Abstract
Recent advances in immunosuppressive therapy have reduced the incidence of acute rejection and improved renal transplantation outcomes. Meanwhile, nephropathy caused by BK virus has become an important cause of acute or chronic graft dysfunction. The usual progression of infection begins with BK viruria and progresses to BK viremia, leading to BK virus associated nephropathy. To detect early signs of BK virus proliferation before the development of nephropathy, several screening tests are used including urinary cytology and urinary and plasma PCR. A definitive diagnosis of BK virus associated nephropathy can be achieved only histologically, typically by detecting tubulointerstitial inflammation associated with basophilic intranuclear inclusions in tubular and/or Bowman’s epithelial cells, in addition to immunostaining with anti-Simian virus 40 large T-antigen. Several pathological classifications have been proposed to categorize the severity of the disease to allow treatment strategies to be determined and treatment success to be predicted. Since no specific drugs that directly suppress the proliferation of BKV are available, the main therapeutic approach is the reduction of immunosuppressive drugs. The diagnosis of subsequent acute rejection, the definition of remission, the protocol of resuming immunosuppression, and long-term follow-up remain controversial.
Highlights
This review summarizes the recent management of BKV associated nephropathy (BKVAN) after renal transplantation
Since BK virus (BKV) replicates focally in the kidneys, allograft biopsy may sometimes miss the characteristic histological findings of BKVAN, especially when needle biopsies are taken during the early phase of disease or there is a lack of medullary tissue [78]
BK viremia-positive patients who have multiple biopsy cores collected at the same time, not all biopsy cores show the BKVAN pathology; this is seen in approximately 30% of cases [79]
Summary
The survival of transplanted kidney grafts has improved with the development of novel immunosuppressive therapies. Under the strong immunosuppression after renal transplantation, latent polyomavirus reactivates in the kidney, causing lytic destruction of renal tubular epithelial cells, and resulting in tubular fluid accumulation in the interstitial compartment, which is characterized by an inflammatory interstitial nephropathy, associated with functional impairment due to tubular fibrosis and atrophy [7]. Regular screening for BKV replication by quantitative PCR and pre-emptive reduction of immunosuppression in viremic patients have become common among kidney transplant centers, resulting in a decreased prevalence of biopsy-proven BKVAN [8]. Reduce immunosuppressive drugs, since BKV-specific anti-viral therapy is not yet available. A reduction in immunosuppressive drugs can lead to immunological rejection and these treatment failures can lead to transplanted kidney loss. This review summarizes the recent management of BKVAN after renal transplantation
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