Vascular Calcification in Chronic Kidney Disease: Diversity in the Vessel Wall

Vascular calcification (VC) is one of the major causes of cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). VC is a complex process expressing similarity to bone metabolism in onset and progression. VC in CKD is promoted by various factors not limited to hyperphosphatemia, Ca/Pi imbalance, uremic toxins, chronic inflammation, oxidative stress, and activation of multiple signaling pathways in different cell types, including vascular smooth muscle cells (VSMCs), macrophages, and endothelial cells. In the current review, we provide an in-depth analysis of the various kinds of VC, the clinical significance and available therapies, significant contributions from multiple cell types, and the associated cellular and molecular mechanisms for the VC process in the setting of CKD. Thus, we seek to highlight the key factors and cell types driving the pathology of VC in CKD in order to assist in the identification of preventative, diagnostic, and therapeutic strategies for patients burdened with this disease.

Automated summary

Vascular calcification (VC) is a major cause of cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD), resembling bone metabolism and driven by factors such as hyperphosphatemia and Ca/Pi imbalance. The process involves various cell types and signaling pathways. In-depth analysis of VC types, therapies, and cellular mechanisms aims to aid in the development of preventive, diagnostic, and therapeutic strategies for CKD patients burdened with this disease.