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Uremic Toxins and Vascular Dysfunction
Isabelle Six1, Nadia Flissi1, Gaëlle Lenglet1
1UR 7517 UPJV, Pathophysiological Mechanisms and Consequences of Cardiovascular Calcifications (MP3CV), Picardie Jules Verne University, 80025 Amiens, France.
Insights
Uremic toxins (UTs) from chronic kidney disease (CKD) disrupt vascular function by altering vasomotricity. This review details how UT accumulation causes inflammation, oxidative stress, and reduced nitric oxide, contributing to cardiovascular disease.
Area of Science:
- Cardiovascular Science
- Nephrology
- Vascular Biology
Background:
- Vascular dysfunction is central to cardiovascular pathologies and conditions with cardiovascular impact, like chronic kidney disease (CKD).
- Altered vasomotricity, an imbalance in vascular relaxing and contracting factors, is a key aspect of vascular dysfunction.
- Vascular dysfunction initiates atherosclerosis and vascular calcification, and is an emerging risk factor in CKD.
Purpose of the Study:
- To review the mechanisms by which uremic toxins (UTs) induce vascular dysfunction in patients with chronic kidney disease (CKD).
Main Methods:
- This review synthesizes current knowledge on the pathophysiological pathways linking UTs to vascular dysfunction.
- Focuses on the role of accumulated UTs, including phosphate, para-cresyl sulfate, indoxyl sulfate, and FGF23, in CKD.
Main Results:
- Accumulation of UTs in CKD is associated with systemic inflammation and oxidative stress.
- UTs contribute to decreased nitric oxide production, impairing vascular relaxation.
- These factors collectively promote vascular dysfunction and associated cardiovascular risks.
Conclusions:
- Uremic toxins significantly contribute to vascular dysfunction in CKD through multiple interconnected mechanisms.
- Understanding these mechanisms is crucial for developing targeted therapies to mitigate cardiovascular risk in CKD patients.
Abstract:
Vascular dysfunction is an essential element found in many cardiovascular pathologies and in pathologies that have a cardiovascular impact such as chronic kidney disease (CKD). Alteration of vasomotricity is due to an imbalance between the production of relaxing and contracting factors. In addition to becoming a determining factor in pathophysiological alterations, vascular dysfunction constitutes the first step in the development of atherosclerosis plaques or vascular calcifications. In patients with CKD, alteration of vasomotricity tends to emerge as being a new, less conventional, risk factor. CKD is characterized by the accumulation of uremic toxins (UTs) such as phosphate, para-cresyl sulfate, indoxyl sulfate, and FGF23 and, consequently, the deleterious role of UTs on vascular dysfunction has been explored. This accumulation of UTs is associated with systemic alterations including inflammation, oxidative stress, and the decrease of nitric oxide production. The present review proposes to summarize our current knowledge of the mechanisms by which UTs induce vascular dysfunction.
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