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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2011  |  Volume : 22  |  Issue : 1  |  Page : 123-125
Nephritic-nephrotic syndrome as a presentation of BK virus infection

Shiraz Nephro-Urology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran

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Date of Web Publication30-Dec-2010


BK virus (BKV) is increasingly found as an important cause of allograft nephro­pathy. Nephrotic syndrome is not a usual manifestation of BKV nephropathy. Here, we report a 12­year-old boy, a case of end-stage renal disease due to nephronophthisis, who got the kidney trans­planted from a 16-year-old cadaver, and after 18 months of uneventful transplantation on triple immunosuppressive therapy (Mycophenolate mofetil (MMF), cyclosporin and prednisolone), pre­sented with nephrotic feature (edema, heavy proteinuria, hypoalbuminemia and hyperlipidema). Kidney biopsy was in favor of BKV infection and eventually ended in graft failure.

How to cite this article:
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

How to cite this URL:
Derakhshan N, Derakhshan D, Torabinejad S, Derakhshan A. Nephritic-nephrotic syndrome as a presentation of BK virus infection. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2021 Jun 21];22:123-5. Available from: https://www.sjkdt.org/text.asp?2011/22/1/123/74382

   Introduction Top

BK virus (BKV) and JC virus, the two human polyomaviruses, were concurrently reported in 1971. [1] They are small, double-stranded DNA vi­ruses of the papovaviridae family and 60-80% of the general population are seropositive for this virus. Although the human polyomaviruses are highly seroprevalent in humans, they appear to cause clinical disease only among immuno­compromised patients. The major diseases caused by BKV are tubulointerstitial nephritis and ure­teral stenosis in renal transplant recipients and hemorrhagic cystitis in bone marrow transplant recipients. [2] In a study of candidates for kidney transplantation, 33.3% of patients with chronic kidney disease were positive for BKV and 33.3% were positive for JC virus. [3] Polyomavirus asso­ciated nephropathy has appeared as an impor­tant cause of renal failure in pediatric and adult kidney recipients and 30-50% of diagnosed ca­ses will lose the graft eventually. BKV associa­ted nephropathy is also seen in native kidneys of other solid organ recipients. [4] In this case re­port, we describe our experience with a case of pediatric transplant that presented with neph­rotic syndrome and his transplanted kidney biopsy revealed inclusion bodies in favor of BKV infection.

   Case Report Top

A 12-year-old boy, a case of end-stage renal disease (ESRD) due to nephronophthisis, re­ceived kidney graft from a 16-year-old cada­veric donor, 6 months after initiation of hemo­dialysis. He had an uneventful transplantation course, and was on triple immunosuppressive regimen (MMF, cyclosporine and prednisolone) for 18 months, with normal renal function. His latest clinical and laboratory findings, one month before his presentation, were as follows: weight 44 kg, height 150 cm, blood pressure 120/75 mmHg, prednisolone 5 mg every other day, cellcept 750 mg twice/day, cyclosporine dose 5 mg/kg, cyclosporine level (c0 110 ng/mL), serum creatinine 0.9 mg/dL and normal lipid profile and urinalysis. One month later, he sud­denly developed periorbital edema that became generalized within a few days. At this time, his weight was 52 kg, blood pressure 160/100 mmHg, ascites, scrotal edema and pitting edema of lower extremities. His serum albumin was 2.3 g/dL, blood urea nitrogen 40 mg/dL, serum creatinine 2.5 mg/dL, serum triglyceride 490 mg/dL, serum cholesterol 410 mg/dL and 24 hour urine protein was 4200 mg. Serum com­plement levels (c3, c4) were normal. He had an enlarged and tender graft with increased paren­chymal echogenicity and resistive index. At first, clinical diagnosis of de novo glomeruloneph­ritis was made but kidney biopsy revealed ede­matous interstitium with marked mononuclear infiltration and tubular cells containing typical viral intranuclear hyperchromatic inclusions in favor of BKV. Reduction of immunosuppres­sive dose and IVIG (high dose intravenous im­munoglobin) administration was ineffective and he had progressive loss of graft function and became dialysis-dependent within three weeks.

   Discussion Top

Polyomavirus BK (BKV) infection has been lately recognized as a major cause of renal allo­graft dysfunction. [5] The prevalence of BKV in­duced nephropathy is estimated to be 1-10%, with a mean of approximately 5%. [4],[5],[6] Aggressive immunosupressive therapy is considered the main risk factor for BKV nephropathy, but no specific immunosuppressive drug is exclusively associated with polyomavirus associated neph­ropathy, even though most cases reported to date arise while the patient is on triple immuno­suppressive combinations, often comprising tac­rolimus and/or mycophenolate mofetil plus cor­ticosteroids. [6] Reduction of immunosuppressive therapy is considered the main point in treatment. However, other treatment options are available now. [6],[7] The diagnosis of BKV nephropathy is suspected clinically and supported by polymerase chain reaction (PCR) and definitive diagnosis of BK-induced nephropathy is by specific findings with allograft biopsy, particularly results with immunohistochemical staining and/or ultrastructural examination of the specimen by electron microscopy. A 2005 consensus conference also stated that a definitive diag­nosis requires an allograft biopsy. [6] There is a similar case in literature, reported with nephrotic syndrome after lung transplantation with sequences of SV40 (but not BK or JC virus) in the patient's kidney biopsy and urine by PCR. [8]

In conclusion, although we had not done immunohistochemical staining and PCR study, pre­sence of inclusions in tubular cells was highly suggestive of BKV nephropathy presenting as nephritic syndrome.

   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(7712):1253-7  Back to cited text no. 1
2.Reploeg MD, Storch GA, Clifford DB. BK virus: a clinical review. Clin Infect Dis 2001; 33:191.  Back to cited text no. 2
3.Kaneko T, Moriyama T, Tsubakihara Y, Horio M, Imai E. Prevalence of human polyoma virus (BK virus and JC virus) infection in patients with chronic renal disease. Clin Exp Nephrol 2005;9:132-7.  Back to cited text no. 3
4.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(3):324-32.  Back to cited text no. 4
5.Ginevri F, Azzi A, Botti G, Comoli P. Polyomavirus BK-associated nephropathy after kidney transplantation. G Ital Nefrol 2006;23 (6):575-84  Back to cited text no. 5
6.Hirsch HH, Brennan DC, Drachenberg CB, et al. Polyomavirus-associated nephropathy in renal transplantation: interdisciplinary analyses and recommendations. Transplantation 2005;79:1277.  Back to cited text no. 6
7.Casadei DH, del C Rial M, Opelz G, et al. A randomized and prospective study comparing treatment with high-dose intravenous immuno­globulin with monoclonal antibodies for rescue of kidney grafts with steroid-resistant rejection. Transplantation 2001;71:53.  Back to cited text no. 7
8.Milstone A, Vilchez RA, Geiger X, Fogo AB, Butel JS, Dummer S. Polyoma virus simian virus 40 infection associated with nephropathy in a lung-transplant recipient. Transplantation 2004;77(7):1019-24.  Back to cited text no. 8

Correspondence Address:
Nima Derakhshan
71937-Pediatric Section, Nemazi Hospital, Shiraz
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PMID: 21196627

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