Mecanismos básicos da encefalopatia urêmica

Scaini, Giselli; Ferreira, Gabriela K.; Streck, Emílio L.

doi:10.1590/s0103-507x2010000200016

Cited by 19 publications

(7 citation statements)

References 51 publications

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“…Distant organ cross talk after AKI cause a significant increase in oxidative stress mediators which can directly change the structure of biomolecules in distant organs cell. One of the suggested reasons of uremic encephalopathy is local oxidative stress in cerebral tissue and the renal failure could increase systemic oxidative stress 21 46 . Evidences reports that renal I/R increase lipid peroxidation index, MDA level, in the hippocampus tissue of rats.…”

Section: Discussionmentioning

confidence: 99%

Prazosin Treatment Protects Brain and Heart by Diminishing Oxidative Stress and Apoptotic Pathways After Renal Ischemia Reperfusion

et al. 2022

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Acute kidney injury (AKI) is a major medical challenge caused from renal ischemia-reperfusion (IR) injury connected with different cellular events in other distant organs. Renal IR-related oxidative stress and inflammation followed by cell apoptosis play a crucial role in IR-induced distant organ pathological damages. Prazosin has shown protective effects against IR-injuries. Thus, the current study intended to investigate the possible protective role of prazosin against the consequents of renal IR in the heart and brain tissues. To reach this goal, rats were randomly divided into 3 groups (n=7): Sham, IR and prazosin pretreatment-IR animals (1 mg/kg intraperitoneally injection of prazosin 45 min before IR induction). After 6 h reperfusion, lipid peroxidation and antioxidant markers levels were evaluated in the both, brain and heart tissue. Moreover, apoptotic pathway in the heart and brain tissues were assessed by western blotting. Accordingly, prazosin pretreatment in IR model rats could significantly increase the antioxidant capacity and attenuate apoptotic pathways by increasing the bcl-2 levels and decreasing the expression of Bax and caspase 3 enzymes (P<0.05). Thus, prazosin suppressed cellular damages of heart and brain tissues post kidney IR by anti-oxidative and anti-apoptotic effects, which suggests the plausible use of prazosin in improving the clinical outcomes during AKI after further investigations.

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Section: Discussionmentioning

confidence: 99%

Prazosin Treatment Protects Brain and Heart by Diminishing Oxidative Stress and Apoptotic Pathways After Renal Ischemia Reperfusion

et al. 2022

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“…The pathophysiology of the uremic encephalopathy is complex and multi-factorial. Some of the proposed mechanisms include accumulation of harmful metabolites (uremic toxins such as creatinine, guanidine, guanidinosuccinic acid, and methyl guanidine), disturbances of energy metabolism (decreased levels of creatine phosphate, ATP, and glucose, and increased levels of AMP, ADP, and lactate), imbalance between excitatory and inhibitory neurotransmitters (N-methyl-D-aspartate receptor [NMDA] vs gamma-aminobutyric acid [GABA]), oxidative stress (increased reactive oxygen species), and hormonal imbalances (elevated parathyroid hormone level) [9, 10, 17]. Uremia results in inappropriate activation of excitatory NMDA receptors and concomitant inhibition of inhibitory GABA neurotransmitters, resulting in excitatory neurotoxicity, and is one of the accepted mechanisms of uremic encephalopathy [17].…”

Section: Discussionmentioning

confidence: 99%

“…Uremic encephalopathy is one of the most severe complications of renal failure (both acute and chronic) in humans [8]. It is characterized by a spectrum of clinical signs such as convulsions, seizures, and lack of cognitive ability [9, 10]. Associated lesions include neuronal necrosis, cerebral edema, neuropil vacuolation, vascular thrombosis, hemorrhage, and arterial fibrinoid necrosis [10].…”

Section: Introductionmentioning

confidence: 99%

Uremic encephalopathy in a rhesus macaque (Macaca mulatta): A case report and a brief review of the veterinary literature

Mustonen

González

Mendoza

et al. 2018

J of Medical Primatology

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“…AKI leads to an imbalance of excitatory and inhibitory neurotransmitters due to deregulation of transporters to across the BBB. Accumulation of guanidine compounds, including creatinine, guanidine, guanidinosuccinic acid, and methyl-guanidine, in the cerebrospinal fluid results in their efflux through the transporters into the circulation, which then has a stimulatory effect on N -methyl-D-aspartate (NMDA) glutamate receptors (GluR) and an inhibitory effect on γ-aminobutyric acid receptors [41]. Almost all peripheral inflammatory diseases are associated with wide-ranging behavioral symptoms from mood alterations to fatigue to cognitive impairments [42,43].…”

Section: Neurotransmitter Derangement and Brain Injurymentioning

confidence: 99%

Brain consequences of acute kidney injury: Focusing on the hippocampus

Malek

2018

Kidney Res Clin Pract.

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The high mortality rates associated with acute kidney injury are mainly due to extra-renal complications that occur following distant-organ involvement. Damage to these organs, which is commonly referred to as multiple organ dysfunction syndrome, has more severe and persistent effects. The brain and its sub-structures, such as the hippocampus, are vulnerable organs that can be adversely affected. Acute kidney injury may be associated with numerous brain and hippocampal complications, as it may alter the permeability of the blood-brain barrier. Although the pathogenesis of acute uremic encephalopathy is poorly understood, some of the underlying mechanisms that may contribute to hippocampal involvement include the release of multiple inflammatory mediators that coincide with hippocampus inflammation and cytotoxicity, neurotransmitter derangement, transcriptional dysregulation, and changes in the expression of apoptotic genes. Impairment of brain function, especially of a structure that has vital activity in learning and memory and is very sensitive to renal ischemic injury, can ultimately lead to cognitive and functional complications in patients with acute kidney injury. The objective of this review was to assess these complications in the brain following acute kidney injury, with a focus on the hippocampus as a critical region for learning and memory.

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Mecanismos básicos da encefalopatia urêmica

Cited by 19 publications

References 51 publications

Prazosin Treatment Protects Brain and Heart by Diminishing Oxidative Stress and Apoptotic Pathways After Renal Ischemia Reperfusion

Prazosin Treatment Protects Brain and Heart by Diminishing Oxidative Stress and Apoptotic Pathways After Renal Ischemia Reperfusion

Uremic encephalopathy in a rhesus macaque (Macaca mulatta): A case report and a brief review of the veterinary literature

Brain consequences of acute kidney injury: Focusing on the hippocampus

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