JC virus‐associated nephropathy in a renal transplant recipient and comparative analysis of previous cases

Abstract

We report JC virus (JCV)-associated nephropathy in a renal allograft recipient and summarize the clinical and laboratory data of the 8 previous cases. A 28-year-old male renal allograft recipient received a preemptive transplant from his father. Six months later, a kidney biopsy was performed because of deterioration of allograft function. Biopsy revealed tubulointerstitial mononuclear infiltrates with normal glomeruli; on hematoxylin and eosin staining, basophilic nuclear inclusions were seen in the nucleus of tubular cells. Urinary cytology failed to demonstrate decoy cells, but polymerase chain reaction of a urinary sample was positive for JCV 3.15 × 10(10) copies/mL. Additionally, polyomavirus (SV40) immunohistochemical staining was performed and was positive in the enlarged nuclei of tubular epithelial cells in the kidney biopsy sample. After the diagnosis of polyomavirus-associated nephropathy (PVAN) was confirmed by kidney biopsy, immunosuppressive agents were reduced. Intravenous immunoglobulin was administered 5 times at a dose of 500 mg/kg every other 3 weeks. Two months after diagnosis, the serum creatinine became stable and urinary viral load of JCV was decreased. Because viruria was still present, tacrolimus was converted to sirolimus. Four months after immunosuppressive agent conversion from tacrolimus to sirolimus, the viruria had disappeared. Review of the literature and our case demonstrates that male gender, previous acute rejection episode, low incidence of JCV viremia, PVAN pattern B histology, and reducing immunosuppression are the diagnostic touchstones for PVAN due to JCV.

A Review on JC Virus Infection in Kidney Transplant Recipients

“…PyVAN with graft dysfunction and premature graft loss has been markedly increased since the 1990s [53, 54]; therefore, a pathogenic potential of JCV should be taken into account. In contrast to the closely related BKV, to date, only few cases of nephropathy have been attributed to JCV [55–59]. Low level of JCV replication and shedding are common in immunocompetent individuals [60, 61] but surprisingly the incidence of asymptomatic viruria is not increased in renal allograft recipients [62, 63].…”

Molecular Characterization of BK and JC Viruses Circulating among Potential Kidney Donors in Kuwait

“…While viruria is generally considered to be insignificant, viremia and nephropathy trigger reduction in immunosuppression and antiviral therapy [4–6]. In addition to BKV, JC virus (JCV) has also been shown to be involved in the development of nephropathy [7, 8]. JCV establishes latency in the kidney and B lymphocytes, and it is associated with the development of progressive multifocal leukoencephalopathy (PML) in immunocompromised individuals, usually those with acquired immune deficiency syndrome (AIDS) [9].…”

Rapid reduction of viruria and stabilization of allograft function by fusidic acid in a renal transplant recipient with JC virus-associated nephropathy

“…JCV-associated nephropathy, in addition to BKV-associated nephropathy, has been increasingly recognized as a cause of allograft dysfunction with graft loss in renal transplant recipients in the past decade [3][4][5]14]. Risk factors include male gender, acute rejection episodes, the use of antithymocyte globulin, and immunosuppressive regimen comprising tacrolimus with mycophenolate mofetil [14].…”

“…Risk factors include male gender, acute rejection episodes, the use of antithymocyte globulin, and immunosuppressive regimen comprising tacrolimus with mycophenolate mofetil [14]. Clinically, polyomavirus-associated nephropathy is characterized by acute deterioration of renal allograft function and lack of treatment response to escalated dosages of immunosuppressive drugs and surgical removal of obstructive lesions [14]. Non-histological diagnostic clues include the presence of decoy cells and a high JCV or BKV DNA load in urine.…”