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chronic allograft dysfunction

Wael M Hamza, Hanan H Ali, Samia M Gabal, Sawsan A Fadda
The chronic dysfunction stands as the most common cause of renal allograft loss. During the nineties of the past century, this condition was referred to as chronic allograft nephropathy (CAN). Since 2005, CAN has been assigned by the eighth Banff schema to four main categories via histopathological and immunohistochemical findings including chronic antibodymediated rejection (CAMR), chronic T-cell-mediated rejection (CTMR), chronic cyclosporine toxicity (CNITOX), and "interstitial fibrosis (IF)/tubular atrophy; not otherwise specified (NOS)" to eliminate the term CAN...
September 2016: Saudi Journal of Kidney Diseases and Transplantation
Yihung Huang, Evan Farkash
As both T cell and antibody-mediated rejection can have a subclinical phase, protocol biopsies provide an early opportunity to intervene before the onset of clinical allograft dysfunction. Protocol biopsies are usually done after reperfusion to establish baseline, between 3 and 6 months to identify subclinical rejection, and at 6-12 months to assess chronicity and persistent inflammation that have prognostic implication. Treatment of both subclinical T cell and antibody-mediated rejection prevents progression of rejection and development of interstitial fibrosis/tubular atrophy or transplant glomerulopathy...
September 2016: Advances in Chronic Kidney Disease
S Pereira, C M Cruz, M Soares, J Gandara, S Ferreira, V Lopes, R Vizcaíno, J Daniel, H P Miranda
INTRODUCTION: In liver transplantation, late graft dysfunction can have several causes, particularly rejection, infection, vascular, biliary complications, and others, usually suspected by abnormal liver tests. However, normal liver tests do not confirm a normal graft and liver biopsy could identify unexpected features with repercussions in immunosuppressive therapy. The aim of this study was to determinate the histological abnormalities in patients 10 years after liver allograft transplantation with sustainably normal liver tests and evaluate the changes in immunosuppressive therapy triggered by histological data...
September 2016: Transplantation Proceedings
Y Yamada, E Vandermeulen, T Heigl, J Somers, A Vaneylen, S E Verleden, H Bellon, S De Vleeschauwer, E K Verbeken, D E Van Raemdonck, R Vos, G M Verleden, W Jungraithmayr, B M Vanaudenaerde
The single most important cause of late mortality after lung transplantation is chronic lung allograft dysfunction (CLAD). However, the pathological development of CLAD was not as simple as previously presumed and subclassification phenotypes, bronchiolitis obliterans syndrome (BOS) and restrictive CLAD (rCLAD), have been introduced. We want to re-investigate how CLAD manifests in the murine orthotopic lung transplant model and investigate the role of interleukin 17A (IL-17A) within this model. Orthotopic LTx was performed in CB57Bl6, IL-17 WT and IL-17 KO mice...
October 10, 2016: Transplant Immunology
Akihiko Kitahara, Seijiro Sato, Terumoto Koike, Masanori Tsuchida
We report here a case of fatal respiratory failure developed during chemotherapy for diffuse large B cell lymphoma that occurred late after lung transplantation. 25-year- old man underwent lung transplantation from brain death donor for respiratory failure due to interstitial pneumonia at the age of 16 years old. Two years after transplantation, his respiratory function decreased gradually. Chronic lung allograft dysfunction including bronchiolitis obliterans( BOS) and restrictive allograft syndrome was suspected and immunosuppression was enhanced...
October 2016: Kyobu Geka. the Japanese Journal of Thoracic Surgery
Tomohito Saito, Masaaki Sato, Yohei Taniguchi, Tomohiro Murakawa, Shaf Keshavjee
Chronic lung allograft dysfunction (CLAD) is a major limitation to long-term success of lung transplantation. Restrictive allograft syndrome (RAS) is a recently discovered subtype of CLAD, showing distinct clinical, pathological and radiological features compared with the major CLAD subtype, bronchiolitis obliterans syndrome (BOS). Introduction of the novel CLAD classification system that differentiates CLAD into BOS and RAS has stimulated research activities aiming delineation of the underlying pathological mechanism in the 2 CLAD subtypes...
October 2016: Kyobu Geka. the Japanese Journal of Thoracic Surgery
Hidemi Suzuki, Atsushi Hata, Yuki Shina, Takamasa Yun, Kazuhisa Tanaka, Yuichi Sakairi, Hironobu Wada, Taiki Fujiwara, Takahiro Nakajima, Takekazu Iwata, Masako Chiyo, Shigetoshi Yoshida, Ichiro Yoshino
Chronic lung allograft dysfunction (CLAD) is a critical impediment to the long-term survival after lung transplantation. A rat orthotopic lung transplantation model was developed in the early 1970s, and using this model, our laboratory has shown that the immunopathogenesis of CLAD involves both allogeneic immunity and autoimmunity. However, further investigation of CLAD is limited by the scarcity of transgenic and knockout strains. The model most widely used to study CLAD, the mouse model of heterotopic tracheal transplantation, has some incomplete pathophysiologic features of CLAD, which limits the utility of this model...
October 2016: Kyobu Geka. the Japanese Journal of Thoracic Surgery
Takeshi Shiraishi, Akinori Iwasaki
The most frequent cause of death within a year after lung transplantation is infectious complications, which shifts to chronic allograft rejection or chronic lung allograft dysfunction(CLAD) thereafter. It is no doubt that minimization of the dose of immunosuppression within the acceptable therapeutic range is a best strategy to avoid infectious complications however, adequate dose of immunosuppressant is mandatory to protect lung allografts from acute or chronic rejection. Carefully balanced therapy of immunosuppression and infection control is extremely important for patient's long term survival after lung transplantation...
October 2016: Kyobu Geka. the Japanese Journal of Thoracic Surgery
Jiexiu Zhang, Zijie Wang, Zhen Xu, Zhijian Han, Jun Tao, Pei Lu, Zhengkai Huang, Wanli Zhou, Chunchun Zhao, Ruoyun Tan, Min Gu
BACKGROUND Chronic allograft dysfunction (CAD) is the major factor endangering the long-term allograft survival in kidney transplantation. The mechanisms of CAD remain unclear. MATERIAL AND METHODS A total of 64 renal transplant recipients were enrolled in our study and divided into a stable group and CAD group according to their allograft function. A group of 32 normal controls (healthy volunteers) were also included. An ELISA was used to detect serum interleukin-33 (IL-33), IL-2, IL-4, IL-10, IL-17, and interferon-gamma (IFN-γ)...
October 4, 2016: Annals of Transplantation: Quarterly of the Polish Transplantation Society
Darlene Vigil, Nikifor K Konstantinov, Marc Barry, Antonia M Harford, Karen S Servilla, Young Ho Kim, Yijuan Sun, Kavitha Ganta, Antonios H Tzamaloukas
Nephropathy secondary to BK virus, a member of the Papoviridae family of viruses, has been recognized for some time as an important cause of allograft dysfunction in renal transplant recipients. In recent times, BK nephropathy (BKN) of the native kidneys has being increasingly recognized as a cause of chronic kidney disease in patients with solid organ transplants, bone marrow transplants and in patients with other clinical entities associated with immunosuppression. In such patients renal dysfunction is often attributed to other factors including nephrotoxicity of medications used to prevent rejection of the transplanted organs...
September 24, 2016: World Journal of Transplantation
M Y Shino, S S Weigt, N Li, A Derhovanessian, D M Sayah, R H Huynh, R Saggar, A L Gregson, A Ardehali, D J Ross, J P Lynch, R M Elashoff, J A Belperio
The impact of allograft injury time-of-onset on the risk of chronic lung allograft dysfunction (CLAD) remains unknown. We hypothesized that episodes of late-onset (≥6 months) allograft injury would produce an augmented CXCR3/ligand immune response, leading to increased CLAD. In a retrospective single-center study, 1894 transbronchial biopsies from 441 lung transplant recipients were reviewed for the presence of acute rejection (AR), lymphocytic bronchiolitis (LB), diffuse alveolar damage (DAD) and organizing pneumonia (OP)...
September 27, 2016: American Journal of Transplantation
Shi Deng, Tao Jin, Li Zhang, Hong Bu, Peng Zhang
Chronic renal allograft dysfunction (CRAD) is the most common cause of graft failure following renal transplantation. However, the underlying mechanisms remain to be fully elucidated. Immunosuppressants and hyperlipidemia are associated with renal fibrosis following long‑term use. The present study aimed to determine the effects of tacrolimus (FK506) and lipid metabolism disorder on CRAD. In vitro and in vivo models were used for this investigation. Cells of the mouse proximal renal tubular epithelial cell strain, NRK‑52E, were cultured either with oxidized low‑density lipoprotein (ox‑LDL), FK506, ox‑LDL combined with FK506, or vehicle, respectively...
September 13, 2016: Molecular Medicine Reports
Julien Guihaire, Ryo Itagaki, Mandy Stubbendorff, Xiaoqin Hua, Tobias Deuse, Sebastian Ullrich, Elie Fadel, Peter Dorfmüller, Robert C Robbins, Hermann Reichenspurner, Udo Schumacher, Sonja Schrepfer
Bronchiolitis obliterans syndrome (BOS) is a main cause of allograft dysfunction and mortality after lung transplantation (LTx). A better understanding of BOS pathogenesis is needed to overcome this treatment-refractory complication. Orthotopic tracheal transplantation using human bronchus was performed in Brown Norway (BN) and nude (RNU) rats. Allografts were recovered in both strains at Day 7 (BN7 , n = 6; RNU7 , n = 7) or Day 28 (BN28 , n = 6; RNU28 , n = 6). Immune response of the host against the bronchial graft was assessed...
September 10, 2016: Transplant International: Official Journal of the European Society for Organ Transplantation
Kartik V Shenoy
No abstract text is available yet for this article.
September 1, 2016: American Journal of Respiratory and Critical Care Medicine
S Izhakian, W G Wasser, B D Fox, B Vainshelboim, J E Reznik, M R Kramer
BACKGROUND: Rabbit antithymocyte globulin (rATG) therapy has been shown to be beneficial in lung transplant recipients as induction therapy for treating acute lung rejection; however, its role in chronic lung rejection has been reported only rarely. We evaluated the effectiveness of rATG therapy in slowing the progression of chronic lung allograft dysfunction (CLAD) syndrome. METHODS: We conducted a retrospective review of 25 lung transplant patients with CLAD who received rATG therapy in the Pulmonary Institute of Rabin Medical Center, Israel, between May 2005 and February 2016...
July 2016: Transplantation Proceedings
Q Yan, H Jiang, B Wang, W Sui, H Zhou, G Zou
BACKGROUND: To investigate the expression of RANTES (regulated upon activation, normal T-cell-expressed and -secreted) and monocyte chemoattractant protein-1 (MCP-1) in renal allografts with chronic renal allograft dysfunction (CRAD), and explore its relationship with interstitial fibrosis and tubular atrophy (IF/TA). METHODS: An immunohistochemical assay and computer-assisted, genuine colored image analysis system were used to detect the expression of RANTES and MCP-1 in renal allografts with CRAD...
July 2016: Transplantation Proceedings
Stefano Di Carlo, Elena Rossi, Gianfranco Politano, Simona Inghilleri, Patrizia Morbini, Fiorella Calabrese, Alfredo Benso, Alessandro Savino, Emanuela Cova, Davide Zampieri, Federica Meloni
The pathogenesis of Bronchiolitis Obliterans Syndrome (BOS), the main clinical phenotype of chronic lung allograft dysfunction, is poorly understood. Recent studies suggest that epigenetic regulation of microRNAs might play a role in its development. In this paper we present the application of a complex computational pipeline to perform enrichment analysis of miRNAs in pathways applied to the study of BOS. The analysis considered the full set of miRNAs annotated in miRBase (version 21), and applied a sequence of filtering approaches and statistical analyses to reduce this set and to score the candidate miRNAs according to their potential involvement in BOS development...
2016: PloS One
Tristan Legris, Christophe Picard, Dilyana Todorova, Luc Lyonnet, Cathy Laporte, Chloé Dumoulin, Corinne Nicolino-Brunet, Laurent Daniel, Anderson Loundou, Sophie Morange, Stanislas Bataille, Henri Vacher-Coponat, Valérie Moal, Yvon Berland, Francoise Dignat-George, Stéphane Burtey, Pascale Paul
Although kidney transplantation remains the best treatment for end-stage renal failure, it is limited by chronic humoral aggression of the graft vasculature by donor-specific antibodies (DSAs). The complement-independent mechanisms that lead to the antibody-mediated rejection (ABMR) of kidney allografts remain poorly understood. Increasing lines of evidence have revealed the relevance of natural killer (NK) cells as innate immune effectors of antibody-dependent cellular cytotoxicity (ADCC), but few studies have investigated their alloreactive potential in the context of solid organ transplantation...
2016: Frontiers in Immunology
Elly Vandermeulen, Stijn E Verleden, Hannelore Bellon, David Ruttens, Elise Lammertyn, Sandra Claes, Jennifer Vandooren, Estafania Ugarte-Berzal, Dominique Schols, Marie-Paule Emonds, Dirk E Van Raemdonck, Ghislain Opdenakker, Geert M Verleden, Robin Vos, Bart M Vanaudenaerde
BACKGROUND: Recently, antibody mediated rejection (AMR) has been associated with a higher incidence of chronic lung allograft dysfunction (CLAD) and mortality after lung transplantation (LTx). We investigated markers related to AMR and matrix remodeling in CLAD, with special attention for its two phenotypes being bronchiolitis obliterans syndrome (BOS) and restrictive CLAD (rCLAD). METHODS: Immunoglobulins (IgA, IgE, IgG1-IgG4, total IgG and IgM) and complement (C4d and C1q) were quantified in lung lavage samples at the moment of BOS (n=15) or RAS (n=16) diagnosis; and were compared to stable transplant patients who served as control (n=14)...
September 2016: Transplant Immunology
Ning Cao, Xiaofang Ma, Zhenzhen Guo, Yaqiu Zheng, Shengnan Geng, Mingjing Meng, Zhenhua Du, Haihong Lin, Yongjian Duan, Gangjun Du
Obesity is a risk factor for cancer and cancer-related mortality, however, its role in lung cancer progression remains controversial. This study aimed to assess whether high-fat diet (HFD)-induced obesity promotes lung cancer progression and whether the promotion can be decreased by Kanglaite injection (KLTI). In vivo, HFD-induced overweight or obesity increases the lung carcinoma incidence and multiplicity in a urethane-induced lung carcinogenic model and cancer-related mortality in a LLC allograft model by increasing oxidative stress and cellular signaling molecules including JAK, STAT3, Akt, mTOR, NF-κB and cyclin D1...
August 11, 2016: Oncotarget
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