Why the study?
Patients with CKD have an increased CV risk only partly explained by established risk factors, with carotid disease playing a role in CV disease and renal disease progression.
This narrative review highlights the arterial phenotype of CKD patients, characterized by carotid stiffening and remodeling, which contributes to their increased cardiovascular and cerebrovascular risk.
Patients with chronic kidney disease (CKD) have an increased cardiovascular (CV) risk that is only in part explained by established risk factors. Carotid arteriosclerosis and atherosclerosis are increased in CKD, play a role in the causation of CV disease in these patients and can affect the progression of renal disease. The arterial stiffening process is evident even in CKD patients with a very mild reduction of glomerular filtration rate (GFR) whereas arterial thickening is evident in more advanced stages. Possible mechanisms include functional and structural alterations of the arterial wall. Arterial stiffness can mediate the effect of CKD on target organs (i.e., brain, kidney and heart). In this review we discuss the arterial phenotype of patients with CKD. This is characterized by increased common carotid artery stiffness and outward remodeling (enlargement and thickening of the arterial wall) and a normal/reduced stiffness paired with an inward remodeling (narrowing of the arterial wall) of muscular arteries. We also discuss the consequences of carotid dysfunction, including the involvement of large elastic arteries stiffness on ventricular-vascular coupling, the mechanisms linking carotid stiffening and increased cardio- and cerebrovascular risk in CKD patients, and the therapeutic options to improve carotid function.
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Zanoli et al. (2021) studied this question.
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