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Published on: May 31, 2016
Role of Uremic Toxins in Early Vascular Ageing and Calcification
Nikolaos C Kyriakidis1, Gabriela Cobo2, Lu Dai3
1One Health Research Group, Faculty of Medicine, Universidad de Las Américas (UDLA), Antigua Vía a Nayón, Quito EC170124, Ecuador.
Abstract:
In patients with advanced chronic kidney disease (CKD), the accumulation of uremic toxins, caused by a combination of decreased excretion secondary to reduced kidney function and increased generation secondary to aberrant expression of metabolite genes, interferes with different biological functions of cells and organs, contributing to a state of chronic inflammation and other adverse biologic effects that may cause tissue damage. Several uremic toxins have been implicated in severe vascular smooth muscle cells (VSMCs) changes and other alterations leading to vascular calcification (VC) and early vascular ageing (EVA). The above mentioned are predominant clinical features of patients with CKD, contributing to their exceptionally high cardiovascular mortality. Herein, we present an update on pathophysiological processes and mediators underlying VC and EVA induced by uremic toxins. Moreover, we discuss their clinical impact, and possible therapeutic targets aiming at preventing or ameliorating the harmful effects of uremic toxins on the vasculature.
Insights
Uremic toxins in chronic kidney disease (CKD) cause vascular damage, leading to vascular calcification (VC) and early vascular aging (EVA). This review updates understanding of these processes and discusses potential therapeutic targets.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Toxicology
Background:
- Advanced chronic kidney disease (CKD) leads to uremic toxin accumulation, impairing cellular functions and causing chronic inflammation.
- Uremic toxins are linked to vascular smooth muscle cell (VSMC) alterations, promoting vascular calcification (VC) and early vascular aging (EVA).
- These vascular complications contribute significantly to the high cardiovascular mortality observed in CKD patients.
Purpose of the Study:
- To provide an updated overview of the pathophysiology and mediators involved in VC and EVA induced by uremic toxins.
- To discuss the clinical impact of uremic toxin-mediated vascular damage.
- To explore potential therapeutic strategies for preventing or mitigating these harmful effects.
Main Methods:
- Literature review and synthesis of current research on uremic toxins and vascular pathology.
- Analysis of pathophysiological mechanisms underlying vascular calcification and early vascular aging in CKD.
- Discussion of clinical implications and emerging therapeutic targets.
Main Results:
- Uremic toxins disrupt biological functions, leading to inflammation and tissue damage.
- Specific toxins contribute to VSMC changes, driving VC and EVA.
- These vascular changes are key drivers of cardiovascular risk in CKD.
Conclusions:
- Understanding the role of uremic toxins in VC and EVA is crucial for managing cardiovascular risk in CKD.
- Targeting uremic toxins and their downstream effects offers potential therapeutic avenues.
- Further research into therapeutic targets could improve outcomes for CKD patients.
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