BK Polyomavirus in Solid Organ Transplantation

Abstract

The human BK polyomavirus (BKV) is the major cause of polyomavirus-associated nephropathy (Py-VAN) putting 1-15% of kidney transplant patients at risk of premature allograft failure, but is less common in other solid organ transplants. Because effective antiviral therapies are lacking, screening kidney transplant patients for BKV replication in urine and blood has become the key recommendation to guide the reduction of immunosuppression in patients with BKV viremia. This intervention allows for expanding BKV-specific cellular immune responses, curtailing of BKV replication in the graft, and clearance of BKV viremia in 70-90% patients. Postintervention rejection episodes occur in 8-12%, most of which are corticosteroid responsive. Late diagnosis is faced with irreversible functional decline, poor treatment response, and graft loss. Adjunct therapies such as cidofovir, leflunomide and intravenous immunoglobulins have been used, but the benefit is not documented in trials. Retransplantation after PyVAN is largely successful, but requires close monitoring for recurrent BKV viremia.

Pretransplantation Donor–Recipient Pair Seroreactivity Against BK Polyomavirus Predicts Viremia and Nephropathy After Kidney Transplantation

“…Disease Community of Practice guideline (38). The added value of our study lies particularly in the integrated evaluation of this serological marker among donor-recipient pairs because this provides leads for future algorithms to predict BKPyV-related disease after transplantation.…”

Potential Impact of Microarray Diagnosis of T Cell–Mediated Rejection in Kidney Transplants: The INTERCOM Study

“…Polyoma virus nephropathy (PVN), which had not been recognized in 1991, renders TCMR lesions of uncertain significance (15), and the 1991 criteria must now be interpreted in biopsies with more aging, injury and scarring. This ''data drift''-a shift in disease prevalence and prior probabilities within the target population-is a common occurrence in epidemiological studies, and is to be expected in a diagnostic system in use for over two decades.…”

Analysis of diagnostic methods as a screening test to detect BK virus nephropathy in kidney transplant patients

“…Negative urine NAT for BKPyV has almost 100% NPV but patients with BKPyV viruria exceeding established thresholds should be tested additionally by NAT on the blood. 1,2 NAT in urine, in the absence of an elevated BKPyV plasma load is not associated with an increased risk for BKPyVAN. Pinto et al 7 concluded that positive BKPyV in two or more urine samples was helpful to predict BKPyV viremia with 100% sensitivity, 94% specificity and a PPV of 50% and NPV of 100%.…”

“…1,6 Currently, available screening tests include: urine cytology to identify virally loaded epithelial cells (also named "decoy cells"), quantitative nucleic acid amplification testing (NAT) by polymerase chain reaction (PCR) to identify BKPyV in urine or plasma or blood samples, or urine electronic microscopy to detect three-dimensional viral aggregates (Haufen). that directly compared the analytical performance of screening methods to predict the diagnosis of BKPyVAN proven by histopathology.…”

“…1 BKPyV is acquired in childhood and persists latent in the urinary tract until its reactivation in the immunosuppression state. The nephropathy is a consequence of BKPyV reactivation in the urinary tract of the donor kidney/ureter with subsequent viremia and invasion of the virus in the graft causing viral cytopathic changes, inflammatory response and functional deterioration.…”