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Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Selenium and selenium-dependent antioxidants in chronic kidney disease
1Department of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, Lodz, Poland; College of Health Sciences, Bydgoszcz, Poland.
Abstract:
Oxidative stress plays a key role in numerous disease processes including chronic kidney disease (CKD). In general, oxygen metabolism leads to the formation of reactive oxygen species (ROS) dangerous to cells. Although enzymes and low-molecular-weight antioxidants protect against ROS, chronic imbalances of formation and elimination can eventually overwhelm endogenous defenses leading to deleterious consequences. In CKD, glutathione peroxidases (GSH-Px) play an important role in ROS metabolism. Plasma GSH-Px is synthesized in the kidney and requires selenium (Se) as a cofactor. Interestingly, Se and plasma GSH-Px are both significantly reduced in CKD, especially for those patients on hemodialysis. Supplementation of Se in these patients results in modest increases of GSH-Px, presumably from residual renal tissue. Kidney transplantation rapidly restores plasma GSH-Px. In this chapter, the relevance of these findings to CKD is explored with emphasis on renal disease processes and impact on attendant disorders including cancer and cardiovascular disease.
Insights
Chronic kidney disease (CKD) is linked to oxidative stress and reduced selenium (Se) levels, impacting glutathione peroxidases (GSH-Px). Kidney transplantation effectively restores GSH-Px levels in CKD patients.
Area of Science:
- Biochemistry
- Nephrology
- Oxidative Stress Biology
Background:
- Oxidative stress, resulting from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, is implicated in various diseases, including chronic kidney disease (CKD).
- Glutathione peroxidases (GSH-Px), crucial enzymes in ROS metabolism, require selenium (Se) as a cofactor and are synthesized in the kidney.
- CKD, particularly in patients undergoing hemodialysis, is characterized by significantly reduced levels of both Se and plasma GSH-Px.
Purpose of the Study:
- To explore the role and significance of selenium and glutathione peroxidases in the context of chronic kidney disease.
- To investigate the impact of reduced Se and GSH-Px on renal disease processes and associated conditions like cardiovascular disease and cancer.
- To examine the effects of selenium supplementation and kidney transplantation on plasma GSH-Px levels in CKD patients.
Main Methods:
- Review and analysis of existing literature on oxidative stress, CKD, selenium, and glutathione peroxidases.
- Examination of clinical data regarding Se and GSH-Px levels in CKD patients, including those on hemodialysis.
- Assessment of the impact of interventions such as Se supplementation and kidney transplantation on GSH-Px levels.
Main Results:
- Plasma GSH-Px and Se levels are notably diminished in patients with CKD, especially those on hemodialysis.
- Selenium supplementation leads to a modest increase in GSH-Px, likely due to residual kidney function.
- Kidney transplantation rapidly and effectively restores plasma GSH-Px levels.
Conclusions:
- Selenium is a critical cofactor for GSH-Px, and its deficiency contributes to impaired antioxidant capacity in CKD.
- The kidney's role in synthesizing plasma GSH-Px highlights the organ's importance in systemic antioxidant defense.
- Restoration of kidney function through transplantation effectively reverses GSH-Px deficiency, underscoring the link between renal health and oxidative balance.
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