Future treatment of vascular calcification in chronic kidney disease

被引:6
|
作者
Cozzolino, Mario [1 ,3 ]
Maffei Faccioli, Federico [1 ]
Cara, Anila [1 ]
Boni Brivio, Giulia [1 ]
Rivela, Francesca [1 ]
Ciceri, Paola [1 ]
Magagnoli, Lorenza [1 ]
Galassi, Andrea [1 ]
Barbuto, Simona [2 ]
Speciale, Serena [2 ]
Minicucci, Carlo [2 ]
Cianciolo, Giuseppe [2 ]
机构
[1] Univ Milan, Dept Hlth Sci, Renal Div, ASST St Paolo & Carlo, Milan, Italy
[2] Alma Mater Studiorum Univ Bologna, IRCCS Azienda Ospedaliero Univ Bologna, Dialysis & Renal Transplant Unit, Nephrol, Bologna, Italy
[3] ASST St Paolo & Carlo, Dept Hlth Sci, Renal Div, Via Rudini, Milan 820142, Italy
关键词
Vascular calcification; chronic kidney disease; cardiovascular disease; mortality; CKD-MBD; CORONARY-ARTERY CALCIFICATION; MATRIX GLA-PROTEIN; LEFT-VENTRICULAR HYPERTROPHY; VITAMIN-D-RECEPTOR; GROWTH-FACTOR; 23; ENDOTHELIAL PROGENITOR CELLS; GLOMERULAR-FILTRATION-RATE; STAGE RENAL-DISEASE; VALVULAR CALCIFICATION; CARDIOVASCULAR CALCIFICATION;
D O I
10.1080/14656566.2023.2266381
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
IntroductionCardiovascular 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 coveredIn this review, we examined the literature and summarized the pathophysiology, biomarkers and focused on the treatments of VC.Expert opinionEven 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.Expert opinionEven 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.
引用
收藏
页码:2041 / 2057
页数:17
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