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Annals of Diagnostic Paediatric Pathology 2006, 10(1–2):13–15
© Copyright by Polish Paediatric Pathology Society Annals of
Polyoma BK virus nephropathy in children after kidney
transplantation
Przemys³aw Kluge 1 , Ewa Œmirska 2 , Sylwester Prokurat 2 , Agnieszka Perkowska 3 ,
Bo¿ena Cukrowska 1
Diagnostic
Paediatric
Pathology
1
Department of Pathology
2
Department of Nephrology, Kidney Transplantation and Arterial Hypertension
The Children's Memorial Health Institute
Warsaw, Poland
3
Institute of Transplantology Medical University
Warsaw, Poland
Abstract
Polyoma BK virus nephropathy in transplanted kidney may lead to premature graft failure in up to 10% of
adult patients. In children there are only very few data from the literature on this problem. We examined
retrospectively the material (kidney biopsies and nephrectomy specimens) collected at the Department of
Pathology, the Children’s Memorial Health Institute from 1997–2004. Two out of 69 patients developed
Polyoma BK virus associated nephropathy (2,9%). In one of them virus caused injury resulted in graft lost.
Key words: children, kidney transplantation, nephropathy, polyoma BK virus
Introduction
Polyomavirus hominis type 1, known also as BK virus represents
a family of DNA viruses. BK virus genome shares a homology
with other viruses of the family: JC virus and SV40
virus [3]. This homology has important implications for some
diagnostic procedures. Primary BK virus infection occurs
during childhood and about 75% of adults are seropositive.
The humoral response results in production of antibodies in
various classes of immunoglobulins. In a host with normal
immunity the infection has a clinically indolent course,
which is subclinical or with slight flu-like symptoms [3].
After primary infection virus particles persist mainly in epithelial
cells of urinary tract including kidneys.
The clinical course is different in immunocompromised
patients [1, 3]. In both inherited and secondary immune
dysfunctions previously „silent” virus undergoes reactivation.
In some patients this results in an injury of infected organs,
viremia and sometimes generalized disease. In practice
BK virus caused organ injury is mainly observed in transplanted
kidneys. In up to 10% of adult patients after kidney
replacement Polyoma BK virus associated nephropathy
(PAN) occurs, sometimes leading to graft failure [1, 3]. The
prevalence of PAN seems to become more and more frequent,
probably because of using modern, potent immunosuppressive
drugs.
According to data from the literature PAN was diagnosed
6–270 weeks after kidney transplantation (KT) – average
44 weeks. In retrospective studies PAN was associated
with graft failure in 10–100% patients after 12–240 weeks of
follow up [3]. In morphological picture kidney injury consist
of necroinflammatory damage of tubules with occurrence of
characteristic nuclear inclusions containing virus particles
[1–4]. This damage, in some patients, subsequently results in
irreversible scarring of renal parenchyma and organ lost.
To classify a morphological pattern of PAN a 3-step
system is proposed [1, 3]. In stage (or pattern) A there is only
focal involvement of tubular medullar epithelium. Nuclear
inclusion and inflammatory cells are not numerous. In this
stage a false-negative diagnosis is probable because of sam-
Address for correspondence
Przemys³aw Kluge, MD Fax: + 48 22 815 19 75
Department of Pathology
The Children’s Memorial Health Institute
Aleja Dzieci Polskich 20
04-730 Warsaw, Poland