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POLYOMAVIRUS ASSOCIATED NEPHROPATHY STAGING, PATTERNS AND VIRAL LOAD:
EXPERIENCE FROM ONE PATHOLOGY UNIT WITH PROTOCOL BIOPSIES
S. Şen1, B. Sarsık1, E. Tatar2, A Zeytinoğlu3, H. Töz2
Departments of Pathology1, Nephrology2, and Microbiology3,
Ege University, School of Medicine, İzmir, Turkey
Objectives: Infection of BK virus can lead to polyomavirus associated nephropathy (PVAN) and graft
failure in renal transplant recipients. Thus effective management of these patients requires early detection
of the virus. Detailed histopathological features of PVAN were described, and consensus on staging is still
evolving.
Methods: All records of renal transplant biopsies reported our pathology center from 2006 to 2011 was
searched for patients diagnosed as PVAN. PVAN biopsies were reevaluated for biopsy adequacy, PVAN
Drachenberg patterns, stages and histologic virus load levels (Banff 2011 draft) and clinical indications.
PVAN was diagnosed amorphous basophilic or amphophilic intranuclear inclusions of the cells, with
positive immunohistochemistry for SV40 T antigen (Calbiochem, DP02). Other histopathological details
including Banff scores were also recorded. The clinical records of the adult patients for demographic,
clinical, and laboratory data were reviewed.
Results: During the study period 2180 allograft biopsy materials including implantation, protocol indication
and second opinion biopsies and transplant nephrectomies were reported. Total 37 PVAN biopsy reports
from 26 patients were found and reevaluated. Patterns of PVAN were evaluated as 11%,and 89% (B1:
27%, B2: 30% and B3: 32%) respectively, for pattern A and B. Banff stages of PVAN were defined as
51%, 46% and 3% respectively, for stage A, B, and C. Banff polyomavirus load levels (pvl) were
diagnosed as 19%, 65% and 16% respectively, for pvl.1, pvl.2 and pvl.3. PVAN was diagnosed nearly
cortical biopsies on the majority of the biopsies (%65).
During the study period a total 422 new renal transplantations were made. Adult 19 PVAN positive
patients (27 positive biopsies) were followed our adult transplantation unit. PVAN was first diagnosed on
the majority of protocol biopsies (53%). Follow-up biopsies were available on 13 adult patients. PVAN
persisted in 8 biopsies from 5 patients. Finally SV40 stain became negative in after lowering of
immunosuppression, biopsies from 10 patients. Two transplant losses occurred related C4d positive
humoral rejection within one year (10,5%).
Conclusions: Protocol biopsies may allow diagnosing of the PVAN before the occurrence of renal
allograft dysfunction. Outcome is good although the persistent PVAN biopsies are observed in some
patients. In our series graft losses related humoral rejection were occurred.