No abstract available.
Electroencephalography* ; Neuronal Ceroid-Lipofuscinoses ; Neurons*

PURPOSE:BK virus associated nephropathy (BKVAN) affects 1-10% of kidney transplant (KT) patients and it produces a progressive destruction of allograft. Reducing immunosuppression is the only way to save the graft, while it needs tight monitoring of the graft rejection and graft survival is poorer in advanced case. Leflunomide has immunosuppressive effect and also antiviral activity. Addition of leflunomide may improve BK virus clearance and graft survival. METHODS:6 KT patients with biopsy proven BKVAN (Histological pattern B) were treated with leflunomide and reduced immunosuppression. All patients were monitored with serial determination of viral load in blood and graft function. RESULTS:BKVAN was diagnosed at 14 months (7-28) post transplant, at that time median serum creatinine concentration was 2.8 mg/dL (1.8-3.6). 12.5 months (6-16) later of leflunomide treatment, median serum creatinine was 2.3 mg/dL and no graft loss was found. CONCLUSION:Leflunomide therapy with reduced immunosuppression may be effective in the treatment for BKVAN.
Biopsy ; BK Virus ; Creatinine ; Graft Rejection ; Graft Survival ; Humans ; Immunosuppression ; Isoxazoles ; Kidney ; Kidney Transplantation ; Transplantation, Homologous ; Transplants ; Viral Load ; Viruses

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.
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