AI Article Synopsis

  • - Trace element deficiency, particularly selenium (Se), is prevalent in end-stage renal disease (ESRD) patients due to dialysis and reduced appetite, leading to serious health issues.
  • - Se plays a crucial role in defending against oxidative stress, and its deficiency can lead to complications like cardiovascular disease, bone loss, elevated uric acid, and anemia, which overlap with ESRD issues.
  • - The article emphasizes the need for further research to clarify whether Se deficiency is a primary cause of ESRD complications and to explore how Se supplementation might help alleviate these problems through well-designed clinical trials.

Article Abstract

Trace element deficiency is common among patients with end-stage renal disease (ESRD); the reason is that since these patients undergo dialysis, they lose these elements more than healthy people, and also the use of trace elements is restricted due to loss of appetite. Selenium (Se) is a trace element that is essential for the oxidative stress defense system. Se deficiency leads to some complications similar to those often seen in ESRD patients, such as all-cause mortality due to cardiovascular diseases, bone loss, uric acid elevation, and anemia. This article aims to review the evidence on consequences of Se deficiency in ESRD patients, as well as effects of Se supplementation in hemodialysis patients. Multiple databases were searched to summarize the available evidence on selenium's role in kidney diseases. Since the complications of ESRD and those of Se deficiency are mostly similar, this triggers the idea that Se deficiency may be considered as a cause of these problems, but it needs to be more assessed that Se deficiency is a single factor or there are other factors participated in. Also the role of Se supplementation on resolving the mentioned complications, needs to be more studied through welldesigned clinical studies.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9235365PMC
http://dx.doi.org/10.4103/jrpp.jrpp_3_22DOI Listing

Publication Analysis

Top Keywords

trace element
8
complications esrd
8
esrd patients
8
patients
6
deficiency
6
potential benefits
4
benefits selenium
4
selenium supplementation
4
supplementation patients
4
patients kidney
4

Similar Publications

Public Health.

Alzheimers Dement

December 2024

College of Public Health, University of Kentucky, Lexington, KY, USA.

Background: Previous studies have shown that SF36 summary scores predict incident dementia. However, it is unclear whether SF36 summary scores follow different temporal trajectories. Thus, the goal of this study is to examine possible trajectories for SF36 summary scores.

View Article and Find Full Text PDF

Public Health.

Alzheimers Dement

December 2024

Univ Rennes, Inserm, EHESP, Irset (Institut de Recherche en Santé, Environnement et Travail), Rennes, NA, France.

Chemicals are ubiquitous in modern life. More than 100,000 chemicals are currently used worldwide, and the production continues to increase. Measuring with accuracy all the components of the chemical exposome represents a tremendous challenge which has been only very partly met so far, and gaps in science remain multiple.

View Article and Find Full Text PDF

Background: The G protein-coupled receptor GPR39 is heavily associated with the pathogenesis of neurologic disorders, including Alzheimer's disease (AD) and related dementia (ADRD). Its dysregulation of zinc 2+ (Zn) processes triggers metallic dyshomeostasis, oxidative stress, neuroinflammation, microtubule destabilization, synaptic dysfunction, and tau phosphorylation-all hallmarks of neurodegeneration. Hence, pharmacologic modulation of GPR39 could offer an effective treatment against AD and ADRD.

View Article and Find Full Text PDF

Background: Alzheimer's Disease (AD) is a neurological disease characterized by two major biological components; amyloid beta (abeta) and hyperphosphorylated tau. Research suggests that the hyperphosphorylated tau aggregation seen in late-onset AD is characterized by two independent pathways, one caused by abeta buildup, and the other potentially caused by Apolipoprotein 4 (APOE4). However, research examining the relationship between hyperphosphorylated tau and APOE4 in the absence of abeta has been both inconsistent and lacks behavioral results.

View Article and Find Full Text PDF

Background: Iron is implicated in Alzheimer's disease (AD) and is bound to β-amyloid (Ab) plaques. AD brains have increased 4-hydroxynonenal (HNE) adducts, a lipid decomposition product bound to proteins originating from iron mediated lipid peroxidation. Increased brain iron may result from cerebral microbleeds which by nature are rich sources of iron.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!