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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2015  |  Volume : 26  |  Issue : 1  |  Page : 94-97
Polyomavirus-associated nephropathy in renal and simultaneous pancreas-kidney transplant recipients: Report of three cases

1 Division of Internal Medicine, Fundación Valle del Lili, Cali, Universidad CES, Medellín, Colombia
2 Division of Nephrology and Transplants, Fundación Valle del Lili, Cali, Colombia

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Date of Web Publication8-Jan-2015


Infection with polyomavirus (BK virus) is the cause of renal graft losses in more than 50% of the infected cases. There should be a high index of suspicion about this disease, although the incidence is only between 2% and 5% as the future of renal graft depends on the early and appropriate management of the same. Herein, we describe three clinical cases: Two were those of kidney transplant and the third, a combined kidney-pancreas transplant. In these cases, by reducing immunosuppression and, in one case, replacing the calcineurin inhibitor by MTOR (mammalian target of rapamycin) in addition, we were able to preserve of the normal function of the transplanted organs.

How to cite this article:
Cadavid D, Mesa L, Schweineberg J, Posada JG. Polyomavirus-associated nephropathy in renal and simultaneous pancreas-kidney transplant recipients: Report of three cases. Saudi J Kidney Dis Transpl 2015;26:94-7

How to cite this URL:
Cadavid D, Mesa L, Schweineberg J, Posada JG. Polyomavirus-associated nephropathy in renal and simultaneous pancreas-kidney transplant recipients: Report of three cases. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2022 Dec 8];26:94-7. Available from: https://www.sjkdt.org/text.asp?2015/26/1/94/148750

   Introduction Top

Polyomavirus was first described by Gardner in 1971. [1] This virus has tropism for the urinary tract [2],[3] and can be present as latent infection in 30-40% of the cases [4],[5] or manifest itself with impaired renal function. [5],[6],[7] Polyomavirus infection in recipients of kidney or kidney pancreas has been an emerging entity causative of renal dysfunction and graft loss. [8],[9],[10],[11],[12] This paper aims to describe the cases of three patients, two of kidney transplant and one combined kidney- pancreas transplant, in whom polyomavirus infection was diagnosed and was confirmed by renal biopsy and immunohistochemistry. [13],[14]

Herein, the immunosuppressive treatment, management and renal graft outcome are described.

   Case Reports Top


A 59-year-old Colombian man with previous history of progressive membranous glomerulonephritis (GMNM), for which he received steroides and mycophenolate mofetil (MMF), until requiring hemodialysis. Dialysis was continued till he received a cadaveric renal transplantation on 26 August 2009. The initial immunosuppressive therapy was with Tacrolimus, MMF and prednisolone. Later on, at six months post transplant, the creatinine level increased from 1.06 to 3.7 mg/dL. A renal biopsy was performed [Figure 1], which showed 11 glomerulus with normal histology, blood vessels without alterations, multifocal inflammatory cell-infiltrated mesangium, tubules with lymphocytic inflammatory infiltrate and nucleomegaly with ground glass inclusions, immunohistochemistry that supports infection with polyomavirus (BK virus). Therefore, it was decided to discontinue MMF and the Tacrolimus doses were reduced with satisfactory improvement and with a reduction of the creatinine and, thereby, preserving graft function.
Figure 1: Immunohistochemistry in renal biopsy. The SV40-T antigen was positive on tubular epithelial cells. Formalin-fixed paraffinembedded tissue section, antibody-directed against the SV-40 T antigen (×400 original magnification).

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Case 2

Case 2 is a 30-year-old woman, Colombian, with previous history of systemic lupus erythematosus (SLE) for which she had received high-dose steroids. However, with uncontrolled lupus nephropathy that steadily progressed, she required hemodialysis and received kidney graft from a cadaveric donor on 10 June 2009. Immunosuppressive therapy was started with cyclosporine, MMF and prednisolone, with appropriate dose regulations on follow-up. At three months after transplantation, the creatinine levels increased from 1.4 to 1.8 mg/dL. A renal biopsy performed showed glomeruli with normal histology with tubular necrosis in 20% tubules but without evidence of tubulitis and lymphocytic inflammatory infiltrates in the interstitium. Characteristic nucleomegaly was observed and, additionally, immunohistochemistry performed was also consistent with infection by polyomavirus (BK virus). Immunohistochemistry for C4d was negative, which ruled out humoral rejection. Therefore, it was decided to discontinue cyclosporine A, to lower the doses of MMF and to initiate treatment with sirolimus (M-TOR inhibitor), which showed improvement in renal function with restoration of baseline creatinine.

Case 3

Case 3 is a 28-year-old Colombian man with diabetes mellitus type 1 and diabetic nephropathy with CKD stage 5 and initiated on renal replacement therapy who received simultaneous pancreas-kidney (SPK) transplant on 1 September 2007. Induction was performed with daclizumab and further immunosuppressive therapy with Tacrolimus, MMF and prednisolone, with normal graft function of both organs. Eighteen months later, he presented with blood urea nitrogen elevation and creatinine increased from 1.3 at baseline to 1.85 mg/dL. A renal biopsy was performed, which showed six glomeruli free of microthrombus without mesangiolysis. Twenty percent of the tubules were with tubular necrosis and without evidence of tubulitis and lymphocytic inflammatory infiltrate in the interstitium. Nucleomegaly with tubular epithelial damage from viral cytopathic effects was observed and immunohistochemistry was consistent with infection by polyomavirus (BK virus). It was decided to discontinue MMF and to reduce the dose of Tacrolimus with satisfactory outcome and reduction of the creatinine with normal kidney and pancreatic graft function.

   Discussion Top

Polyomavirus infection is reported to be the cause of renal graft dysfunction and graft loss up to approximately 50% of the cases. [4],[5],[6] The virus is acquired at an early age and is latent in 80% of the general population. It affects the urinary tract due to its specific tropism for the urinary system [3] and manifests with active infection in renal transplant patients due to the immunosuppressed state. The incidence is greater now with the advent of more potent immunosuppressive drugs and polyclonal or monoclonal antibodies, more often used for the induction of combined transplants as SPK. [2],[3],[4],[5],[6],[7],[8]

Awareness about polyomavirus infection in renal transplant patients or SPK is highly necessary and a great degree of suspicion about this diagnosis should be there when facing a renal transplant patient having graft dysfunction. This will help in on-time intervention that establishes the appropriate diagnosis, as its main differential diagnosis is acute humoral or cellular rejection [15] where the therapeutic intervention needed is exactly the opposite of the treatment for polyomavirus infection, which is to decrease immunosuppression. It has to be borne in mind that an early diagnosis is absolutely essential for better graft survival. [2],[11],[16]

In this paper, we describe three cases of patients who received kidney or simultaneous SPK who developed graft dysfunction. Renal biopsy showed histological findings suggestive of polyoma viral infection and immunohistochemistry confirmed the diagnosis. The time of infection after transplantation by BK virus was about six months, consistent with the reported literature. [17] While there is still no global consensus on the management of polyomavirus infection in renal transplant patients or SPK, by far the strongest evidence is to reduce the immunosuppression. [10],[11],[12] There are some reports where leflunomide (pyrimidine synthesis inhibitor) [18] or quinolones have been used for the prevention of infection by BK virus [19],[20] and may even play a role in the management of these patients. However, still, the preferred initial therapy is to decrease the dose of immunosuppressive medication [21] and withdraw the antiproliferative drugs. This has shown good results even in difficult cases, as in combined SPK where immunosuppression requirements are higher. It is seen that replacing calcineurin inhibitors by M-Tor inhibitors is also successful, [10],[22] as was seen in our second case. A high degree of suspicion and timely renal biopsy is essential for initiating early intervention.

   Acknowledgment Top

The authors would like to thank Dr. Andres Felipe Echeverri and Dra. Yaneth Aljure.

Conflict of interest: None

   References Top

Gardner SD, Field AM, Coleman DV, Hulme B. New human papovavirus (BK) isolated from urine after renal transplantation. Lancet 1971;1:1253-7.  Back to cited text no. 1
Rivero AM, Eiros J, Rodríguez A, Navarro JF. Emerging viruses in nephrology: polyomavirus. Nefrología 2002;22:414-24.  Back to cited text no. 2
Meehan SM, Kraus MD, Kadambi PV, Chang A. Nephron segment localization of polyoma virus large T antigen in renal allografts. Hum Pathol 2006;37:1400-6.  Back to cited text no. 3
Chester PM, Heritage J, McCance DJ. Persistence of DNA sequences of BK virus and JC virus in normal human tissue and diseased tissues. J Infect Dis 1983;147:676-84.  Back to cited text no. 4
Nickeleit V, Klimkait T, Binet IF, et al. Testing for Polyoma virus type BK DNA in plasma to identify renal-allograft recipients with viral nephropathy. N Engl J Med 2000;342:1309-15.  Back to cited text no. 5
Nickleit V, Milhatsch MJ. Polyoma virus nephropathy: Pathogenesis, morphological and clinical aspects. Verh Dtsch Ges Pathol 2004;88:69-84.  Back to cited text no. 6
Hirsch HH, Knowles W, Dickenmann M, et al. Prospective study of polyomavirus type BK replication and nephropathy in renal-transplant recipients. N Engl J Med 2002;347:488-96.  Back to cited text no. 7
Ison MG, Parker M, Stosor V, Kaufman DB. Development of BK nephropathy in recipients of simultaneous pancreas-kidney transplantation. Transplantation 2009;87:525-30.  Back to cited text no. 8
Bonvoisin C, Weekers L, Xhignesse P, Grosch S, Milicevic M, Krzesinski JM. Polyoma virus in renal transplantation: A hot problem. Transplantation 2008;85(7 Suppl):S42-8.  Back to cited text no. 9
Johnston O, Jaswal D, Gill JS, Doucette S, Fergusson DA, Knoll GA. Treatment of Polyomavirus Infection in Kidney Transplant Recipients: A Systematic Review. Transplantation 2010;89:1057-70.  Back to cited text no. 10
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. 11
Wiseman AC. Polyoma virus nephropathy: A current perspective and clinical considerations. Am J Kidney Dis 2009;54:131-42.  Back to cited text no. 12
Nickeleit V, Hirsch HH, Zeiler M, et al. BKvirus nephropathy in renal transplants-tubular necrosis, MHC-class II expression and rejection in a puzzling game. Nephrol Dial Transplant 2000;15:324-32.  Back to cited text no. 13
John R, Herzenberg AM. Our approach to a renal transplant biopsy. J Clin Pathol 2010;63:26-37.  Back to cited text no. 14
Ito Y, Nishi S, Imai N, et al. The case of BK virus infection in which it was difficult to differentiate from acute rejection. Clin Transplant 2011;25 Suppl 23:44-8.  Back to cited text no. 15
Randhawa P, Brennan DC. BK virus infection in transplant recipients: An overview and update. Am J Transplant 2006;6:2000-5.  Back to cited text no. 16
Hirsch HH, Steiger J. Polyomavirus BK. Lancet Infect Dis 2003;3:611-23.  Back to cited text no. 17
Geetha D, Sozio SM, Ghanta M, et al. Results of repeat renal transplantation after graft loss from BK virus nephropathy. Transplantation 2011;92:781-6.  Back to cited text no. 18
Sharma BN, Li R, Bernhoff E, Gutteberg TJ, Rinaldo CH. Fluoroquinolones inhibit human polyomavirus BK (BKV) replication in primary human kidney cells. Antiviral Res 2011;92:115-23.  Back to cited text no. 19
Gabardi S, Waikar SS, Martin S, et al. Evaluation of fluoroquinolones for the prevention of BK viremia after renal transplantation. Clin J Am Soc Nephrol 2010;5:1298-304.  Back to cited text no. 20
Derakhshan N, Derakhshan D, Torabinejad S, Derakhshan A. Nephritic-nephrotic syndrome as a presentation of BK virus infection. Saudi J Kidney Dis Transpl 2011;22:123-5.  Back to cited text no. 21
[PUBMED]  Medknow Journal  
Chon WJ, Josephson MA. Leflunomide in renal transplantation. Expert Rev Clin Immunol 2011;7:273-81.  Back to cited text no. 22

Correspondence Address:
Dr. Dahyana Cadavid
Division of Internal Medicine, Fundación Valle del Lili, Cali
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.148750

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