View clinical trials related to Kidney Transplantation.
Filter by:Delayed graft function (DGF), delineated by the necessity for dialytic intervention within the initial week post-transplantation, afflicts approximately 20%-50% of recipients. The primary objective of this study is to investigate the potential efficacy of norepinephrine infusion in conjunction with goal-directed fluid therapy (GDFT) in mitigating the occurrence of DGF among individuals undergoing kidney transplantations. The findings of this investigation have the potential to advance the field of perioperative care in kidney transplantations by providing insights into optimized management strategies.
The purpose of this study is to investigate the safety, tolerability, pharmacokinetics and pharmacodynamics of escalating doses of TCD601 when compared to rATG in de novo renal transplant patients.
Investigator led, prospective, observational cohort study to detect genomic features which can predict outcomes following kidney transplantation. 1. Determine non-HLA genomic mismatches between donor-recipient pairs which impact kidney allograft survival following transplantation 2. Derive polygenic risk scores on pre-transplant blood and/or kidney biopsy samples which predict kidney allograft dysfunction 3. Derive polygenic risk scores on post-transplant blood and/or kidney biopsy samples which predict kidney allograft dysfunction
The goal of this observational study is to develop a machine learning algorithm for early detection of infections in kidney transplant recipients using data recorded by wearable digital health technologies. The main questions it aims to answer are: 1. What are the biometric data pattern changes in impending infections? 2. What accuracy the machine learning algorithm can achieve? Participants will be given/use their own wearable device that will record biometric data. Any infection event will be recorded and an algorithm will be trained to recognize changes in biometric data preceding symptomatic infection.
Using CDW data from 5 tertiary hospitals in Korea, this study identify the optimal range of trough level that can prevent adverse outcome in the early periods after transplantation.
Context Cytomegalovirus (CMV) infection is a frequent and potentially severe event in solid organ transplant (SOT) recipients. Most of available treatment display adverse effects that limit their use. Therefore, in case of an infection, it is of primary importance to identify the patients at high risk of severe infection and/or disease, and who ill benefit the most from antiviral therapy. As CMV infection is mainly controlled by cellular immunity, measuring specific anti-CMV T lymphocyte immunity could be an interesting tool for identifying these at-risk individuals. One of these tests is the QuantiFERON-CMV (QF-CMV) assay (QuiagenTM, Courtabœuf, France). Aim of the study The aim of the study is to determine the extent to which the QF-CMV can be use to identify, among SOT recipients with a CMV viremia, those that may not need antiviral therapy. Methods Participation to the study will be proposed to SOT recipients with an asymptomatic CMV infection with a blood viral load between 1,000 and 15,000 IU/mL. The QF-CMV will be performed in included participants, and the result will be given or not to the clinician in charge (according to the attributed group through randomisation). - In the group without result communication, the clinician in charge will determine whether a treatment is needed according to the guidelines and the local practices. - in the group with result communication, the clinician in charge will be advised not to introduce antiviral therapy if the result is positive, and to determine whether a treatment is needed according to the guidelines and the local practices if the result is positive. In the following weeks, the viral load will be monitored, along with creatininemia, cell blood count, and kalemia (to detect antiviral adverse effect). The participants will be sampled: - 5 to 12 days after QF-CMV sampling (V2) ; - 7 to 14 days days after V2 (V3 - between D12 and D26) ; - 7 to 14 days days after V3 (V4 - between D19 and D40) . Endpoints The primary endpoint is the rate of uncontrolled infection 5 to 12 days after QF-CMV sampling, defined as follows: - Blood CMV viral load >10,000 IU/mL [4 log]; - And/or increase in blood viral load ≥0.5 log IU/mL with CV otherwise >5000 IU/mL; - And/or the onset of CMV disease. The secondary endpoint is the is the occurrence antiviral adverse effects (hematoxicity or nephrotoxicity).
The goal of this observational study is to compare outcomes of robot-assisted kidney transplantation and open kidney transplantation. The main questions are - comprehensively analyze our early experience of robot-assisted kidney transplant patients and compare the results with those of open kidney transplant patients
The goal of the Australian Genomics of Chronic Allograft Dysfunction (AUSCAD) study is a single centre (Westmead Hospital), prospective, observational study, which enrols patients at time of kidney (or kidney-transplant) transplant and tracks the post transplant course. The AUSCAD study aims to generate new knowledge and improve outcomes following kidney transplantation. The primary aim is to determine whether important outcomes (including chronic rejection and graft loss) are correlated with patterns of allograft reactivity, gene expression and susceptibility profiles.
Solid Organ Transplantation (SOT) is made possible by the use of a lifelong immunosuppressive treatment. This treatment limits the response of the immune system, enabling long-term survival of the transplanted organ, but also leading to weaker anti-infectious responses. In this study, we will compare the response to a booster Hepatitis B vaccination (HBV) in SOT patients, either after kidney or liver transplantation. We will also compare the immune response depending on the immunosuppressive treatment. In order to provide a detailed picture of the immune response, we will investigate the usual serological response (anti-HBs antibodies), but also the cellular memory (both T and B) using ELISpot assays and flow-cytometry, over a 6 months period following booster vaccination.
Antibody mediated rejection (ABMR) is a major cause of graft loss after kidney transplantation (KT) and is mainly associated with preformed anti-HLA donor specific antibodies (DSAs) (phenotype 1) or de novo DSAs (dnDSAs) (phenotype 2). Preexisting DSA-associated ABMR have superior graft survival compared with dnDSA-associated ABMR, which could partly be explained by the fact that patients with de novo DSA-associated ABMR have biopsy later, when graft dysfunction and/or proteinuria are already present. ABMR is a progressive process with an early stage called subclinical ABMR (sABMR), in which histological lesions are present in the kidney graft without clinical graft dysfunction. These early lesions are now well recognized as risk factors for transplant glomerulopathy and poor graft survival in phenotype 1 ABMR (ref 5). The impact of sABMR associated with dnDSA at any time post-transplant has been less studied and reported. Recently, we published a retrospective multicenter study within the Spiesser Group that included 123 patients without graft dysfunction who underwent graft biopsy because of the presence of dnDSA (One Lambda, MFI > 1000). Performing a kidney graft biopsy after dnDSA indentification without renal dysfunction leads to the diagnosis of active sABMR in 35 % of cases. Nevertheless, we did not observe any effect of standard of care treatment in active sABMR. Very recently, an expert consensus for the recommended treatment for ABMR after KT was published. They concluded the clear lack of evidence but a standard of care for ABMR was nevertheless defined. Therefore, we propose to evaluate a new strategy for active sABMR, testing a conversion from calcineurin inhibitor (CNI) to belatacept associated with the recently recommended standard of care (SOC) compared to continuing CNI. Belatacept might help to manage nonadherence, decrease the toxicity of CNI on an endothelium already affected by microvascular inflammation, and reduce DSA titers. The monitoring of dnDSA after KT and an indication graft biopsy in case of appearance, even in the absence of graft dysfunction, is not part of a routine clinical practice in all KT centers. This strategy could be a valuable option, in order to begin treatment of ABMR before graft dysfunction occurs, and therefore to improve prognosis associated with phenotype 2 ABMR. Parajuli et al.4 suggested that early diagnosis and treatment of sABMR with SOC, using DSA monitoring may improve outcomes after KT, but this is a retrospective and no-randomized study. This study will be the first prospective randomized study in the context of de novo DSA. We will evaluate a new combination of treatment for ABMR in the context of dnDSA with subclinical lesions and in the same time may help to determine the real incidence of sABMR in KT recipients with subclinical dnDSA. The use of belatacept in the context of sABMR to improve the non-adherence and to decrease the endothelial toxicity had never been evaluated in a prospective way.