Introduction: Cardiovascular disease (CVD) is one of the global leading causes of morbidity and mortality in chronic kidney disease (CKD) patients. Vascular calcification (VC) is a major cause of CVD in this population and is the consequence of complex interactions between inhibitor and promoter factors leading to pathological deposition of calcium and phosphate in soft tissues. Different pathological landscapes are associated with the development of VC, such as endothelial dysfunction, oxidative stress, chronic inflammation, loss of mineralization inhibitors, release of calcifying extracellular vesicles (cEVs) and circulating calcifying cells. Areas covered: In this review, we examined the literature and summarized the pathophysiology, biomarkers and focused on the treatments of VC. Expert opinion: Even though there is no consensus regarding specific treatment options, we provide the currently available treatment strategies that focus on phosphate balance, correction of vitamin D and vitamin K deficiencies, avoidance of both extremes of bone turnover, normalizing calcium levels and reduction of inflammatory response and the potential and promising therapeutic approaches liketargeting cellular mechanisms of calcification (e.g. SNF472, TNAP inhibitors). Creating novel scores to detect in advance VC and implementing targeted therapies is crucial to treat them and improve the future management of these patients.
Cozzolino M., Maffei Faccioli F., Cara A., Boni Brivio G., Rivela F., Ciceri P., et al. (2023). Future treatment of vascular calcification in chronic kidney disease. EXPERT OPINION ON PHARMACOTHERAPY, 24(18), 2041-2057 [10.1080/14656566.2023.2266381].
Future treatment of vascular calcification in chronic kidney disease
Barbuto S.;Speciale S.;Minicucci C.;
2023
Abstract
Introduction: Cardiovascular disease (CVD) is one of the global leading causes of morbidity and mortality in chronic kidney disease (CKD) patients. Vascular calcification (VC) is a major cause of CVD in this population and is the consequence of complex interactions between inhibitor and promoter factors leading to pathological deposition of calcium and phosphate in soft tissues. Different pathological landscapes are associated with the development of VC, such as endothelial dysfunction, oxidative stress, chronic inflammation, loss of mineralization inhibitors, release of calcifying extracellular vesicles (cEVs) and circulating calcifying cells. Areas covered: In this review, we examined the literature and summarized the pathophysiology, biomarkers and focused on the treatments of VC. Expert opinion: Even though there is no consensus regarding specific treatment options, we provide the currently available treatment strategies that focus on phosphate balance, correction of vitamin D and vitamin K deficiencies, avoidance of both extremes of bone turnover, normalizing calcium levels and reduction of inflammatory response and the potential and promising therapeutic approaches liketargeting cellular mechanisms of calcification (e.g. SNF472, TNAP inhibitors). Creating novel scores to detect in advance VC and implementing targeted therapies is crucial to treat them and improve the future management of these patients.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.