Polyomavirus nephropathy (PVN) is a common viral infection of renal allografts, with biopsy-proven incidence of approximately 5%. A generally accepted morphologic classification of definitive PVN that groups histologic changes, reflects clinical presentation, and facilitates comparative outcome analyses is lacking. Here, we report a morphologic classification scheme for definitive PVN from the Banff Working Group on Polyomavirus Nephropathy, comprising nine transplant centers in the United States and Europe. This study represents the largest systematic analysis of definitive PVN undertaken thus far. In a retrospective fashion, clinical data were collected from 192 patients and correlated with morphologic findings from index biopsies at the time of initial PVN diagnosis. Histologic features were centrally scored according to Banff guidelines, including additional semiquantitative histologic assessment of intrarenal polyomavirus replication/load levels. In-depth statistical analyses, including mixed effects repeated measures models and logistic regression, revealed two independent histologic variables to be most significantly associated with clinical presentation: intrarenal polyomavirus load levels and Banff interstitial fibrosis ci scores. These two statistically determined histologic variables formed the basis for the definition of three PVN classes that correlated strongest with three clinical parameters: presentation at time of index biopsy, serum creatinine levels/renal function over 24 months of follow-up, and graft failure. The PVN classes 1-3 as described here can easily be recognized in routine renal biopsy specimens. We recommend using this morphologic PVN classification scheme for diagnostic communication, especially at the time of index diagnosis, and in scientific studies to improve comparative data analysis.
Our findings support the idea that rapamycin may be of value for patients with RCC and that its antitumor efficacy is realized by cell cycle arrest and targeted reduction of VEGF-A and TGF-beta1. A regimen of rapamycin and cyclosporine, demonstrated to be effective in reducing acute rejection of renal allografts, may prevent RCC progression as well, and has the potential to prevent mortality due to RCC in patients with ESRD who have received renal allografts.
Health researchers and policy-makers increasingly urge both patient and clinician engagement in shared decision making (SDM) to promote patient-centered care. Although SDM has been examined in numerous clinical settings, it has received little attention in solid organ transplantation. This paper describes the application of SDM to the kidney transplantation context. Several distinctive features of kidney transplantation present challenges to SDM including fragmented patient-provider relationships, the timesensitive and unpredictable nature of deceased organ offers, decision-making processes by transplant providers serving as both organ guardians (given the organ scarcity) versus advocates for specific patients seeking transplantation, variable clinical practices and policies among transplant centers, and patients' potentially compromised cognitive status and literacy levels. We describe potential barriers to and opportunities for SDM, and posit that SDM is feasible, warranting encouragement in kidney transplantation. We propose strategies to promote and overcome obstacles to SDM in kidney transplantation. We contend that engagement in SDM can be facilitated by re-organization of clinical care, communication and education of providers and patients.
A fter renal transplantation, the clinical outcome is dependent upon various recipient factors and upon donor characteristics such as donor brain death, prolonged cold ischemia, age, sex, and race (1-9). Nonetheless, delayed graft function (DGF) and acute rejection (AR) are interrelated posttransplant complications that can contribute to impaired intermediate-and long-term graft function and survival (1,2,5-11). We have tested the hypothesis that molecular evidence of intragraft inflammation and active T cell immunity present intraoperatively at the zero-hour and detected via PCRbased transcriptional profiling are linked to adverse posttransplant clinical outcomes such as DGF, AR within 3 mo following transplantation, and the quality of graft function 6 mo posttransplantation. A predictive role for suboptimal expression of anti-apoptotic genes, some expressed in response to inflammation (hemoxygenase-1 and A20) (12-17) and others not triggered by inflammation, was also investigated. In short, identification of pertinent molecular markers at the zero-hour provides a keen insight into future clinical outcomes. Materials and Methods Study SubjectsWe studied 75 renal allografts (31 cadaver and 44 living donor) and the clinical course of transplant recipients. Transplants were performed at Beth Israel Deaconess Medical Center. The Beth Israel Deaconess Medical Center Committee on Clinical Investigations approved the study. Each patient gave informed consent. Patients with a bleeding diathesis or on anticoagulant therapy were excluded from the study. Immunosuppressive RegimenThe intraoperative immunosuppressive regimen consisted of 1.5 mg/kg of thymoglobulin (Sangstat, Fremont, CA) given in a slow infusion begun before the transplant procedure or 20 mg of anti-CD25 mAb (Simulect; Novartis, East Hanover, NJ) and solumedrol 500 mg intravenously. Maintenance immunosuppressive regimens consisted of the calcineurin inhibitors tacrolimus (Fujisawa, Deerfield, IL) or cyclosporine (Novartis), prednisone, and mycophenolate mofetil (Roche, Nutley, NJ). Five patients received sirolimus (Wyeth-Ayerst, St. David's, PA), prednisone, and mycophenolate mofetil. Renal BiopsyAn intraoperative allograft wedge biopsy was performed 15 minutes after vascular reperfusion. One half of the biopsy was subjected to stanPublished online ahead of print. Publication date available at www.jasn.org.
Background The recommendation by the American Society of Transplantation for annual trivalent inactivated influenza vaccination greater than 3 to 6 months post-kidney transplantation provides a unique opportunity to test the in vivo impact of immunosuppression on recall T- and B-cell responses to influenza vaccination. Methods This study took advantage of recent breakthroughs in the single-cell quantification of human peripheral blood B-cell responses to prospectively evaluate both B- and T-cell responses to the seasonal (2010 and 2011) influenza vaccine in 23 stable renal transplant recipients and 22 healthy controls. Results and Conclusion The results demonstrate that the early B-cell response to influenza vaccination, quantified by the frequency of influenza-specific antibody-secreting cells (ASC) in peripheral blood, was significantly reduced in stable transplant recipients compared to healthy controls. The magnitude of the seroresponse and the rate of sero-conversion were also blunted. The influenza-specific interferon-gamma (IFNγ) T-cell response was significantly reduced in transplant recipients; however, there was no correlation between the magnitude of the influenza-specific IgG ASC and IFNγ responses. The induction of memory T- and B-cell responses to influenza vaccination supports the recommendation to vaccinate while the blunted responses demonstrate the efficacy of immunosuppression in controlling memory responses individual transplant recipients.
The use of cell phone technology and text messaging was ubiquitous and comparable between groups, but computer and Internet access and frequency of use were not. Reaching out to the African American community may best be accomplished by using cell phone/text messaging as opposed to Internet-based platforms.
We conducted this study using the updated 2005‐2016 Organ Procurement and Transplantation Network database to assess clinical outcomes of retransplant after allograft loss as a result of BK virus–associated nephropathy (BKVAN). Three hundred forty‐one patients had first graft failure as a result of BKVAN, whereas 13 260 had first graft failure as a result of other causes. At median follow‐up time of 4.70 years after the second kidney transplant, death‐censored graft survival at 5 years for the second renal allograft was 90.6% for the BK group and 83.9% for the non‐BK group. In adjusted analysis, there was no difference in death‐censored graft survival (P = .11), acute rejection (P = .49), and patient survival (P = .13) between the 2 groups. When we further compared death‐censored graft survival among the specific causes for first graft failure, the BK group had better graft survival than patients who had prior allograft failure as a result of acute rejection (P < .001) or disease recurrence (P = .003), but survival was similar to those with chronic allograft nephropathy (P = .06) and other causes (P = .05). The better allograft survival in the BK group over acute rejection and disease recurrence remained after adjusting for potential confounders. History of allograft loss as a result of BKVAN should not be a contraindication to retransplant among candidates who are otherwise acceptable.
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