Risk factors for the development of delayed graft function in deceased donor renal transplants.

INTRODUCTION: Delayed renal graft function (DGF) is associated with various factors and with a higher complication rate in the posttransplant period. Determination of center-specific risk factors may help to reduce the incidence of DGF and improve transplantation results. The aim of this study was to define risk factors for the development of DGF after renal transplantation. PATIENTS AND METHODS: This study included 290 consecutive deceased donor renal transplantations performed in a single center between January 1, 2004, and November 30, 2007. All cases were examined for the presence of DGF, defined as the need for at least 1 dialysis during the first posttransplant week. The subjects were divided into 2 groups: immediate graft function and DGF. Both groups were compared for donor and recipient transplantation factors as well as early posttransplant results. RESULTS: DGF was observed in 61 cases (21%). Our analysis revealed associations of DGF with recipient age (P = .011), female gender (P = .028), donor age (P = .033), body mass index (P = .007), severe hemodynamic disturbances (P = .005) preexistent glomerular or interstitial sclerosis (P = .002 or P = .028, respectively); and cold ischemia time (CIT; P = .019). Trends toward significance were observed with recipient weight > 100 kg (P = .078), and diabetes mellitus (P = .109). Recipients who experienced DGF showed on higher rate of acute rejection, a longer hospital stay, and an higher level serum creatinine at discharge (P < .001 for all). CONCLUSION: DGF had deleterious effects in the early posttransplant period. Careful allocation and reduction of CIT may improve transplantation results.

Reactivation of BK Virus in the Early Period After Kidney Transplantation.

BACKGROUND: Typically, polyoma BK virus (BKV) remains latent in the urogenital tract after primary infection. Reactivation of BKV in recipients of kidney allografts can cause progressive graft dysfunction known as BK virus nephropathy (BKVN). The cornerstone of treatment for BKVN is prevention; therefore, it is important to detect BKV reactivation early and reduce immunosuppression. We sought to identify the BKV reactivation rate and associated factors in a prospective study. MATERIALS AND METHODS: We studied 37 consecutive unselected adult recipients who underwent deceased donor kidney transplantation in 2007 and completed at least 3 months of observation. Qualitative nested polymerase chain reaction (PCR) testing was performed to detect BKV DNA in urine and plasma specimens. RESULTS: In all cases, BK viremia or viruria was not detected on the postoperative day or 2 weeks thereafter. At 3 months, BKV reactivation developed in 6 (16%) of 37 recipients. Simultaneous viremia and viruria were present on 5 patients and viremia only in 1 patient. Significant risk factors for BK viremia were body mass index >30 kg/m(2) (P = .02), retransplantation (P =.04), and use of tacrolimus (P = .02). Serum creatinine values at 3 months after transplantation were significantly higher among patients with active BKV infection (P = .008). CONCLUSIONS: Early BKV reactivation is associated with worse graft function as early as 3 months after transplantation. Obesity, retransplantation, and use of tacrolimus were factors promoting early development of BKV viremia.

Influence of Pretransplant Dialysis Vintage on Repeated Kidney Transplantation Outcomes.

Dialysis has a dose-dependent effect on first kidney transplantation outcomes, and a shorter waiting time on dialysis is associated with superior graft function. There are not enough data to support this statement in the case of a repeated transplantation. As such, we aimed to evaluate the influence of the dialysis vintage before the last transplantation on graft function as well as patient and graft survival in repeated transplantation situations. Patients who underwent repeated kidney transplantations were included in the retrospective study. Specifically, 79 patients were included who were divided into 4 groups according to the dialysis vintage before the last transplantation. We assessed graft function and patient and graft survival rates after 1- and 3-year follow-up. One-year graft function was worse for patients with a dialysis vintage of more than 31 months (P = .005), but there was no difference after 3 years. One- and 3-year graft survival was better for patients with a dialysis vintage of less than 12 months (P = .017). We concluded that a longer waiting time on dialysis was associated with worse graft function and diminished long-term graft survival after repeated kidney transplantation.

Progressive multifocal leukoencephalopathy following fludarabine treatment in a chronic lymphocytic leukemia patient.

UNLABELLED: Progressive multifocal leukoencephalopathy (PML) is a neurological disease caused by infection of the central nervous system (CNS) with the JC polyomavirus (JCV). JCV is endemic and infects a large proportion (70-90%) of healthy individuals worldwide, but infection is latent. JCV reactivation may occur, if the immune function is compromised. AIM: To present a PML case in a CLL patient after a long course of disease and treatment with fludarabine. JCV virus infection in this patient was proven both in brain biopsy material and blood. METHODS: Patient with a nine-year history of CLL was hospitalized with the weakness in the right leg and left hand, tremors, speech difficulties. An MRI diagnosed infiltrative glial tumor of the left hemisphere, proliferating predominantly in the frontal lobe, more in the gyrus frontalis superior region. CNS tumor biopsy performed. RESULTS: Morphology and immunoprofile of the lesion consistent with progressive multifocal leukoencephalopathy. The material from biopsy was diagnosed as positive for JCV DNA. JCV and HHV-7 genomic sequences were found in patient's PBL DNA sample. In a plasma DNA sample, only genomic sequences were detected. CONCLUSION: The present case draws attention to the fact that the use of fludarabine and its combinations in CLL therapy increases the risk of JCV infection reactivation and development of serious complications like PML.

Association of HHV-6 and HHV-7 reactivation with the development of chronic allograft nephropathy.

BACKGROUND: The long-term effect of HHV-6 and HHV-7 infections on chronic allograft nephropathy (CAN) development after renal transplantation is uncertain. OBJECTIVES: To determine HHV-6 and HHV-7 reactivation during the post-transplantation period and to evaluate its effect on CAN development in renal transplant patients. STUDY DESIGN: Eighty-one renal allograft recipients (28 with CAN, 53 with normal transplant function) were studied to determine the frequency of HHV-6 and HHV-7 reactivation during 36.4+/-7.8 months after renal transplantation using nested PCR. HHV-6 variants were identified using restriction endonuclease analysis. Patients were monitored for the development of CAN. RESULTS: The frequency of HHV-6 and/or HHV-7 plasma DNA was significantly higher in CAN patients (25/28, 89.3%) compared to control patients (15/50, 30.0%, p=0.0001). CAN patients also had an increased incidence of dual active infections (20/25, 80% and 2/15, 13.3%, p=0.007, respectively). In all 34 HHV-6 positive cases, the HHV-6B variant was identified. The presence of HHV-7 DNA in plasma preceded the presence of HHV-6 DNA. Early development of CAN and graft loss was detected only in patients with simultaneous HHV-6 and HHV-7 plasma DNA. CONCLUSIONS: Reactivation of HHV-6 and HHV-7 in renal graft recipients is a risk factor for CAN development. The presence of concurrent HHV-6 and HHV-7 DNA in the plasma is an unfavorable prognostic factor.