Targeting oxidative stress, a crucial challenge in renal transplantation outcome (original) (raw)
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Role of ischemia-reperfusion in oxidative stress-mediated injury during kidney transplantation
Clinical research and trials, 2019
Renal transplant (RT) is the definitive treatment for end-stage renal disease, which is known as a high prevalence pathology with strong economic repercussion both for patients and health systems. Solid organ transplantation is a classically described clinical setting in which massive amounts of reactive oxygen species (ROS) are produced due to ischaemia-reperfusion, thus becoming an essential pathophysiological element involved in delayed graft function in the context of RT. Nevertheless, no clinical protocol yet exists to counteract the damage mediated by ROS intensively produced throughout the transplant process. The available evidence shows a number of successful experiences in the use of antioxidant supplementation and reinforcement over other oxidative stress-related pathologies. This article addresses the pathophysiological role of oxidative stress in RT and its known consequences in function and structure of the allograft, with the objective of gathering consistent information that demonstrates the central role of oxidative stress in this pathology, and to consider it as a possible therapeutic approach in the future.
Ischemia/Reperfusion Injury in Kidney Transplantation: Mechanisms and Prevention
Transplantation Proceedings, 2008
Ischemia has been an inevitable event accompanying the procedure of kidney transplantation. Ischemic changes start with brain death which is associated with severe homodynamic disturbances: increasing intracranial pressure results in bradycardia and decrease in cardiac output; Cushing reflex causes tachycardia and increase of blood pressure, and after short period of stabilization, systemic vascular resistance declines with hypotension leading to cardiac arrest. Free radical mediated injury occurs and release of pro-inflammatory cytokines and activation of the innate immunity develops. It has been is suggested that all of these changes -the early innate response and the ischemic tissue damage play a role in development of adaptive response which in turn may lead to acute kidney rejection, Hypothermic kidney storage of various duration before transplantation adds to ischemic tissue damage. The final stage of ischemic injury occurs during reperfusion. Reperfusion injury, as an effector phase of ischemic injury, develops hours or days after initial insult. Repair and regeneration process occur along with cellular apoptosis, autophagy and necrosis, and the fate of the organ depends on whether cell death or regeneration prevails. The whole process has been described as the ischemia/reperfusion injury. It has profound influence not only on the early, but also late function of the transplanted kidney. Prevention of I/R injury should be started before recovery of the organs (donor pretreatment).
2017
Renal transplantation (RT) is considered the "gold standard" treatment for end-stage renal disease patients. Efforts should be made to reduce ischaemia-reperfusion (IR) injury, which unavoidably occurs in RT as long as several clinical settings, i.e. open-heart surgeries, prosthesis implantation, among others. It is well known that IR is primarily responsible for injury associated with RT. Consequently, tissue inflammation and organ dysfunction will ensue due to the occurrence of oxidative stress (OS) in the reperfused tissue, a condition generated when endogenous antioxidant defences become overwhelmed by a massive production of reactive oxygen species. Furthermore, OS is involved in the impairment of renal function, leading to deleterious conditions such as delayed graft function (DGF), which is a common clinical expression of IR injury in RT. Omega-3 polyunsaturated fatty acids (n-3 PUFA) have been widely used in different clinical settings to counteract the deleterious effects of OS. Thus, based on the currently available literature, the central aim of this review was to propose an n-3 PUFA-based strategy targeting the key role of OS in the pathophysiology of renal IR injury in order to encourage protection against the occurrence of DGF.
Modulation Factors of Oxidative Status in Stable Renal Transplantation
Transplantation Proceedings, 2005
Reactive oxygen species (ROS) trigger a biomolecular alteration that causes functional and structural changes. In renal transplantation, there is an increase in oxidative phenomena related to endothelial dysfunction, inflammation, and atherosclerosis, the main cause of cardiovascular complications and chronic allograft failure. The present study was designed to assess the oxidative state of transplant patients with stable renal function, in order to establish differences in oxidative, biochemical, and clinical parameters between patients treated with tacrolimus versus cyclosporine. We studied 67 stable kidney transplant patients treated with calcineurin inhibitors who were not receiving cholesterollowering therapy, and 14 healthy subjects. Data were collected on biochemical parameters: lipid profile (apoA, apoB, total cholesterol and fractions, and triglycerides); urea; and creatinine; oxidative parameters: malondialdehyde (MDA) as a lipid peroxidation marker, glutathione peroxidase (GPx), catalase, superoxide dismutase (SOD), glutathione reductase (GR), and antibodies against oxidized LDL; and clinical variables. Transplanted patients showed a higher oxidative status (MDA increase and GPx decrease) than healthy subjects. The oxidative status did not differ between the cyclosporine and tacrolimus cohorts. Some factors during the posttransplant period, such as delayed graft function, cytomegalovirus infection, and microalbuminuria, which may damage renal function, produce a decreased antioxidant capacity (lower GPx).
Role of Oxidative Stress and Cytokines in Renal Ischemia Reperfusion Injury
Annals of Tropical Medicine and Public Health
Ischemia reperfusion injury is the principal and the most severe cause of acute kidney injury. This is the result of a generalized or localized degeneration in the transportation of oxygen and nutrients to cells and the removal of waste products from kidney cells. Ischemia reperfusion injury is the main chance element for the development of persistent kidney disorder; this is explained in terms of renal or instantaneous system irregularity for more than 3 months. Throughout various clinical cases, kidneys are exposed to the ischemia reperfusion injury, interpreted by interruption of the kidney blood out glide by continued by successive perfusion development, such as resuscitation circulatory arrest, cardiac and vascular surgery, kidney transplantation and trauma. This article offers the literature's basic information to evaluate the most relevant details about the Oxidative stress and cytokines that act in renal ischemia reperfusion injury.
Clinical Research and Trials
Liver transplantation is the definitive therapy for most patients with end-stage liver failure. During this surgical procedure, hepatic ischemia-reperfusion is an unavoidable phenomenon known to be involved in graft injury, often resulting in postoperative complications and liver dysfunction. Although the pathophysiology behind ischemia reperfusion injury (IRI) comprises various mechanisms, oxidative stress (OS) has been recognized as a key factor. The aims of this review are to provide an updated overview of the role of OS in liver IRI, providing some bases for therapeutic interventions based on counteracting the OS-related mechanism of injury and thus suggesting novel possible strategies in the prevention of IRI in liver transplants.