Arterial stiffness and increased cardiovascular risk in chronic kidney disease

Abstract

Chronic kidney disease (CKD) is a global public health problem. Cardiovascular disease (CVD) is a common comorbidity and a major cause of mortality in CKD population. While CVD-related mortality is relatively uncommon in young population, it accounts for most deaths in young CKD adults. There are numerous risk factors for CVD in CKD patients including conventional (hypertension, diabetes, dyslipidemia) and nonconventional (oxidative stress, inflammation, anemia, mineral metabolism disorder) factors. Recent studies have placed great emphasis on the association of arterial stiffness (AS) and CVD. AS is traditionally known as an aging marker of the artery; however, increased AS is observed in young and even in pediatric CKD patients; it is also shown that AS progresses in consistent with kidney function decline. Unparallel AS in young CKD population and excessive risk of CVD in young CKD adults show an indication that AS probably offers one of the underlying mechanisms for linking CKD and CVD. AS in CKD patients has multifactorial causes. Comorbidities such as hypertension, diabetes, dyslipidemia, and mineral metabolism disorder which are risk factors for CVD also show great contribution to AS in CKD patients. Increased systolic blood pressure and decreased diastolic blood pressure resulting from AS cause elevated ventricular afterload, lead to impaired coronary perfusion, myocardial ischemia, and ventricular hypertrophy, and consequently develop into CVD event. In this review, we summarized the role of AS in CKD and CVD, aiming to explore the linkage of AS between CKD and CVD.

Oxidative stress in chronic kidney disease

“…Arterial stiffness and medial vascular calcification are already present in up to 35% of patients with early CKD stages (KDIGO G3-4), and this process already starts in children [163]. A role of oxidative stress in the occurrence of arteriosclerosis and arterial stiffness in CKD has also been reported [164]. Several uremic toxins such as AGEs, IS, and p-cresyl sulfate and eNOS uncoupling have been shown to induce arterial stiffness through increased oxidative stress [165][166][167][168][169].…”

The Biology of Hemodialysis Vascular Access Failure

“…[47][48][49][50] Increased WSS increases inflammatory cytokines such as Il-1β, TNF-α, and interferon (IF-γ). [51][52][53] Additionally, WSS has been shown to increase VEGF-A, MMP2, MM9, intercellular adhesion molecule-1 (ICAM-1), and other cytokines implicated in the proliferative aspect of negative remodeling. 54 Many of these changes are likely tied to nuclear factors such as decreased Krüppel-like factor 2 (KLF-2) and increased AKT signaling.…”

Bowel movement frequency, oxidative stress and disease prevention

“…However, it remains unclear whether the cumulative effect is of a sufficient magnitude to prevent cardiovascular disease. Chronic kidney disease is characterized by oxidative stress and increased incidence of cardiovascular mortality (32,33). In a rat model of chronic kidney disease, a high amylose-resistant starch diet was shown to ameliorate oxidative stress, inflammation and progression of chronic kidney disease (34).…”