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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
LETTER TO THE EDITOR  
Year : 2011  |  Volume : 22  |  Issue : 1  |  Page : 136-138
B.K. polyoma virus nephropathy in renal allograft recipient


1 Department of Pathology, Lab Medicine, Transfusion Services and Immunohematology, G. R. Doshi and K. M. Mehta Institute of Kidney Diseases & Research Centre (IKDRC) Dr. H.L. Trivedi Institute of Transplantation Sciences (ITS), Civil Hospital Campus, Asarwa, Ahmedabad 380016, Gujarat, India
2 Department of Nephrology and Transplantation Medicine, G. R. Doshi and K. M. Mehta Institute of Kidney Diseases & Research Centre (IKDRC) Dr. H.L. Trivedi Institute of Transplantation Sciences (ITS), Civil Hospital Campus, Asarwa, Ahmedabad 380016, Gujarat, India

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Date of Web Publication30-Dec-2010
 

How to cite this article:
Vanikar AV, Shah PR, Trivedi HL. B.K. polyoma virus nephropathy in renal allograft recipient. Saudi J Kidney Dis Transpl 2011;22:136-8

How to cite this URL:
Vanikar AV, Shah PR, Trivedi HL. B.K. polyoma virus nephropathy in renal allograft recipient. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2019 Aug 22];22:136-8. Available from: http://www.sjkdt.org/text.asp?2011/22/1/136/74390
To the Editor,

B.K. polyoma virus nephropathy (BKN) occurs in renal allograft recipients after reactivation of the latent virus in the renal epithelium. [1] About 1-10% of all renal allograft recipients are affected by BKN around 44 weeks post­transplantation, and about 40% progress to irreversible graft failure. [2],[3],[4] We would like to share our experience with a 22-year-old man who underwent renal transplantation from his father as the donor through clonal deletion pro­tocol without immunosuppression. On the 7 th post-operative day, he had a rise in serum creatinine (SCr) from 1.7 to 2.1 mg/dL, which was associated with high donor-specific and non-specific antibody levels of 3,000 mean fluorescent intensity (measured by luminex platform). He was treated with anti-rejection therapy comprising of methylprednisone 500 mg IV × 5, anti-thymoglobulin × 3, plasmaphe­resis eight sessions and Rituximab. He was discharged on prednisone 15 mg/day and Myco­fenolate mofetil (MMF) 360 mg twice a day (BID) after 1 week, but was readmitted after 28 weeks of transplantation for a rise in the SCr to 4.19 mg/dL. His 24-hour urinary pro­tein was 4.5 grams and the serum CMV DNA was negative. A graft biopsy revealed glome­ruli with partially obliterated capillary lumina lined with membranes of normal thickness, heavily infiltrated with cell debris and mixed leukocyte population with RBCs. The tubules were severely degenerated and several tubular epithelial cells showed cytomegaly, with amor­phous basophilic, eosinophilic granular, finely granular without halo/vesicular intranuclear in­clusions that were positive for anti-SV 40 anti­body [Figure 1]. The peritubular capillaries were dilated and occasionally filled with RBCs/mononuclear cells. No C4d deposits were seen on their membranes. All blood vessels were unremarkable. His urine also showed decoy cells and was diagnosed as acute BK polyoma virus nephropathy stage B. Subse­quently, MMF was discontinued and predni­sone was tapered to 10 mg/day. He was ini­tiated on Lefunamide 50 mg BID × 3 days, which was decreased to 20 mg BID subse­quently. He recovered and, on the last follow­up after 11 months of transplantation, his SCr was 1.6 mg/dL on no immunosuppression.

Histopathology is the gold standard for diag­nosis and/or staging of BKN. [5] In the early stage of the disease, there is a focal medullary in­volvement with limited cytopathy of tubular epithelial cells. However, with advancement to stage B, there is extensive renal involvement showing diffuse/multifocal cytopathy with nec­rosis, nuclear smudging of tubular epithelial cells and accompanying diffuse mixed leuco­cytic infiltration. It is sometimes difficult to differentiate BKN from acute cellular rejec­tion. Acute humoral rejection is ruled out with the absence of C4d deposits on the peritubular capillaries. However, anti-S 40 antibody stai­ning becomes inevitable in many cases to con­firm BKN and rule out cellular rejection. Pro­per diagnosis is crucial as management of re­jection is different from that for BKN. It has been observed that it is the overall immuno­suppressive load rather than an individual im­munosuppressant that accounts for the ina­bility of the host to mount a successful anti­viral immune response. [6] Leflunomide is used to treat BK virus infection on a long-term basis, and reduction of immunosuppression is essential for its cure. Cidofovir, a phosphonate purine analogue of cytosine that potentially in­hibits viral DNA polymerases, has a broad spectrum of activity against herpes, papilloma and pox viruses. Its exact mode of action against polyoma viruses is not established. [7] Fluoroquinolines and intravenous immunoglo­bulins have also helped in arresting BK virus replication. [8] Our patient, who was not subjec­ted to conventional immunosuppression at any time, contracted BKN probably due to clonal deletion, which proved to be severe for him. However, early diagnosis and aggressive ma­nagement helped in curing the disease and regaining adequate stable graft function with­out any immunosuppression.
Figure 1: Left: Hematoxylin and eosin, ×200, intranuclear inclusions in the tubular epithelial cells; the
arrow shows the amorphous basophilic inclusion and the arrow head shows the vesicular inclusion.
Right: anti-SV 40 antibody-stained inclusions in the same cells, ×100.


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   References Top

1.Randhawa PS, Demetris AJ. Nephropathy due to polyomavirus type BK. N Engl J Med 2000;342(18):1361-3.  Back to cited text no. 1
    
2.Hirsch HH, Brennan DC, Drachenberg CB, et al. Polyomavirus-associated nephropathy in renal transplantation: interdisciplinary analyses and recommendations. Transplantation 2005;79(10): 1277-86.  Back to cited text no. 2
    
3.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(3): 429-31.  Back to cited text no. 3
    
4.Ramos E, Drachenberg CB, Papadimitriou JC, et al. Clinical course of polyoma virus nephro­pathy in 67 renal transplant patients. J Am Soc Nephrol 2002;13:2145-51.  Back to cited text no. 4
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5.Buehrig CK, Lager DJ, Stegall MD, et al. Influence of surveillance renal allograft biopsy on diagnosis and prognosis of polyomavirus­associated nephropathy. Kidney Int 2003;64: 665-73.  Back to cited text no. 5
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6.Blanckaert K, De Wriese AS. Current recom­mendations for diagnosis and management of BK virus nephropathy in renal transplant recipients. Nephrol Dial Transplant 2006;21: 3364-7.  Back to cited text no. 6
    
7.Andrei G, Snoeck R, Vandeputte M, De Clercq E. Activities of various compounds against murine and primate polyomaviruses. Antimi­crobe Agents Chemother 1997;41:587- 93.  Back to cited text no. 7
    
8.Rinaldo CH, Hirsch HH. Antivirals for the treatment of polyomavirus BK replication. Expert Rev Anti Infect Ther 2007;5(1):105-15.  Back to cited text no. 8
    

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Correspondence Address:
Aruna V Vanikar
Department of Pathology, Lab Medicine, Transfusion Services and Immunohematology, G. R. Doshi and K. M. Mehta Institute of Kidney Diseases & Research Centre (IKDRC) Dr. H.L. Trivedi Institute of Transplantation Sciences (ITS), Civil Hospital Campus, Asarwa, Ahmedabad 380016, Gujarat
India
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