Successful retransplantation after renal allograft loss to polyoma virus interstitial nephritis

Abstract

Poduval et al. (1) have reported on successful retransplantation after renal-allograft loss to polyoma virus nephritis. They conclude that previous graft loss secondary to polyoma virus infection is not a contraindication to retransplantation. Although we do agree that retransplantation should be considered as a therapeutic option, our experience suggests that specific circumstances and actions may be indispensable for long-term success. A 35-year-old man with end-stage renal failure caused by diabetic nephropathy underwent a simultaneous pancreas and kidney transplantation from a six antigen-mismatched cadaveric donor on January 11, 1999. Immunosuppression consisted of antithymocyte globulin (ATG) induction, tacrolimus, mycophenolate mofetil (MMF), and prednisone (discontinued at posttransplant month [PTM] 5). Except for prolonged wound healing, the postoperative course was uneventful with an excellent function of both organs. On PTM 11 and 16, short courses of methylprednisolone were given because of creatinine increases with borderline changes and acute rejection (type 1A, Banff 97) on kidney biopsy, respectively. On PTM 20, after another biopsy revealed tubular-cell intranuclear inclusions, polyoma virus nephritis was suspected and tacrolimus and MMF doses were reduced. However, the deterioration of renal function was not halted, and thus, because of full function of the bladder-drained pancreatic graft and past intolerance of dialysis treatment, a decision on preemptive renal retransplantation was undertaken. Retransplantation was performed on April 22, 2001 with the kidney graft harvested from a 2 antigen-matched cadaveric donor. The removed graft showed interstitial nephritis of viral etiology with intranuclear inclusions (polyoma virus confirmed by immunohistochemistry: SV40 T-Ag, Oncogene Research Products, San Diego, CA). The postoperative period was complicated by delayed graft function with a creatinine level of 198 μmol/L (2.2 mg/dL) at time of hospital discharge. Prednisone was added to tacrolimus and MMF in the early postoperative period. An increase of creatinine necessitated a kidney biopsy at PTM 3, which showed only mild benign nephrosclerosis and no signs of acute rejection. At PTM 5, immunosuppression was changed to low-dose tacrolimus and sirolimus in an attempt to minimize nephrotoxicity and reduce risk of recurrence of viral nephritis. Another biopsy done at PTM 5 for progressive deterioration of graft function showed nonsuppurative tubulointerstitial nephritis of viral origin (polyoma etiology was confirmed by immunohistochemistry with urinalysis being negative for decoy cells). A short course of steroid therapy was tried with some transient effect because of a simultaneous finding of 1B rejection. However, polyoma virus nephritis was reconfirmed by biopsy at PTM 8, and graft function further declined later with dialysis treatment restarted at PTM 12. As suggested by others (2), retransplantation in patients with graft loss caused by polyoma nephritis should be considered only in cases where evidence of lytic infection is no longer present. Qualitative or quantitative plasma or urine polymerase chain reaction (PCR) monitoring (3) (unfortunately unavailable to us in the described case) may be necessary, while urine cytology is probably of insufficient sensitivity. These and other important preconditions, such as preceding allograft nephrectomy and specific adjustments of immunosuppression, will have to be defined more precisely to ensure a lasting success of kidney retransplantation in cases of polyoma nephritis. Petr Boucek1 Ludek Voska2 Frantisek Saudek1