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Transplantation immunology
Published in Gabriel Virella, Medical Immunology, 2019
Satish N. Nadig, Jane C. Kilkenny
Chronic rejection, including chronic allograft nephropathy in the setting of kidney transplantation, is characterized by an insidiously progressive loss of function of the grafted organ. In all transplanted organs with chronic rejection, there is arterial intimal thickening, called transplant arteriosclerosis or transplant vasculopathy. Both immune (HLA mismatch, inadequate immunosuppression, acute rejection episodes) and non-immune-mediated (ischemia time, brain-dead donors, ischemia/reperfusion injury) stimuli may upregulate pathways that lead to progressive graft failure.
Transplantation
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
The single most important risk factor for chronic rejection after kidney transplantation is acute rejection (with vascular inflammation) and recurrent episodes of acute rejection. As non-immune factors often contribute significantly to the long-term failure of a kidney transplant, the term ‘chronic allograft nephropathy’ is sometimes used.
Cellular Imaging of Macrophage Activity in Infection and Inflammation
Published in Michel M. J. Modo, Jeff W. M. Bulte, Molecular and Cellular MR Imaging, 2007
Martin Rausch, Markus Rudin, Peter R. Allegrini, Nicolau Beckmann
Although numerous experimental and human studies have emphasized their presence during acute renal allograft rejection,35,37 early infiltration by macrophages is considered to be a poor prognostic sign for allograft survival.38 Nevertheless, several studies support the hypothesis that macrophage-derived inflammation is a cofactor for chronic allograft nephropathy,39–41 monocytes/macrophages and T-cells being the predominant graft-invading cells of rat renal allografts with chronic rejection.42–44 In view of the fact that chronic graft dysfunction represents the leading cause for the still unsatisfactory long-term results after organ transplantation, investigating macrophage infiltration into allografts during chronic rejection constitutes an important paradigm.
Prognostic value of the 7-year protocol biopsy of adult kidney allografts: impact of mesangiosclerosis and proteinuria
Published in Renal Failure, 2023
Yoshihiro Itabashi, Hideyo Oguchi, Tetuo Mikami, Noriyuki Kounoue, Taichi Arai, Kazunobu Shinoda, Masaki Muramatsu, Seiichiro Shishido, Ken Sakai
The Organ Procurement and Transplantation Network (OPTN)/Scientific Registry of Transplant Recipients (SRTR) 2019 annual report stated that maintaining long-term kidney graft survival is still challenging [1]. A previous report suggested that the long-term protocol biopsy has potential significance in detecting non-immunological factors that may lead to the deterioration of allograft function [2], although there has been little evidence supporting the usefulness of the long-term protocol biopsy in detecting chronic allograft rejection. Nankivell et al. [3] demonstrated that chronic allograft nephropathy progressively develops by 10 years post-transplantation in the natural course after kidney transplantation, with about 60% of cases severely affected in 10 years regardless of preceding rejection episodes. Furthermore, another study of 145 patients who underwent protocol biopsies at both 5 and 10 years after kidney transplantation showed that 54% of patients at 5 years and 82% of patients at 10 years had non-immune pathological injuries including arteriolar hyalinosis, mesangial sclerosis, and glomerulosclerosis [4]. As these changes presumably lead to allograft dysfunction, it may be necessary to perform protocol biopsies earlier than 10 years after transplantation.
Shear wave elastography parameters adds prognostic value to adverse outcome in kidney transplantation recipients
Published in Renal Failure, 2023
Tian-yi Zhang, Jiayi Yan, Jiajia Wu, Wenqi Yang, Shijun Zhang, Jia Xia, Xiajing Che, Hongli Li, Dawei Li, Liang Ying, Xiaodong Yuan, Yin Zhou, Ming Zhang, Shan Mou
Kidney transplantation has become a promising choice for patients with kidney failure to prolong life and improve the quality of life. Both short- and long-term survival of kidney transplantation recipients have improved substantially during the last few decades, resulting from advances in immunosuppression, more precise cytotoxic antibody detection and better human lymphocyte match [25–27]. However, evolving challenges such as chronic allograft dysfunction, infection, and cardiovascular diseases are still a concern [28]. Beyond one year after the transplantation, chronic allograft nephropathy was characterized by microvascular and glomerular injury [29]. The use of calcineurin inhibitors (tacrolimus and cyclosporin a) could lead to luminal narrowing, glomerulosclerosis, and tubulointerstitial damage [29]. All the above histological alterations cause increase stiffness of kidney parenchyma.
Impact of Proinflammatory Cytokine Gene Polymorphisms and Circulating CD3 on Long-Term Renal Allograft Outcome in Egyptian Patients
Published in Immunological Investigations, 2021
Sabah Farouk El-Abd, Nagwa Mansour Badr Eldin, Salwa Mahmoud Elwasif, Nora Abdel Sameaa Ahmed, Eman Salah El-Shafey, Eslam Elsherbiny
Particularly, upregulation of the genetically estimated pro-inflammatory TNF-α and IFN-γ (Th1 cytokines) were demonstrated to be the chief cytokines implicated in cell-induced immunity, that caused allograft rejection (Nikolova et al. 2008; Sánchez-Fructuoso et al. 2016; Vu et al. 2014). Moreover, the activity of TNF-α was suggested be associated with stimulation of a cascade of inflammatory events, promoting the expression of adhesion molecules, triggering of neutrophils beside its activity as a co-stimulator for T cell stimulation and antibody release (Serrano et al. 2006). The single-nucleotide polymorphism (SNP) TNF-α − 308 G/A (rs1800629) is situated on chromosome 6p21.3, within the class III region of MHC. The TNF-α − 308 A allele was reported as a potential transcriptional stimulator in vitro relative to the mutual G allele. Consequently, the frequency of A allele known to be associated with the risk factors that mediate chronic allograft nephropathy (CAN) development (Nikolova et al. 2008; Tinckam et al. 2005)..