Review delineates coronary artery abnormalities in chronic kidney disease, indicating a need for targeted cardiovascular risk prevention.
Cardiovascular disease represents the primary cause of morbidity and mortality among patients with chronic kidney disease (CKD). Emerging evidence suggests that coronary artery pathology in CKD diverges from the traditional atherosclerotic phenotype seen in individuals with maintained renal function. This review delineates coronary artery-specific alterations in CKD, focusing on mechanisms that expedite atherogenesis, characteristics of plaques, calcific remodeling, and dysfunction of the coronary microvasculature. CKD fosters a pro-inflammatory, pro-oxidative, and pro-calcific environment, which results in endothelial damage and vascular calcification remodeling. Furthermore, coronary plaques in CKD are more likely to exhibit larger lipid-rich necrotic cores, heightened inflammatory cell infiltration, a significant calcific burden, and vulnerability indicators such as cholesterol crystals and microdisruptions. Impaired coronary microvascular function is also prevalent and may account for ischemia with non-obstructive coronary arteries. In summary, CKD is linked to a rapid, calcification- and inflammation-driven form of coronary disease characterized by both macrovascular plaque remodeling and microvascular dysfunction. This underscores the necessity of early identification and prevention of cardiovascular risk, targeting CKD-specific mechanisms in conjunction with conventional risk factors.
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Hanke et al. (2026) studied this question.
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