Kidney diseases are often associated with the progression of atherosclerosis. This still enigmatic relationship does not seem to be an accidental artefact, but a clinically important effect of uraemia - an excessive accumulation of uraemic toxins poorly excreted from the body due to renal failure.

Some uraemic toxins, like homocysteine, have been well characterized with regard to their cardiovascular toxicity, while there are hardly any reports on some compounds, such as indoxyl sulphate, lanthionine and others. Current data clearly suggests that oxidative stress is a significant factor in cardiovascular risk in kidney diseases. The list of uraemic toxins is still expanding, however, the exact atherogenic potential of old and new molecules is still far from the final estimation and remains a challenge. Moreover, the usefulness of antioxidants as potential drugs that inhibit the progression of atherosclerosis in uremia, although seemingly promising, still requires reliable experimental confirmation.

The aim of this Special Issue is to summarize the most recent data describing the molecular mechanisms that lead to atherosclerosis from uraemia, through reactive oxygen species (playing the role of initiators, mediators, or effectors). Since atherogenesis is a multifactorial process, we welcome papers presenting redox studies in all branches of uraemia-associated atherosclerosis. We would also like to summarize the current state of knowledge of the possible use of antioxidants (natural and synthetic) in the prevention of uremia-associated atherosclerosis. We encourage researchers to submit original research articles based on in vitro, animal, and clinical studies as well as short or comprehensive reviews. Reports about well-known and newly identified or even potential uraemic toxins are welcomed.

Potential topics include but are not limited to the following:

• The role of reactive oxygen species induced by uraemic toxins in the dysregulation of primary and secondary haemostasis
• Metabolism of (anti)atherogenic molecules (glucose, lipoproteins, triglycerides, uric acid, and others) under conditions of oxidative stress caused by uraemic toxins
• Biology of the heart and coronary vessels under oxidative stress triggered by uraemic toxins
• Biology of cells of the vascular wall exposed to reactive oxygen species in uraemia
• Reactive oxygen species induced by uremic toxins as modulators of the inflammatory reaction leading to atherosclerosis
• Structural and functional changes of endogenous antioxidant systems in the cardiovascular system under uraemic stress
• Natural and synthetic antioxidants as possible antiatherogenic factors in uraemia-associated atherogenesis