Contributed by Ibrahim Batal, M.D.
This patient is a 36 year-old male who is 216 days status post-kidney transplantation due to hypertension induced kidney failure. He had high creatinine (Cr) values with difficulties controlling his serum Cr which reached a value of 3.1 mg/dl. At that time, the patient was found to shed BK virus in his urine (BKV DNA: 7.7E05 copies/ml), however, no BKV DNA was detected in plasma. A renal allograft biopsy was performed. (Figure 1)
The biopsy revealed tubulitis and interstitial inflammation which was interpreted as mild to moderate acute cellular rejection, and was classified as Banff type IB according to Banff 1997 criteria . No viral nuclear inclusions were seen and the in-situ hybridization for BKV was negative. Peritubular capillary C4d immunohistochemical stain (a marker for antibody-mediated rejection) was negative. An immune cell function assay (Cylex) was performed to evaluate T cell activation and revealed a low value of (30 ng ATP/ml).
Based on the biopsy result, intravenous steroid was given as an anti-rejection therapy (Solumedrol 500 mg) and the tacrolimus dose was increased.
A follow-up biopsy performed 26 days later revealed improvement in the degree of tubulitis as well as interstitial inflammation and was interpreted as borderline for acute rejection (Figure 2). However, renal function deteriorated and serum Cr increased (4 mg/dl), also the viral load increased more than 25 folds in the urine (2.9E07 copies/ml). In addition, BKV DNA was detected for the first time in the plasma (2884 copies/ml). The patient continued deteriorating and lost his graft 1 year later due to chronic allograft nephropathy.