Abstract
Chronic kidney disease (CKD) is a major public health concern that affects around 10 percent of the world’s population. The severity of CKD is mainly due to the high prevalence of cardiovascular (CV) complications in this population. The aim of this review is to describe the arterial remodelling associated with CKD, to provide a quick overview of the mechanisms involved and to review the recent pharmacological approaches aimed at improving vascular health in CKD. CKD patients are exposed to metabolic and haemodynamic disorders that may affect the CV system. Large artery functional and geometric abnormalities have been well documented in CKD patients and are associated with an increase in arterial stiffness and a maladaptive remodelling. Uraemic toxins, such as indoxyl sulphate, p-cresyl sulphate, protein carbamylation and advanced glycation products, exert various effects on vascular smooth muscle cell functions. The low-grade inflammation associated with CKD may also affect arterial wall composition and remodelling. It is worth noting that the CV risk for CKD patients remains high despite the pharmacological control of traditional CV risk factors, suggesting the need for innovative therapeutic strategies. An interventional study targeting the NLRP3 inflammasome has provided some interesting preliminary results that need to be confirmed, especially in terms of safety.
Highlights
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Between 2010 and 2017, Chronic kidney disease (CKD) increased from the 27th to the 17th most prevalent cause of death in the world according to the Global Burden of Disease study [3]
In 2012, the Kidney Disease: Improving Global Outcomes (KDIGO) working group published a classification of CKD based on the following criteria: cause of CKD, glomerular filtration rate (GFR) and presence of albuminuria
Summary
Cardiovascular (CV) diseases are the main cause of death and morbidity in patients with CKD [7]. Epidemiological studies have shown that patients with a preserved GFR and isolated microalbuminuria have a higher risk of CV mortality than the general population [10]. The epidemiology of CV diseases in CKD patients is different than in patients with a high CV risk but with normal kidney function. Heart failure is three to four times more common in CKD patients than in patients with preserved GFR [14]. An alteration in kidney structure and/or function leads to haemodynamic and metabolic disorders that can affect the CV system. These uraemia-related CV risk factors include, among others, oxidative stress, inflammation, insulin resistance and accumulation of toxins that are usually excreted by the kidneys. In patients with ESRD, interventional studies focussed on traditional CV risk factors such as dyslipidaemia failed to improve survival rates [16,17,18,19,20]
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