The above case also shows mild intimal arteritis (v1) in addition to BK virus infection.  BK virus infection also causes tubulitis, indistinguishable from acute T-cell-mediated rejection. But the endoarteritis is the strong evidence of acute T-cell-mediated rejection. I learned from consultation cases that some transplant pathologist takes the extent of tubulitis into consideration.  In their report, it states that " Interpretation of the tubulointerstitial nephritis in the setting of BK nephropathy is problematic.  The tubular epithelial cells with BK virus infection, which are highlighted by immunohistochemical stains for SV-40, only exist in some tubules.  However, the tubulitis is more diffuse, involving the tubules without positive BK virus stains. This raises the possibility of co-existing acute cellular rejection.  Clinical judgment and close follow up are suggested."

Can acute T-cell-mediated rejection co-exist with BK virus infection? The answer is YES. The problem is how to diagnose these conditions. If we only depend on arteritis to diagnose co-existing acute rejection, probably we underdiagnose the co-existing acute rejection.

There are protocols to treat BK virus infection with acute rejection. One of the protocols is that nephrologist will first bolus the patient with steroids and then do the reduction.  The above patient was treated in this way and improved. The following up biopsy demonstrated negative SV40 stain. But the tubulitis and glomerulitis persist. The creatinine went up again several weeks later. The nephrologist had to increase the immunosuppression.

I do not have much experience about this subject. I am still in the learning process. I welcome your input.

 谢谢frankbj老师的讲解和references. Based on your experience and/or references, how do you diagnose co-existing rejection?