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Adipose tissue and inflammation in chronic kidney disease
Jonas Axelsson1, Olof Heimbürger, Peter Stenvinkel
1Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Division of Renal Medicine, Stockholm, Sweden.
Insights
Inflammation, driven by altered adipokines from fat tissue, significantly impacts cardiovascular disease in dialysis patients. Further research is needed to understand these complex interactions and improve patient outcomes.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Cardiovascular disease (CVD) is a leading cause of death in end-stage renal disease (ESRD) patients.
- Traditional risk factors do not fully explain the high CVD prevalence in ESRD.
- Inflammation, insulin resistance, oxidative stress, wasting, and endothelial dysfunction are implicated in ESRD-related CVD.
Purpose of the Study:
- To explore the role of adipose tissue-derived adipokines and cytokines in ESRD.
- To investigate the link between altered adipokine levels and CVD in ESRD patients.
- To highlight the need for further research into the complex interactions involved.
Main Methods:
- Review of recent studies on adipose tissue function and adipokine secretion.
- Analysis of serum adipokine and cytokine levels in chronic kidney disease (CKD) patients.
- Examination of the proposed pro-inflammatory and metabolic effects of these factors.
Main Results:
- Adipose tissue secretes various adipokines (leptin, adiponectin, visfatin) and cytokines (resistin, TNF-α, IL-6).
- Serum levels of these factors are elevated in CKD, likely due to reduced kidney excretion.
- These factors may exert pro-inflammatory effects and contribute to metabolic disturbances.
Conclusions:
- Altered adipokine profiles in CKD may contribute to CVD.
- Complex interactions between adipose tissue, muscle, inflammation, and vascular health require further investigation.
- Understanding these mechanisms is crucial for improving outcomes in high-risk ESRD populations.
Abstract:
Cardiovascular disease remains a major cause of morbidity and mortality in end-stage renal disease patients. As traditional risk factors cannot alone explain the unacceptable high prevalence and incidence of cardiovascular disease in this high-risk population, inflammation (interrelated to insulin resistance, oxidative stress, wasting and endothelial dysfunction) has been suggested to be a significant contributor. Recent studies show that the adipose tissue is a complex organ with functions far beyond the mere storage of energy. Indeed, it has been shown that fat tissue secretes a number of adipokines including leptin, adiponectin and visfatin, as well as a cytokines (here defined as signaling proteins mainly secreted by other cells present in adipose tissue, but sometimes also to a lesser degree by adipocytes per se), such as resistin, tumor-necrosis factor-alpha and interleukin-6. Adipokine serum levels are markedly elevated in chronic kidney disease, probably due to decreased renal excretion. Evidence suggests that they may have pro-inflammatory effects as well as contribute to metabolic derangements. Much research is thus still needed to elucidate the likely complex interactions between different fat tissue depots, muscle tissue and its' effects on inflammation, vascular health and outcome in this high-risk population.
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