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Gleisner M.A.,University of Chile | Rosemblatt M.,University of Chile | Rosemblatt M.,Andres Bello University | Fierro J.A.,Transplantation Unit | Bono M.R.,University of Chile
Transplantation Proceedings | Year: 2011

Background: Dendritic cells (DCs) are professional antigen-presenting cells able to induce immunity or tolerance. The interactions of immature DCs with naive T lymphocytes induce peripheral tolerance through mechanisms that include anergy or deletion of lymphocytes or the generation of regulatory T cells. Because of the central role of DCs in the immune response, they are potential targets for the induction of experimental tolerance. Thus, the generation of immature (tolerogenic) DCs able to capture and present alloantigens to T cells represents an important aim in our efforts to achieve better transplant acceptance. Methods: In this work, we generated immature DCs by using vitamin D 3 (VD3) during the process of DC differentiation. Results: The VD3DCs showed an immature phenotype characterized by a low expression of major histocompatibility complex antigens of class II, CD86, and CD80 molecules and the secretion of a tolerogenic cytokine pattern. Furthermore, we showed that VD3DCs phagocytose apoptotic allogeneic cells efficiently without inducing DC maturation or activation. Most important, our experiments demonstrated that mice treated with VD3 produce immature DCs in vivo, and that DCs from VD3-treated mice immunized with allogeneic apoptotic cells maintained their tolerogenic phenotype. Conclusion: Our results show that allogeneic apoptotic cells in combination with VD3 generate DCs with tolerogenic characteristics that could be used to induce tolerance towards alloantigens. © 2011 by Elsevier Inc. All rights reserved. Source


Stravodimos K.G.,Athens Medical School | Adamis S.,National and Kapodistrian University of Athens | Tyritzis S.,Athens Medical School | Georgios Z.,Transplantation Unit | Constantinides C.A.,Athens Medical School
Journal of Endourology | Year: 2012

Background and Purpose: Renal transplant lithiasis represents a rather uncommon complication. Even rare, it can result in significant morbidity and a devastating loss of renal function if obstruction occurs. We present our experience with graft lithiasis in our series of renal transplantations and review the literature regarding the epidemiology, pathophysiology, and current therapeutic strategies in the management of renal transplant lithiasis. Patients and Methods: In a retrospective analysis of a consecutive series of 1525 renal transplantations that were performed between January 1983 and March 2007, 7 patients were found to have allograft lithiasis. In five cases, the calculi were localized in the renal unit, and in two cases, in the ureter. A review in the English language was also performed of the Medline and PubMed databases using the keywords renal transplant lithiasis, donor-gifted lithiasis, and urological complications after kidney transplantation. Several retrospective studies regarding the incidence, etiology, as well as predisposing factors for graft lithiasis were reviewed. Data regarding the current therapeutic strategies for graft lithiasis were also evaluated, and outcomes were compared with the results of our series. Results: Most studies report a renal transplant lithiasis incidence of 0.4% to 1%. In our series, incidence of graft lithiasis was 0.46% (n=7). Of the seven patients, three were treated via percutaneous nephrolithotripsy (PCNL); in three patients, shockwave lithotripsy (SWL) was performed; and in a single case, spontaneous passage of a urinary calculus was observed. All patients are currently stone free but still remain under close urologic surveillance. Conclusion: Renal transplant lithiasis requires vigilance, a high index of suspicion, prompt recognition, and management. Treatment protocols should mimic those for solitary kidneys. Minimally invasive techniques are available to remove graft calculi. Long-term follow-up is essential to determine the outcome, as well as to prevent recurrence. © 2012, Mary Ann Liebert, Inc. Source


Sund F.,Uppsala University Hospital | Lidehall A.,Uppsala University Hospital | Claesson K.,Uppsala University Hospital | Foss A.,Transplantation Unit | And 3 more authors.
Clinical Transplantation | Year: 2010

Cytomegalovirus (CMV) infection is still the leading opportunistic infection following solid organ transplantation. The aim of this prospective study of renal transplant recipients was to evaluate the dynamics of CMV-specific T-cells, viral load, and clinical symptoms of CMV infection. Methods: Levels of tetramer-selected CD8+ T-cells (TetraCD8), CMV-specific interferon-γ producing CD8+ T-cells (IFNγCD8), and CD4+ T-cells (IFNγCD4), measured using major histocompatibility complex-tetramer and cytokine flow cytometry techniques, and CMV DNA were monitored monthly in 17 CMV-seropositive patients up to one yr (median 12 months, range 3-12) after transplantation and correlated to clinical outcome. Results: CMV DNAemia was detected in 94% of the patients, but only one patient developed CMV disease. CMV DNAemia >1 million copies/mL was seen in asymptomatic patients. CMV-specific T-cells decreased rapidly after transplantation. TetraCD8 and IFNγCD8 regenerated within three months, whereas IFNγCD4 recovery was impaired up to one yr after transplantation. The proportion of IFNγCD4 at two months post-transplantation as compared with baseline, correlated strongly with the magnitude of the CMV DNAemia. Conclusions: Monitoring the reduction of IFNγCD4 compared with baseline during the first months after transplantation could be considered in predicting risk for high-grade CMV DNAemia and in deciding strategic approaches for pre-emptive and prophylactic therapy. © 2009 Wiley Periodicals, Inc. Source


Arnold M.-L.,Friedrich - Alexander - University, Erlangen - Nuremberg | Ntokou I.-S.,National Tissue Typing Center | Doxiadis I.I.N.,Leiden University | Spriewald B.M.,Friedrich - Alexander - University, Erlangen - Nuremberg | And 2 more authors.
Transplant International | Year: 2014

Human leukocyte antigen alloantibodies have a multitude of damaging effects on the allograft, both complement (C′) activation and Fc-independent ones. To date, the clinical significance of non-C′ fixing (NCF) HLA donor-specific antibodies (DSA) is still unclear. In this study, we investigated whether renal transplant recipients with NCF-DSA subclasses (IgG2/IgG4, IgA1/IgA2) are at higher risk of graft loss compared to patients with exclusively C′ fixing (IgG1/IgG3). Blood samples from 274 patients were analyzed for HLA IgG and IgA subclasses using a modified single-antigen bead assay. We identified 50 (18.2%) patients with circulating NCF antibodies either DSA (n = 17) or against third-party HLA (n = 33). NCF-DSAs were preferentially of IgG2/IgG4 isotype (11/17) and were mainly directed against HLA class II (13/17). NCF DSA were present as a mixture with strong C′ fixing IgG1/IgG3. Graft survival was similar between patients with exclusively C′ fixing antibodies and those with a mixture panel (log rang test P = 0.162), and also among patients with different immunoglobulin isotype and subclasses (long-rank test, P = 0.732). We conclude that expansion of DSA to NCF subclasses postrenal transplantation does not seem to be associated with worse graft survival as compared to the presence of exclusive C′ fixing subclasses. © 2013 Steunstichting ESOT. Source


Karaolanis G.,Transplantation Unit | Lionaki S.,Nephrology and Transplantation Unit | Moris D.,Transplantation Unit | Palla V.-V.,Transplantation Unit | Vernadakis S.,Transplantation Unit
Transplantation Reviews | Year: 2014

Secondary hyperoxaluria is a multifactorial disease affecting several organs and tissues, among which stand native and transplanted kidneys. Nephrocalcinosis and nephrolithiasis may lead to renal insufficiency. Patients suffering from secondary hyperoxaluria, should be promptly identified and appropriately treated, so that less renal damage occurs.The aim of this review is to underline the causes of hyperoxaluria and the related pathophysiologic mechanisms, which are involved, along with the description of seven cases of irreversible renal graft injury due to secondary hyperoxaluria. © 2014 Elsevier Inc. Source

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