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Table of Contents
CASE REPORT
Year : 2022  |  Volume : 16  |  Issue : 3  |  Page : 346-349

Partial pelviureteric junction obstruction secondary to BK virus infection early posttransplantation - A case report


1 Department of Nephrology, Yashoda Hospitals, Secunderabad, Telangana, India
2 Department of Pathology, Apollo Hospitals, Hyderabad, Telangana, India
3 Department of Nuclear Medicine, Yashoda Hospitals, Hyderabad, Telangana, India

Date of Submission14-Mar-2021
Date of Acceptance08-May-2021
Date of Web Publication30-Sep-2022

Correspondence Address:
Dr. Urmila Anandh
Department of Nephrology, Yashoda Hospitals, Alexander Road, Secunderabad, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijot.ijot_27_21

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  Abstract 


A 63-year-old female presented to our hospital with progressive allograft dysfunction, declining urine output and fluid overload. She had undergone a second transplant 4 months before. Her evaluation revealed partial pelviureteric obstruction in her ultrasound. She underwent a renal biopsy which revealed BK virus infection. The pelviureteric obstruction improved with oral diuretics and her mycophenolate sodium was discontinued. The case illustrates a rare urological manifestation of BK virus infection which can present with symptomatic allograft dysfunction early posttransplantation.

Keywords: BK virus, pelvi-ureteric junction, renal transplantation, simian virus 40 stain


How to cite this article:
Anandh U, Gowrishankar S, Aurangabadkar H. Partial pelviureteric junction obstruction secondary to BK virus infection early posttransplantation - A case report. Indian J Transplant 2022;16:346-9

How to cite this URL:
Anandh U, Gowrishankar S, Aurangabadkar H. Partial pelviureteric junction obstruction secondary to BK virus infection early posttransplantation - A case report. Indian J Transplant [serial online] 2022 [cited 2022 Nov 27];16:346-9. Available from: https://www.ijtonline.in/text.asp?2022/16/3/346/357606




  Introduction Top


BK virus was first isolated from the urine sample of a renal transplant recipient in 1971.[1] This DNA virus is often present in latent state and gets reactivated when there is relative state of immunodeficiency (renal transplantation).[2] In the kidney transplant recipient, it can manifest as progressive renal dysfunction, urinary tract infection, hemorrhagic cystitis, and ureteric stenosis.[3] In nephrology practice, most patients have asymptomatic allograft dysfunction over years.[4] Our patient presented with BK virus infection very early posttransplant with predominant urologic manifestation of pelviureteric obstruction.


  Case Report Top


A 63-year-old female of African descent was evaluated in our hospital for a second transplantation. She gave a history of undergoing a transplantation in another center in 2014. Her native kidney was affected by focal segmental glomerulosclerosis. Her allograft functioned well for the first 5 years. Subsequently, her kidney function worsened, and she was restarted on dialysis in 2019. She gave a history of multiple blood transfusions after reinitiation of dialysis.

Her pretransplant evaluation revealed that she had severe renal failure, anemia, hyperphosphatemia, and hyperparathyrodism. She was dialyzed through her arteriovenous fistula. She had no cardiac comorbidities. Her daughter came forward as a prospective donor. She was evaluated and found to have no medical issues [Table 1]. After all legal formalities, the patient underwent a renal transplantation. She received lymphocyte-depleting induction. Her steroids were tapered rapidly (discharge prednisolone 10 mg/day). The second kidney was placed in the left iliac fossa. The allograft functioned well, and the discharge creatinine was 1.1 mg/dl. The double J stent was removed after 3 weeks.
Table 1: Investigations during her admission posttransplantation

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Four weeks after transplantation, she came to hospital with worsening renal function (creatinine 2.1 mg/dl), fever, and edema. Her evaluation showed the presence of multidrug-resistant Klebsiella pneumoniae. She received 14 days of oral fosfomycin. Her fever subsided, and her renal functions improved (creatinine 1.5 mg/dl). She was asymptomatic over the next 4 months when she developed puffiness of face, pedal edema, and decreasing urine output. She was re-admitted and found to have worsening renal function (creatinine 2.2 mg/dl), hyponatremia (serum S-128 meq/L), and leukopenia (white blood cell 3970 cells/μL). Her urine analysis and liver function tests were normal.

During her hospital stay, her urine output progressively declined. Her radiological evaluation showed moderate hydronephrosis with predominantly dilated pelvis [Figure 1]. The cortical thickness was 1.51 cm. As she was a high-risk transplant, she underwent an ultrasound-guided renal biopsy which showed evidence of interstitial inflammation. Immunohistochemistry with C4D staining was negative. The simian virus 40 stain showed the presence of BK virus nephropathy [Figure 2]. Her renal scintigraphy showed impaired perfusion and cortical tracer uptake. Gradual pooling of tracer activity was noted in the dilated pelvicalyceal system with slow tracer clearance. Persistent tracer activity was noted in the prevoid and the postvoid images and in the delayed 3 h–5 h static images [Figure 3]. This was suggestive of partial obstruction at the pelviureteric junction. Her BK virus blood (143900copies/ml) and urine (56490 copies/ml) levels were tested and they confirmed the presence of active viral replication.
Figure 1: Renal allograft showing mild to moderate hydronephrosis with disproportionate diltation of the renal pelvis

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Figure 2: Renal allograft biopsy showing simian virus 40 stain positivity

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Figure 3: Tc 99 diethylenetriamine pentaacetic acid transplant scintigraphy showing delayed tracer clearance suggestive of partial pelviureteric junction obstruction

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She was started on everolimus and ciprofloxacin, and mycophenolate mofetil was slowly withdrawn. She was also started on leflunomide, however, the drug had to be discontinued because of profound lymphopenia. She was also started on long-term diuretics. Her urine output normalized, and her follow-up serum creatinine is 1.0 mg/dl. A repeat BK virus plasma level done 3 months later showed a decrease in viral replication (4600 copies/ml). An urological review was done, and a repeat ultrasound was done which showed no progression of the pelviureteric obstruction. The surgeons advised conservative management with periodic follow-up.


  Discussion Top


With the advent of potent immunosuppression, BK virus nephropathy has emerged as an important cause of progressive allograft dysfunction.[5] Over the years, various risk factors have been investigated, and younger age, male recipients, recipients without diabetes, female donors, thymoglobulin induction, and tacrolimus maintenance have all been found to increase the risk of BK virus infection.[6] Our patient had many of the risk factors mentioned above.

BK virus nephropathy is the predominant manifestation of the viral infection and has been noted in 1%–10% of transplants and can lead to graft loss in 50% of patients.[7] Studies from India have shown variable incidence of allograft dysfunction.[8],[9]

Urologic presentation in the early transplant period is a rare manifestation of BK virus infection. Ureteric stenosis is seen in 3% of transplant recipients who develop BK virus infection within the first 3–6 months of transplantation.[10],[11] Most are managed conservatively, and patients need surgical intervention if the obstruction progresses. Our patient is currently stable (creatinine 1.0 mg/dl 15 months posttransplantation) and may need surgical intervention in future if her ureteric obstruction worsens.


  Conclusions Top


Our case reflects the myriad manifestations and unpredictable clinical course of BK virus nephropathy in renal allograft recipients. Ureteric obstruction is a rare manifestation which requires surgical intervention. Concomitant modification of immunosuppression and antivirals are also required to prevent progressive interstitial fibrosis and tubular atrophy in these patients.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Gardner SD, Field AM, Coleman DV, Hulme B. New human papovavirus (B.K.) isolated from urine after renal transplantation. Lancet 1971;1:1253-7.  Back to cited text no. 1
    
2.
Nickeleit V, Hirsch HH, Binet IF, Gudat F, Prince O, Dalquen P, et al. Polyomavirus infection of renal allograft recipients: From latent infection to manifest disease. J Am Soc Nephrol 1999;10:1080-9.  Back to cited text no. 2
    
3.
Vögeli TA, Peinemann F, Burdach S, Ackermann R. Urological treatment and clinical course of BK polyomavirus-associated hemorrhagic cystitis in children after bone marrow transplantation. Eur Urol 1999;36:252-7.  Back to cited text no. 3
    
4.
Rosen S, Harmon W, Krensky AM, Edelson PJ, Padgett BL, Grinnell BW, et al. Tubulo-interstitial nephritis associated with polyomavirus (BK type) infection. N Engl J Med 1983;308:1192-6.  Back to cited text no. 4
    
5.
Hirsch HH. Polyomavirus BK nephropathy: A (re-) emerging complication in renal transplantation. Am J Transplant 2002;2:25-30.  Back to cited text no. 5
    
6.
Schold JD, Rehman S, Kayle LK, Magliocca J, Srinivas TR, Meier-Kriesche HU. Treatment for BK virus: Incidence, risk factors and outcomes for kidney transplant recipients in the United States. Transpl Int 2009;22:626-34.  Back to cited text no. 6
    
7.
Patel R. Infections in recipients of kidney transplants. Infect Dis Clin North Am 2001;15:901-52.  Back to cited text no. 7
    
8.
Sachdeva MS, Nada R, Jha V, Sakhuja V, Joshi K. The high incidence of BK polyoma virus infection among renal transplant recipients in India. Transplantation 2004;77:429-31.  Back to cited text no. 8
    
9.
Gupta P, Gupta A, Bhalla AK, Malik M, Gupta A, Bhargava V, et al. BK virus nephropathy in living donor renal allograft recipients: An observational study from a large transplant center in India. Saudi J Kidney Dis Transpl 2018;29:1366-70.  Back to cited text no. 9
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10.
Coleman DV, Mackenzie EF, Gardner SD, Poulding JM, Amer B, Russell WJ, et al. Human polyoma-virus (BK) infection and ureteric stenosis in renal allograft recipients. J Clin Pathol 1978;31:338-47.  Back to cited text no. 10
    
11.
Muhsin SA, Wojciechowski D. BK virus in transplant recipients: current perspectives. Transplant Res Risk Manage 2019;11:47-58.  Back to cited text no. 11
    


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