Calcificaciones cardiovasculares en la enfermedad renal crónica: potenciales implicaciones terapéuticas

Cardiovascular (CV) calcification is a highly prevalent condition at all stages of chronic kidney disease (CKD) and is directly associated with increased CV and global morbidity and mortality. In the first part of this review, we have shown that CV calcifications represent an important part of the C...

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Detalles Bibliográficos
Autores: Bover, Jordi|||0000-0003-3577-2273, Ureña-Torres, Pablo|||0000-0001-6757-1906, Górriz, J.L., Lloret, Maria Jesus|||0000-0002-1632-7062, da Silva, I.|||0000-0001-5502-071X, Ruiz-García, C., Chang, P., Rodríguez, M., Ballarín Castan, José Aurelio|||0000-0002-4556-8164
Tipo de recurso: artículo
Fecha de publicación:2016
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:español
OAI Identifier:oai:ddd.uab.cat:290010
Acceso en línea:https://ddd.uab.cat/record/290010
https://dx.doi.org/urn:doi:10.1016/j.nefro.2016.05.023
Access Level:acceso abierto
Palabra clave:Calcificación vascular
Calcifilaxis
Calcimimetics
Calcimiméticos
Calciphylaxis
Chronic kidney disease
Chronic kidney disease-mineral and bone disorders
Enfermedad renal crónica
Fosfato
Phosphate
Vascular calcification
Vitamin D
Vitamina D
Descripción
Sumario:Cardiovascular (CV) calcification is a highly prevalent condition at all stages of chronic kidney disease (CKD) and is directly associated with increased CV and global morbidity and mortality. In the first part of this review, we have shown that CV calcifications represent an important part of the CKD-MBD complex and are a superior predictor of clinical outcomes in our patients. However, it is also necessary to demonstrate that CV calcification is a modifiable risk factor including the possibility of decreasing (or at least not aggravating) its progression with iatrogenic manoeuvres. Although, strictly speaking, only circumstantial evidence is available, it is known that certain drugs may modify the progression of CV calcifications, even though a direct causal link with improved survival has not been demonstrated. For example, non-calcium-based phosphate binders demonstrated the ability to attenuate the progression of CV calcification compared with the liberal use of calcium-based phosphate binders in several randomised clinical trials. Moreover, although only in experimental conditions, selective activators of the vitamin D receptor seem to have a wider therapeutic margin against CV calcification. Finally, calcimimetics seem to attenuate the progression of CV calcification in dialysis patients. While new therapeutic strategies are being developed (i.e. vitamin K, SNF472, etc.), we suggest that the evaluation of CV calcifications could be a diagnostic tool used by nephrologists to personalise their therapeutic decisions.