A Case of Retransplantation in A Patient with Graft Loss Caused by Polyoma Virus Nephropathy.
- Author:
Jee Min JEON
1
;
Ji Hwan KIM
;
Mi Jung PARK
;
Chang Sue PARK
;
Sung Min KIM
;
Hyae Joo OH
;
Yong Kee PARK
;
Yong Hun SHIN
;
Joong Kyung KIM
;
Kill HUH
Author Information
1. Department of Internal Medicine, Bong Saeng Hospital, Busan, Korea. kidney119@hotmail.com
- Publication Type:Case Report
- Keywords:
Polyoma virus nephropathy;
Renal retransplantation;
Nephroureterectomy
- MeSH:
Allografts;
Azathioprine;
Biopsy;
Cadaver;
Creatinine;
Cyclosporine;
Delayed Graft Function;
Graft Rejection;
Humans;
Inclusion Bodies;
Kidney Transplantation;
Male;
Nephritis, Interstitial;
Polyomavirus*;
Recurrence;
Renal Dialysis;
Tacrolimus;
Thrombocytopenia;
Thrombotic Microangiopathies;
Transplants*;
Young Adult
- From:Korean Journal of Nephrology
2005;24(3):489-493
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Polyoma virus (PV) nephropathy is a known cause of graft loss after renal transplantation. In a renal transplant patient suspected of graft rejection, it is important to discriminate between PV induced interstitial nephritis and acute cellular rejection, because of similar pathologic findings. After the loss of the first allograft secondary to PV nephropathy, transplant graft nephroureterectomy before retransplantaton may have an influence in the recurrence of PV nephropathy. However, this question has not been completely resolved. Case: A 23-year-old male underwent first renal transplantation from his HLA haploidentical 25 year-old-sister. His renal function had been good with cyclosporine, steroid and azathioprine until 9 months after transplantation, when his serum creatinine level rose to 2.2 mg/dL. A renal biopsy revealed features of tubulitis and we confirmed PV nephropathy through a positive PV monoclonal antibody reaction to inclusion body. After gradual loss of graft function, he underwent hemodialysis. After 48 months of hemodialysis, the patient underwent cadaveric renal retransplantation without transplant graft nephroureterectomy. Thrombocytopenia and suspected delayed graft function occurred after 2 days of transplantation. A graft biopsy revealed thrombotic microangiopathy. Improved graft function was attained after a temporary stop of tacrolimus and ATGAM(R) bridging therapy. The patient is maintaining satisfactory graft function 33 months after retransplantation without clinical and serological evidence of recurrent PV infection.
