BK polyomavirus nephropathy in two kidney transplant patients with distinct diagnostic strategies for BK virus and similar clinical outcomes: two case reports

Abstract

BackgroundBK polyomavirus-associated nephropathy is an important cause of post-transplantation renal failure. We present two cases of BK polyomavirus-associated nephropathy who were submitted to contrasting strategies of clinical follow-up to BK polyomavirus reactivation, but progressed to a similar final outcome.Case presentationCase 1 is a 37-year-old white man whose graft had never presented a good glomerular filtration rate function, with episodes of tacrolimus nephrotoxicity, and no urinary monitoring for BK polyomavirus; stage B BK polyomavirus-associated nephropathy was diagnosed by biopsy at 14 months post-transplant. Despite clinical treatment (dosage decrease and immunosuppressive drug change), he progressed to stage C BK polyomavirus-associated nephropathy and loss of graft function 30 months post-transplant. Case 2 is a 49-year-old mulatto man in his second renal transplantation who was submitted to cytological urinary monitoring for BK polyomavirus; he presented early, persistent, and massive urinary decoy cell shedding and concomitant tacrolimus nephrotoxicity. Even with decreasing immunosuppression, he developed BK polyomavirus-associated nephropathy 1-year post-transplant. Loss of graft function occurred 15 months post-transplant.ConclusionsCytological urinary monitoring was an efficient strategy for monitoring BK virus reactivation. Decoy cell shedding may be related to BK polyomavirus-associated nephropathy when extensive and persistent. The presence of associated tacrolimus nephrotoxicity may be a confounding factor for the clinical diagnosis of BK polyomavirus-associated nephropathy.

Kidney graft failure induced by BKPyV replication despite a strong reduction of the immunosuppressive therapy

“…In our study, the finding of a NCCR identical to the prototypic NCCR BKPyV strain, both in plasma and in urine samples, suggested that other factors, such as the immune‐competence of the host and the level of immunosuppression might have had a role in determining the poor outcome of PyVAN. The attempt to significantly reduce the level of immunosuppression as indicated by the immediate, complete weaning of Mycophenolic acid, and gradual tapering and subsequent weaning of Tacrolimus failed.…”

“…Reactivation can occur in the context of an immunosuppression state after kidney transplantation. BKPyV replication within the renal epithelial tubular cells causes inflammation that can progress to polyomavirus‐associated nephropathy (PyVAN) and eventually graft loss . The present study describes the case of a kidney transplant patient who developed 7 months after transplant a PyVAN because of a high replication rate of BKPyV that brought to kidney failure.…”

BKV Related Hemorrhagic Cystitis—An Insight into Risk Factors and Later Complications—An Analysis on Behalf of Polish Adult Leukemia Group

“…When the BK virus reactivates in immunocompromised hosts (such as HCT or solid organ transplant recipients) or immunocompromised (such as AIDS patients), it can lead to severe clinical diseases. For example, BKV reactivation can lead to polyomavirus-associated nephropathy in kidney transplant patients [4,5]. Additionally, BKV reactivation may result in renal failure and allograft failure in kidney transplant patients.…”

Merkel cell polyomavirus and its etiological relationship with skin tumors

“…About 10% of kidney transplant patients develop BKPyV-associated nephropathy, with loss of graft function in up to 50% of the cases. 23 …”