*Purpose: JC virus(JCV) is a member of the Polyomaviridae family. Few studies have been published regarding the replication of JCV in transplant recipients. The incidence of JCV allograft nephropathy (JCVAN) has been been reported to be 0.9%. Most cases were diagnosed early post-transplant. The clinical course of late occurring JCVAN is not well studied. We describe two cases of JCVAN occurring beyond 2 years after transplant and the clinical course.

*Methods: We reviewed two cases of kidney transplant recipients diagnosed with biopsy proven Polyoma virus associated allograft nephropathy (PVAN) due to JCV.

*Results: CASE 1: 67-year-old Polish male with ESRD due to hypertensive nephrosclerosis on hemodialysis for 6 years and peritoneal dialysis for 1 year, underwent a deceased donor kidney transplant in 4/2014. His post-operative course was complicated by nephrolithiasis that required a nephrostomy tube. In 11/2017, he developed acute kidney injury(AKI) with creatinine of 2.1 mg/dl. Renal allograft biopsy showed PVAN. His immunosuppression consisted of Astagraf and Myfortic. His Myfortic dose was reduced. Blood BK virus PCR was not detected. Blood JCV PCR was 270,000 copies/ml and urine JCV PCR ws 338,000 copies/ml.His Astagraf dose was reduced to maintain a trough of 3-5 ng/ml. His Myfortic was subsequently stopped. Prednisone 10 mg daily was added. 11 months post followup his Blood JCV PCR is at 2,100 copies/ml and creatinine remains 1.91 mg/dl.CASE 2: 48-year-old Filipino male with a history of polycystic kidney disease underwent deceased donor kidney transplant in November 2003 with stable good kidney function on maintainance tacrolimus and mycophenolate mofetil (MMF). He underwent a renal allograft biopsy in 6/2017 to evaluate AKI, microscopic hematuria and albuminuria. The biopsy showed PVAN. Blood BK virus PCR was undetectable. Blood JCV PCR 600 copies/ml and urine JCV PCR 14 million copies/ml. Tacrolimus dose was adjusted to keep trough between 3 and 5ng/ml and MMF reduced to 500mg BID. Blood JCV PCR continued to increase to 4,200 copies/ml and urine JCV PCR 24 millions copies/ml in 1/2018. MMF was stopped. Prednisone 7.5 mg daily was added and tacrolimus dose was adjusted to maintain a trough level between 2 and 5 ng/ml. Blood JCV PCR decreased to 282 copies/ml and urine JCV PCR 6.3 million copies/ml in 6/2018. Due to worsening renal function: creatinine 1.66mg/dl in 7/2018, renal allograft biopsy was done, showing persistent PVAN. With rising blood JCV PCR to 1,000 copies/ml, IVIG 2g/kg was given in 8/2018. Creatinine improved to 1.4-1.5 mg/dl and JCV PCR decreased to 700 and urine JCV PCR to 354,000 copies/ml in 11/2018.

*Conclusions: JCVAN is an uncommon cause of late-onset AKI in kidney transplant recipients. Reduction in immunosuppression remains the mainstay of management of JCVAN. IVIG can be an adjunctive treatment. Renal function appears stable in the short term despite persistent JCV viremia and viruria, and persistent JCVAN. This may suggest an indolent course of JCVAN. Long-term follow up will better define the natural course of JCVAN.

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