| Abstract|| |
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 2019 Aug 19];22:123-5. Available from: http://www.sjkdt.org/text.asp?2011/22/1/123/74382
| Introduction|| |
BK virus (BKV) and JC virus, the two human polyomaviruses, were concurrently reported in 1971.  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.  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.  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.  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|| |
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|| |
Polyomavirus BK (BKV) infection has been lately recognized as a major cause of renal allograft dysfunction.  The prevalence of BKV induced nephropathy is estimated to be 1-10%, with a mean of approximately 5%. ,, 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.  Reduction of immunosuppressive therapy is considered the main point in treatment. However, other treatment options are available now. , 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.  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. 
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|| |
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71937-Pediatric Section, Nemazi Hospital, Shiraz