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        "resumen" => "<p class="elsevierStylePara">El fosfato no goza de buena reputaci&#243;n entre los nefr&#243;logos&#46; Se asocia con la calcificaci&#243;n vascular y con una gran mortalidad cuando sus niveles en sangre son elevados&#46; Provoca da&#241;os en las c&#233;lulas endoteliales vasculares y transformaci&#243;n osteobl&#225;stica en las c&#233;lulas de los m&#250;sculos lisos vasculares en cultivos&#46; Aunque muchos de los resultados adversos en los pacientes con enfermedad renal cr&#243;nica &#40;ERC&#41; se atribuyen al fosfato&#44; se desconoce el mecanismo molecular preciso que hay detr&#225;s de los problemas que causa&#46; Este d&#233;ficit de conocimiento ha limitado las opciones terap&#233;uticas a la restricci&#243;n del fosfato en la dieta&#44; a captores del fosfato y a la eliminaci&#243;n forzada del fosfato a trav&#233;s de di&#225;lisis&#46; El objetivo de esta revisi&#243;n es llamar la atenci&#243;n de los nefr&#243;logos sobre un metabolito del fosfato denominado part&#237;culas de calciprote&#237;nas &#40;PCP&#41;&#46; Se est&#225; discutiendo la posibilidad de las PCP como pat&#243;geno y nuevo objetivo terap&#233;utico de la ERC&#46;</p>"
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Vol. 34. Núm. 1.enero 2014
Páginas 0-138
Vol. 34. Núm. 1.enero 2014
Páginas 0-138
Acceso a texto completo
Partículas de calciproteínas (PCP): ¿verdaderas culpables de los problemas causados por el fósforo?
Calciprotein particle (CPP): a true culprit of phosphorus woes?
Visitas
12807
Makoto Kuro-oa
a Center for Molecular Medicine. Jichi Medial University, Shimotsuke, Tochigi (Japan), Department of Pathology, Center for Mineral Metabolism, University of Texas Southwestern Medical Center, Dallas, Texas, U.S.A.,
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El fosfato no goza de buena reputación entre los nefrólogos. Se asocia con la calcificación vascular y con una gran mortalidad cuando sus niveles en sangre son elevados. Provoca daños en las células endoteliales vasculares y transformación osteoblástica en las células de los músculos lisos vasculares en cultivos. Aunque muchos de los resultados adversos en los pacientes con enfermedad renal crónica (ERC) se atribuyen al fosfato, se desconoce el mecanismo molecular preciso que hay detrás de los problemas que causa. Este déficit de conocimiento ha limitado las opciones terapéuticas a la restricción del fosfato en la dieta, a captores del fosfato y a la eliminación forzada del fosfato a través de diálisis. El objetivo de esta revisión es llamar la atención de los nefrólogos sobre un metabolito del fosfato denominado partículas de calciproteínas (PCP). Se está discutiendo la posibilidad de las PCP como patógeno y nuevo objetivo terapéutico de la ERC.

Palabras clave:
Captores del fosfato
Palabras clave:
Calcificación vascular
Palabras clave:
Fetuina A
Palabras clave:
Enfermedad renal crónica (ERC)
Palabras clave:
Partículas de calciproteínas (PCP)

Phosphate is a “bad guy” among nephrologists. Phosphate is associated with vascular calcification and high mortality when it is elevated in the blood. It induces damages to vascular endothelial cells and osteoblastic transformation in vascular smooth muscle cells in culture. Although people believe that many adverse outcomes in patients with chronic kidney disease (CKD) are attributed to phosphate, nobody knows the precise molecular mechanism behind these phosphate woes. This knowledge gap has limited therapeutic options to dietary phosphate restriction, phosphate binders, and forced removal of phosphate by dialysis. The purpose of this review is to call nephrologists’ attention to a phosphate metabolite termed calciprotein particles (CPPs). The possibility of CPPs as a pathogen and a novel therapeutic target of CKD is discussed.

Keywords:
Phosphate binders
Keywords:
Vascular calcification
Keywords:
Fetuin-A
Keywords:
Chronic kidney disease (CKD)
Keywords:
Calciprotein particles (CPPs)
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Bibliografía
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