showed pronounced secondary changes due to prolonged urinary tract obstruction, including chronic pyelonephritis with resultant hydronephrosis, peri- and paranephritis, severe glomerular sclerosis, vascular hyalinosis, focal interstitial sclerosis, and dystrophic changes in the tubular epithelium.
Thus, the disease course was characterized by a prolonged period of control following radical surgical removal of localized prostate cancer. Eight years after the operation, the patient developed oligometastatic lesions involving a regional lymph node; these were successfully controlled with radiation and androgen deprivation therapy, resulting in a complete metabolic and biochemical response. Thirteen years after radical prostatectomy, the patient was diagnosed with an extremely rare metastatic involvement of the left ureter, which preoperatively mimicked primary urothelial carcinoma of the upper urinary tract. The final diagnosis was established only after surgical intervention and comprehensive pathomorphological and IHC examination. The patient had no significant comorbid somatic conditions, such as diabetes mellitus or metabolic syndrome, that could materially affect the disease course. Throughout the monitoring period, the patient’s general condition remained satisfactory (ECOG 1), allowing the team to plan further specialized treatment.
¹⁸F-PSMA PET-CT (Biograph Horizon 4R; Siemens, Germany) revealed no pathological foci of radiopharmaceutical accumulation in the bed of the removed left kidney and ureter or in the prostate bed. However, de novo PSMA-positive metastatic lymph nodes were visualized in the retrocrural, retroperitoneal, and pelvic regions; the largest was a left common iliac node measuring up to 17 mm (SUVmax 6.36). These foci were not detected on the previous examination. There were no signs of visceral or bone metastases. Compared with the examination of 28.01.2026, the disease had progressed with new PSMApositive lymph nodes. After radical nephroureterectomy, PSA levels rose. Laboratory tests on 05.05.2026 showed a PSA level of 0.98 ng/mL and a testosterone level of 1.32 nmol/L, consistent with castrate levels. Thus, in the setting of ongoing androgen deprivation therapy and stable castrate testosterone levels, the disease demonstrated radiologic progression with new PSMA-positive metastatic lymph nodes and an increase in PSA to 0.98 ng/mL. The totality of clinical, laboratory, and radiological data was consistent with a castration-resistant course, leading to a diagnosis of metastatic castration-resistant prostate cancer (mCRPC).
The special characteristic of this case is the dissociated course of the disease: the initial ureteral metastasis developed with an extremely low PSA level (0.03 ng/ml), whereas after surgical removal of this lesion, the PSA rose up to 0.98 ng/ml, and there appeared new PSMA-positive metastatic lymph nodes. This highlights the need to assess the progression of CRPC using not only the fluctuations of the PSA level but also clinical data and results of instrumental examinations.
Drugs from the gonadotrophin-releasing hormone agonist group were recommended as a hormonal therapy option: buserelin (3.75 mg IM once every 28 days or 11.25 mg IM once every 90 days), in accordance with current clinical guidelines. Given the signs of disease progression against the background of androgen-deprivation therapy, it was also recommended to escalate systemic therapy by adding a second-generation antiandrogen (enzalutamide) or by prescribing docetaxel chemotherapy.
Case discussion
Metastatic ureteral lesion in prostate cancer is an extremely rare variant of disease progression. The lesion can mimic a primary tumor of the upper urinary tract. In this case, the neoplasm that involved the left ureter developed 13 years after radical prostatectomy and a long period of disease control.
Diagnosing was complicated: initial biopsy suggested classification of the tumor as a urothelial carcinoma. The diagnosis was adjusted after surgical intervention and an IHC examination that revealed PSA expression in the absence of CK7 and CK20 expression, confirming metastatic origin. The special feature of this case is the dissociated course of the disease. Metastatic ureteral lesion was diagnosed at a PSA level of 0.03 ng/ml, whereas after radical nephroureterectomy, the said level increased to 0.98 ng/ml. At the same time, ¹⁸F-PSMA PET-CT performed on 06.05.2026 revealed new PSMA-positive metastatic lymph nodes of retrocrural, retroperitoneal, and pelvic localization, and the testosterone was at 1.32 nmol/l, i.e. the castration level. The combination of an increased PSA level and radiological progression in the setting of persistent castration-level testosterone corresponds to a castrationresistant disease course and supports classifying the situation as mCRPC.
This case also demonstrates the limitations of assessing the activity of the disease solely based on the dynamics of PSA. When the ureteral metastasis was detected, the PSA level was minimal, despite the morphologically confirmed tumor. After the removal of this lesion, the growth of the PSA level was accompanied by the appearance of new PSMA-positive lymphatic metastases. This suggests that assessment of the disease progression should be based on a combination of laboratory, clinical, morphological, and radiological data.
We did not evaluate neuroendocrine differentiation in this case. Given the pronounced PSA expression and the confirmed prostatic origin of the tumor, the presence of neuroendocrine differentiation cannot be confirmed on the basis of the available data and remains a hypothesis requiring dedicated morphological and immunohistochemical examination. MSI/ dMMR status and HRR mutation status were not determined, and no molecular genetic testing results are available.
Taking into account the revealed systemic progression of the disease against the background of ADT, it is necessary to escalate systemic treatment in accordance with modern approaches to the treatment of mCRPC.
This case demonstrates that a correct diagnosis requires factoring in the possibility of late and atypical metastasis of prostate cancer with the appearance of urinary tract obstruction, as well as comprehensive pathomorphological and immunohistochemical examinations. Treatment, in turn, requires an individual approach, taking into account the local manifestations of the disease and the systemic nature of the tumor process. In the presented case, surgical intervention allowed to eliminate the obstruction and establish a definitive diagnosis, and the further progression of the disease determined the continuation of androgen-deprivation therapy with the need to escalate systemic treatment.
Conclusion
Metastasis of prostate cancer to the ureter is a rare variant of the disease progression that may mimic primary urothelial carcinoma. When a patient with prostate cancer history presents with a ureteral neoplasm, it is necessary to consider its metastatic origin, even if the PSA level is low and the radical surgery was performed a long time ago. In such cases, the differential diagnosis options should include primary urothelial carcinoma, and IMH verification of the tumor origin with assessment of PSA, CK7 and CK20 expression is crucial. If a metastatic lesion is confirmed and there are signs of further systemic disease progression, it is advisable to assess the need for correction or escalation of systemic therapy, taking into account modern approaches to the treatment of advanced prostate cancer.