Background: JC virus (JCV) inflection is more common than BK virus (BKV) in general population. But in kidney transplants, polyomavirus nephropathy (PVAN) is primarily caused by BKV. Few cases of PVAN have been attributed to JCV. Systematic studies on the characteristics of JC virus-associated nephropathy (JCVAN) are lacking. Therefore, we summarize 4 cases of JCVAN in renal transplant recipients, which were diagnosed in our center in recent 10 years.

Methods: 183 cases of PVAN from 2006 to 2017 were diagnosed in our center. 4 cases of JCVAN were diagnosed through the negative BKV but high JCV load in urine and blood, and positive SV40T in the biopsy samples. Meanwhile, clinical-pathological data were collected.

Results: At diagnosis (85.8±43.1months after transplantation), the median level of urinary decoy cells and JC viruria were 5 /10HPF, 4.65[times]10^8copy/ml, respectively, only one JC viremia was positive with 327 copy /ml. The mean level of serum creatinine (Scr) and 24-hour urinary protein was 147[mu]mol/L and 1g. Immunohistochemistry showed SV40T positive region of the 4 cases were all in the renal medulla. 2 of the 4 cases combined IgA nephropathy and 1 of the 4 cases combined with antibody mediated rejection. In the latest follow-up, 1 of the 4 transplant was dysfunctional due to IgA nephropathy with 13y of graft survival time while the others were in good function, the mean level of Scr was 134[mu]mol/L.

Conclusions: What is different from BK virus-associated nephropathy is that most of the JCVAN are diagnosed in the late after kidney transplantation, the level of serum creatinine is not so high, viremia is very rare, viral induced injury is not so significant. The overall prognosis is relatively good.

CITATION INFORMATION: Huang G., Wang M., Chen X., Yang S-.C., Chen L. JC Virus-Associated Nephropathy in Renal Transplant Recipient Am J Transplant. 2017;17 (suppl 3).

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