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pling error, particularly in kidney core biopsies. In stage B
a pattern of necroinflammatory injury is evident occurring
multifocally or diffusely. Nuclear inclusions are numerous,
they may be observed in tubular as well as Bowman capsule
epithelial cells. The inflammatory infiltrates include lymphocytes,
plasma cells and polymorphonuclears. The differential
diagnosis in such cases may sometimes be difficult. It
includes acute cellular rejection, other viral infections (particularly
CMV virus and Adenovirus) as well as tubular cells
nuclear pleomorphism occurring during regeneration after
acute tubular necrosis or recovery from acute cellular rejection.
In difficult cases immunomorphology should be used
with SV40 antibody. This antibody, originally developed for
SV40 virus, is useful because of above mentioned homology
of BK and SV40 viruses. „In situ” hybridization also may
be used for more precise diagnosis. In stage C diffuse, chronic
injury is seen with fibrosis and scarring of kidney parenchyma.
In this stage virus specific changes may be very focal
and again difficult to observe.
When PAN is diagnosed antiviral therapy should be
considered, but there are no specific drugs against BK virus.
In some cases therapy with cidofovir is helpful [3].
Little is known about PAN in children after kidney
transplantation but probably it occurs comparable to adults
[5, 6]. The aim of our study is to examine the prevalence of
PAN after KT in our, pediatric group of patients.
function injury (creatynine level was 5 mg%) and severe
pneumonia. As the patient did not improved after therapy
with antibiotics, the immunosuppression was stopped and nephrectomy
was decided. Macroscopically the kidney was enlarged
(12 × 7 × 6 cm) and firmed. Microscopically there were
changes in kidney cortex and medulla (Fig. 1). Numerous
nuclear inclusions of characteristic morphology were found
in tubular cells as well as in epithelium of Bowman capsule
of numerous glomeruli. The infected cells were also seen in
tubular lumina. Extensive inflammatory infiltrates were observed.
They consisted of lymphocytes, plasma cells and polymorphonuclears.
Interstitial oedema was also found. No
necrotic foci were observed. There were no morphological
signs of cellular vascular rejection (no arteritis). The number
of inflammatory cells (lymphocytes) not exceeded 4 per 10
tubular epithelium cells (pattern t1 according to Banff classification).
Reaction with SV40 antibody was strongly positive
in infected cells (Fig. 2). The pattern found was consistent
with stage B changes. It was found that in this patient
core kidney biopsy was performed 3 months earlier. Origi-
Material and methods
Patients
Retrospectively, 102 microscopic slides collected at the Department
of Pathology, the Children’s Memorial Health Institute.
Material including core biopsies and nephrectomy
specimens were obtained from 69 KT pediatric patients. All
biopsies were performed in 1997–2004 because of transplanted
organ injury. There were no protocol biopsies. In all patients
calcineurin inhibitors have been used as basic immunosuppression.
PAN diagnosis
PAN was primarily diagnosed with light microscopy from
HE slides. The diagnosis was confirmed by the immunohistochemical
method using SV40 T Ag antibody (Calbiochem).
Anti-mouse IgG labeled with biotin was used as the
secondary antibody (Vector). The reaction was visualized by
Vectastatin ABC kit (Vector) and AEC substrate chromogen
(Dakocytomation).
Fig. 1 PAN – Stage B pattern in transplanted kidney. Numerous nuclear
inclusions in tubular epithelium as well as inflammatory infiltrates. HE 200×
Results
PAN was microscopically diagnosed in 2 out of 69 patients
(2,9%).
Case 1
In the first patient (6 year old girl) the diagnosis was established
from the nephrectomy specimen. The operation was
performed 12 months after KT in the patient with allograft
Fig. 2 PAN in transplanted kidney. Numerous cells are positive vith SV40
antibody. 100×