Case series reveals diverse presentations of PVN in renal transplant recipients, impacting management strategies.
Polyomavirus nephropathy (PVN) is a major cause of renal allograft dysfunction, and balancing immunosuppression remains the mainstay of therapy. However, PVN has varied clinical and histopathological presentations, complicating its assessment and management. Here, we present four unusual cases in allograft recipients following renal transplantation. The first case is that of a 21-year-old woman with no preceding detectable viruria or viremia who developed concurrent PVN and recurrent immunoglobulin A nephropathy. The second case involves a 30-year-old man with a lower respiratory tract infection who subsequently developed PVN with concurrent chronic active antibody-mediated rejection. The third case concerns a 32-year-old man who developed focal sclerosing and crescentic glomerulonephritis with concurrent PVN. Finally, the fourth case involves PVN-induced crescentic glomerulonephritis and C4d deposition (C4d=2) in a 34-year-old man with hypertension; simian virus 40 (SV40) displayed positivity in glomerular crescents, while C4d showed additional deposition along the tubular basement membrane. In all of the above cases, histological confirmation by renal biopsy-demonstrating viral cytopathic changes and SV40 nuclear positivity in the tubules-was considered the gold standard for PVN diagnosis. PVN may induce crescents or C4d deposition, or it may coexist with rejection. Accurate diagnosis across these scenarios is imperative to guide appropriate immunomodulation.
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Sarwala et al. (2026) studied this question.
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