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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
A kidney from a living or deceased donor can be transplanted into the pelvis of the recipient by attaching the kidney's blood vessels to the iliac vessels and implanting the ureter in the bladder. To reduce the chances of rejection of the kidney, the donor and the recipient are matched whenever possible for their blood group and HLA types and the recipient is given immunosuppressive drugs. The drugs commonly include steroids, tacrolimus or ciclosporin and mycophenolate or azathioprine. Biological therapies such as the monoclonal antibody basiliximab are also used. If transplant rejection occurs, immunosuppression is increased.
Miscellaneous Drugs during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Among 38 pregnancies to 29 women with liver transplants, 13 percent of mothers had signs of organ rejection (Radomski et al., 1995). There were 31 live births (eight abortions) and 32 percent had low birth weight, with 39 percent premature. Infection complicated >25 percent of the liver transplant pregnancies. Immunosuppression is a mainstay of treatment to prevent transplant rejection. Two of 15 infants born to liver transplant patients had birth defects (Kallen et al., 2005). A review of 450 pregnancies in 306 liver transplant recipients (systematic review, 8 studies) indicated that miscarriage was 17.1 percent, pregnancy induced hypertension 21.9 percent and C-section 44.6 percent (Deshpande et al., 2012). Compared to renal transplant obstetric patients, liver transplant pregnancies lasted longer (36.5 vs. 35.6 weeks) had greater birth weight (2866 g vs. 2420 g).
Therapeutic apheresis
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
In the context of renal transplantation, apheresis is generally considered in one of the following three settings: (i) reduction of circulating antibodies that would preclude transplantation; (ii) the treatment of post-transplant rejection, and (iii) the treatment of post-transplant recurrent disease.
Uncover diagnostic immunity/hypoxia/ferroptosis/epithelial mesenchymal transformation-related CCR5, CD86, CD8A, ITGAM, and PTPRC in kidney transplantation patients with allograft rejection
Published in Renal Failure, 2022
Long He, Boqian Wang, Xueyi Wang, Yuewen Liu, Xing Song, Yijian Zhang, Xin Li, Hongwei Yang
In recent years, kidney transplantation has been considered as the best therapeutic intervention for patients with end-stage organ failure [1]. However, kidney transplantation brings the risk of allograft rejection. If leaving unchecked, allograft rejection reaction can destroy the graft. With the use of immunosuppressive agents, the incidence of transplant rejection has reduced [2]. Although the annual survival rate of kidney transplant has reached more than 90%, there is a 4–5% loss of function of the kidney graft. The 5-year survival rate of kidney transplant is 70%, whereas the 10-year survival rate is only 50% [2]. Regular monitoring of serum creatinine is an insensitive predictor and only increases upon the deficiency in kidney function [3]. Thus, it is important to identify potential diagnostic and therapeutic markers that associated with different molecular mechanisms in the process of allograft rejection in kidney transplant patients.
Lessons from transmissible cancers for immunotherapy and transplant
Published in Immunological Medicine, 2022
Rafael Cardoso Maciel Costa Silva, Carolina Panis, Bruno Ricardo Barreto Pires
Transplant rejection is mediated mostly by the adaptive immune system [3]. There are three main mechanisms by which adaptive immunity is triggered to mediate allogeneic tissue rejection: direct, indirect, and semi-direct [4]. The direct pathway is based on the ability of dendritic cells (DCs) from the donor tissue (or transmissible cancer) to present allopeptides and activate host T cells through a non-self MHC. Around 1–10% of T cells can recognize the complex non-self MHC-peptide and mount a specific immune response [5]. The direct pathway is believed to be the dominant immune response during acute rejection. The ability of non-self MHC to present more than one allopeptide, referred as the multiple binary complex model, seems to contribute to the amplification of immune responses and graft rejection [6,7]. The indirect pathway is related to the presentation, by host DCs, of peptides from polymorphic antigens (or neoantigens, in the case of tumors) of the donor [2]. This pathway is associated with late chronic rejection of the transplanted tissues, and it is believed that the T cells clones reactive to this polymorphic alloantigens are distinct from those activated by the direct pathway [2]. The semi-direct pathway is related to the shedding by exosomes, from donor cells, of peptide-loaded MHC into the membrane of recipient DCs, which will present donor MHC-allopeptides to T cells. Several murine studies demonstrated the acquisition of intact alloantigens to recipient DCs after vascularized allograft challenge [8–10]. The semi-direct anddirect pathway would lead to activation of the same T cell clones [2].
Cost, healthcare utilization, and outcomes of antibody-mediated rejection in kidney transplant recipients in the US
Published in Journal of Medical Economics, 2021
Allyson Hart, David Zaun, Robbin Itzler, David Schladt, Ajay Israni, Bertram Kasiske
Kidney transplant is the gold standard for the treatment of end-stage kidney disease (ESKD), but 10-year kidney allograft and patient survival remains suboptimal, at only 50% for deceased donors and 80% for living donor transplants1. Patients with failing transplants experience high mortality rates2, and those who survive must return to dialysis or seek a subsequent kidney transplant, resulting in high costs both financially and for quality of life3. A major cause of graft loss is the rejection of the transplanted kidney. Two types of kidney transplant rejection can occur: T-cell mediated and antibody-mediated rejection (AMR). Previously underrecognized as a clinically significant issue beyond hyperacute rejection at the time of transplantation, antibody-mediated rejection (AMR) is now recognized as a major cause of late kidney graft failures4–6.