International Urology and Nephrology

, Volume 44, Issue 5, pp 1585–1588

Polyoma virus nephropathy-related mass lesion in an apparently immunocompetent patient


  • Stephanie Go
    • Department of PathologyOregon Health & Science University
    • School of MedicineOregon Health & Science University
  • Michael Conlin
    • Department of Surgery, Division of UrologyOregon Health & Science University
  • Jody E. Hooper
    • Department of PathologyOregon Health & Science University
    • Department of PathologyOregon Health & Science University
Nephrology – Case Report

DOI: 10.1007/s11255-011-9985-y

Cite this article as:
Go, S., Conlin, M., Hooper, J.E. et al. Int Urol Nephrol (2012) 44: 1585. doi:10.1007/s11255-011-9985-y


Polyoma virus is a recognized cause of hemorrhagic cystitis, viral nephropathy, and ureteral stricture in renal and stem cell transplant recipients. Rarely, polyoma virus causes native kidney and bladder pathology in heavily immunosuppressed patients. We report a unique case of native kidney polyoma virus nephropathy, urothelial ulceration, and renal pelvic fibrosis presenting as a mass lesion in a non-debilitated, apparently immunocompetent man. Based on radiologic, ureterorenoscopic, and urine cytologic findings, a laparoscopic nephrectomy was performed. However, nephrectomy revealed a hemorrhagic scar-like lesion, with urothelial ulceration, but no neoplasm or malignancy. Histopathologic evaluation and immunostaining revealed polyoma viral infection in the nearby renal medulla. This case adds polyoma virus nephropathy to the differential diagnosis of non-neoplastic and reactive masses, which may mimic renal malignancy.


BK nephropathyImmunocompromisedPolyoma virusRenal mass


BK polyoma virus is a pathologic polyoma virus, with family members JC, SV40, and the recently discovered Merkel Cell Polyomavirus [13]. Over 80% of the population is seropositive for BK polyoma virus; latent virus persists in kidney, ureters, brain, and lymphoid cells [13]. Local and asymptomatic reactivation may occur with transiently diminished immune status and may be prolonged and serious in immunocompromised hosts [2, 3].

Case report

A 79-year-old man undergoing abdominal CT was incidentally found to have a 2.1 × 1.4 cm mass in the right upper renal collecting system (Fig. 1). The patient had a history of prostate cancer, diagnosed 18 months previously, Gleason grade 5+5, bilateral. He was treated with androgen deprivation therapy alone (Lupron) for his prostate cancer, and he had no other history of immunocompromise. His peak prostate-specific antigen (PSA) value was 9.7 μg/l at the time of prostate cancer diagnosis, while his current PSA was 0.64 μg/l. Blood count revealed mild anemia (hematocrit 37.2%), with a normal white blood cell count (6.9 × 109/l) and platelet count (251 × 109/l;). Serum creatinine was 0.97 mg/dl (86 μmol/l). He had hematuria but no flank pain. Proteinuria was 100 mg/dl 1 month prior to surgery, but trace to negative at other time points. His medical history included depression, sciatica neuralgia, reflux esophagitis, and hypothyroidism. His medications included the following: Lupron, atorvastatin, levothyroxine, metoclopramide, ranitidine, baby aspirin, vitamins, and supplements. Previous surgical history consisted only of an L3-4 laminectomy and left foraminotomy for disk herniation.
Fig. 1

Radiologic, cytologic, histologic results. a Post-contrast computed tomography scan shows renal pelvic mass, upper pole (arrow). bc Bladder wash cytology specimens show atypical papillary clusters and atypical cells with enlarged, irregular nuclei b. Nuclei with central clearing and chromatin margination are suspicious for viral cytopathic change (example, arrowc). d Pelvic urothelium in the nephrectomy is denuded, with granulation tissue polyp. Surface fibrin is seen at left, and remnant reactive urothelium is seen at right. ef Viral inclusions are present in medullary tubules (arrowheads). In f, normal tubules are at left; scattered lymphocytes are at right. g Immunohistochemical stain for polyoma virus, shows positivity (brown staining) in a number of tubules in the medulla. (original magnifications, B, E–F-400×, C-630×, D-50×, G-200×)

Workup of the renal mass included a retrograde pyelogram, demonstrating a filling defect in the right renal pelvis. Ureterorenoscopy showed the right upper pole to be apparently replaced with a high-grade papillary tumor. Cytologic washings of the right renal pelvis revealed atypical papillary clusters, and bladder washings were suggestive of malignancy (Fig. 1).

Materials and methods

Ureter and bladder washing cytologic specimens were fixed in CytoRich® Red solution, and a SurePath™ preparation (both TriPath Imaging, Burlington, NC) was stained with the Papanicolaou stain. Cell blocks were prepared with Shandon Cytoblock® Cell Preparation System (Shandon, Pittsburgh, PA), according to manufacturer’s instructions, and stained with hematoxylin and eosin (H&E).

The nephrectomy was fixed in formalin and processed for paraffin embedding, sectioning, and H&E staining using standard methods. Polyoma virus primary antibody was polyclonal PAb416 (Calbiochem/Merck/EMD Chemicals, Gibbstown NJ) 1:400 on a Ventana XT instrument using Ultraview detection (Ventana, Tucson AZ).


The laparoscopic nephrectomy specimen grossly revealed a 1 × 0.5 × 0.2 cm area of apparently thickened renal pelvis in the anterior superior aspect. Upon histologic examination, this area was a medullary scar with granulation tissue, abundant hemosiderophages, ulceration, and reactive change of the overlying urothelium (Fig. 1). There was no evidence of neoplasm or malignancy. There was patchy but widespread corticomedullary inflammation. Tubules in the medulla demonstrated nuclear atypia and possible viral cytopathic changes. Immunostaining for SV40 revealed positive staining in many medullary nuclei, representing polyoma virus nephropathy (Fig. 1). Focal nephrogenic metaplasia/adenoma was identified in sections of ureter. A PSA immunostain was negative in these glands, ruling out prostatic adenocarcinoma; SV40 immunostaining was negative in this focus, as well as in the residual urothelium.

Retrospective review of the cytologic specimens revealed few nuclei with probable viral cytopathic changes, with a background of cellular debris. Although retrospective immunostaining of the one available cell block was negative for polyomavirus, our suspicion for polyoma virus in the cytology specimens remains high. Neither pre- nor post-operative urine or serum polyoma virus PCR studies were available. Serum creatinine was stable at 1.40 mg/dl (124 μmol/l) nineteen months post-nephrectomy.


We report a unique case of polyoma virus nephropathy in a native kidney associated with a mass lesion suspicious for tumor based on radiologic, endoscopic, and cytologic data. To our knowledge, this case represents the first report of polyoma virus nephropathy in the native kidney of an apparently immunocompetent patient, and the first instance of a polyoma virus associated mass lesion of the kidney. There is rare precedent for renal viral infection-associated mass lesions, with one case report of an adenovirus-associated abscess presenting as a mass lesion in an allograft kidney [4].

In the setting of a compromised immune system, reactivation of BK polyoma virus in the genitourinary system may lead to hemorrhagic cystitis, interstitial nephritis/nephropathy, and in renal transplant recipients, ureteral stenosis [3]. Sustained and pathologic reactivation of BK virus is a known complication of renal transplantation, affecting up to 8% of renal allograft recipients, and leading to graft loss in a substantial fraction of patients [13]. Non-kidney solid organ transplant recipients have a much lower rate of BK viral nephropathy in their native kidneys, despite immunosuppression, suggesting interplay between the immunosuppressed state, the organ allograft, and/or tissue injury [5]. Pathologic polyoma virus infection of bladder or native kidneys occurs in the settings of bone marrow/stem cell transplantation (hemorrhagic cystitis in 8% of patients), CLL, HIV, and rarely aggressive chemotherapy in debilitated patients [1, 6, 7].

Remarkably, this patient with polyoma virus nephropathy was neither debilitated, nor receiving immunosuppression, nor cytotoxic chemotherapy. Although he was elderly and had another malignancy (prostate cancer), his treatment involved only androgen deprivation. Active polyoma virus replication was demonstrated in medullary tubules by immunostaining. We considered BK polyoma virus more likely than JC based on renal tubular involvement [1]. We hypothesize that active viral infection and urothelial ulceration led to the atypical cytologic findings, along with hematoma, granulation tissue, and fibrosis, resulting in the renal mass lesion.

In summary, we illustrate a case of renal mass associated with polyoma virus nephropathy, representing a novel and extremely rare cause of a benign renal mass lesion. Surgeons, cytopathologists, and surgical pathologists should be aware of atypical presentations of polyoma virus infection in apparently immunocompetent patients.


This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. The authors wish to thank Drs. Alicia Liang, Ashley Pyle, and Anuja Mittalhenkle for critical reading of the manuscript, and Dr. Nora Dobos for assistance with radiologic images.

Copyright information

© Springer Science+Business Media, B.V. 2011