Abstract
BK polyomavirus nephropathy (BKVN) and allograft rejection are two closely-associated diseases on opposite ends of the immune scale in kidney transplant recipients. The principle of balancing the immune system remains the mainstay of therapeutic strategy. While patient outcomes can be improved through screening, risk factors identification, and rapid reduction of immunosuppressants, a lack of standard curative therapy is the primary concern during clinical practice. Additionally, difficulty in pathological differential diagnosis and clinicopathology’s dissociation pose problems for a definite diagnosis. This article discusses the delicate evaluation needed to optimize immunosuppression and reviews recent advances in molecular diagnosis and immunological therapy for BKVN patients. New biomarkers for BKVN diagnosis are under development. For example, measurement of virus-specific T cell level may play a role in steering immunosuppressants. The development of cellular therapy may provide prevention, even a cure, for BKVN, a complex post-transplant complication.
Highlights
BK polyomavirus nephropathy (BKVN) and allograft rejection are two significant post-transplant complications on opposite ends of the immune spectrum (Figure 1)
BK-specific T cell response was noted in the viremia-resolved group, while the response was only noted after reduced IS in the developed BKVN group [28,31]
The primary endpoint showed de novo donor-specific antibody (dnDSA) development was associated with worse graft survival (p < 0.001), while tacrolimus intra-patient variability (IPV) was associated with dnDSA development (p = 0.002)
Summary
BK polyomavirus nephropathy (BKVN) and allograft rejection are two significant post-transplant complications on opposite ends of the immune spectrum (Figure 1). BKVN and rejection are both prominent causes of kidney damage, renal function 3 years after diagnosis was worse for BKVN than for rejection [1]. The leading cause of BKVN is over-immunosuppression that reactivated the latent BK polyomavirus (BKPyV) within the recipient or reinforced BKPyV infection inside the allograft. Diagnosis based on onset time and clinical manifestation is difficult due to similar clinical presentation of graft rejection and BKVN. This article discusses the evaluations needed for optimal immunosuppression to avoid infection or reactivation of the BKPyV in kidney transplant recipients (KTRs). In the case of confirmed BKPyV infection, control of the disease progression to preserve the graft function is reviewed
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