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Phosphate overload accelerates vascular aging in uremic patients
Vascular calcification is a very common event in atients affected by diabetes and chronic kidney disease (CKD). Recently, it has been well documented that abnormalities in mineral and bone metabolism in CKD patients are associated with increased morbidity and mortality. Elevated serum phosphate and...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
PAGEPress Publications
2006
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3184654/ https://www.ncbi.nlm.nih.gov/pubmed/21977245 http://dx.doi.org/10.4081/hi.2006.6 |
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author | COZZOLINO, MARIO GALLIENI, MAURIZIO GALASSI, ANDREA BRAMBILLA, CLAUDIA BRANCACCIO, DIEGO |
author_facet | COZZOLINO, MARIO GALLIENI, MAURIZIO GALASSI, ANDREA BRAMBILLA, CLAUDIA BRANCACCIO, DIEGO |
author_sort | COZZOLINO, MARIO |
collection | PubMed |
description | Vascular calcification is a very common event in atients affected by diabetes and chronic kidney disease (CKD). Recently, it has been well documented that abnormalities in mineral and bone metabolism in CKD patients are associated with increased morbidity and mortality. Elevated serum phosphate and calcium-phosphate product levels play an important role in the pathogenesis of vascular mineralization in uremic patients and also appear to be associated with increased cardiovascular mortality. Together with classical passive precipitation of calcium-phosphate in soft tissues, during the last decade it has been demonstrated that inorganic phosphate may cause extraskeletal calcification directly through a real “ossification” of the tunica media in the vasculature of CKD patients. Therefore, control of phosphate retention is now an even more crucial target of treatment in patients affected by chronic kidney disease. |
format | Online Article Text |
id | pubmed-3184654 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | PAGEPress Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-31846542011-10-05 Phosphate overload accelerates vascular aging in uremic patients COZZOLINO, MARIO GALLIENI, MAURIZIO GALASSI, ANDREA BRAMBILLA, CLAUDIA BRANCACCIO, DIEGO Heart Int Article Vascular calcification is a very common event in atients affected by diabetes and chronic kidney disease (CKD). Recently, it has been well documented that abnormalities in mineral and bone metabolism in CKD patients are associated with increased morbidity and mortality. Elevated serum phosphate and calcium-phosphate product levels play an important role in the pathogenesis of vascular mineralization in uremic patients and also appear to be associated with increased cardiovascular mortality. Together with classical passive precipitation of calcium-phosphate in soft tissues, during the last decade it has been demonstrated that inorganic phosphate may cause extraskeletal calcification directly through a real “ossification” of the tunica media in the vasculature of CKD patients. Therefore, control of phosphate retention is now an even more crucial target of treatment in patients affected by chronic kidney disease. PAGEPress Publications 2006-05-28 /pmc/articles/PMC3184654/ /pubmed/21977245 http://dx.doi.org/10.4081/hi.2006.6 Text en © Wichtig Editore, 2006 |
spellingShingle | Article COZZOLINO, MARIO GALLIENI, MAURIZIO GALASSI, ANDREA BRAMBILLA, CLAUDIA BRANCACCIO, DIEGO Phosphate overload accelerates vascular aging in uremic patients |
title | Phosphate overload accelerates vascular aging in uremic patients |
title_full | Phosphate overload accelerates vascular aging in uremic patients |
title_fullStr | Phosphate overload accelerates vascular aging in uremic patients |
title_full_unstemmed | Phosphate overload accelerates vascular aging in uremic patients |
title_short | Phosphate overload accelerates vascular aging in uremic patients |
title_sort | phosphate overload accelerates vascular aging in uremic patients |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3184654/ https://www.ncbi.nlm.nih.gov/pubmed/21977245 http://dx.doi.org/10.4081/hi.2006.6 |
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