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Calcification Propensity of Serum is Independent of Excretory Renal Function
Vascular calcification is a component of cardiovascular disease, which is leading cause of death in patients with chronic kidney disease (CKD). A functional assay (T50-test) measuring the propensity of human serum to calcify associates with mortality and cardiovascular events in CKD patients. Calcif...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5738386/ https://www.ncbi.nlm.nih.gov/pubmed/29263429 http://dx.doi.org/10.1038/s41598-017-18336-4 |
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author | Bielesz, Bernhard Reiter, Thomas Marculescu, Rodrig Gleiss, Andreas Bojic, Marija Kieweg, Heidi Cejka, Daniel |
author_facet | Bielesz, Bernhard Reiter, Thomas Marculescu, Rodrig Gleiss, Andreas Bojic, Marija Kieweg, Heidi Cejka, Daniel |
author_sort | Bielesz, Bernhard |
collection | PubMed |
description | Vascular calcification is a component of cardiovascular disease, which is leading cause of death in patients with chronic kidney disease (CKD). A functional assay (T50-test) measuring the propensity of human serum to calcify associates with mortality and cardiovascular events in CKD patients. Calcification propensity is known to increase with CKD stage. We investigated whether the T50 readout is directly dependent on excretory kidney function (eGFR) or rather explained by deranged parameters of bone and mineral metabolism in the course of CKD. T50, along with markers implicated in calcification and mineral metabolism, were measured in a cross-sectional cohort of 118 patients with CKD stage 1–5. Associations of T50 with measured parameters were analysed and partial correlations performed to test to which extent the association of T50 with eGFR can be attributed to variation of these parameters. T50 correlates with eGFR, but serum levels of phosphate and calcium largely explain this association. Phosphate, magnesium, fetuin A, albumin, bicarbonate, and serum cross-laps but not Parathyroid Hormone or Fibroblast Growth Factor 23 are associated with T50 in multivariate adjusted models. These findings indicate that T50 values depend mainly on the concentration of promoters and inhibitors of calcification in serum, but not excretory kidney function. |
format | Online Article Text |
id | pubmed-5738386 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57383862017-12-22 Calcification Propensity of Serum is Independent of Excretory Renal Function Bielesz, Bernhard Reiter, Thomas Marculescu, Rodrig Gleiss, Andreas Bojic, Marija Kieweg, Heidi Cejka, Daniel Sci Rep Article Vascular calcification is a component of cardiovascular disease, which is leading cause of death in patients with chronic kidney disease (CKD). A functional assay (T50-test) measuring the propensity of human serum to calcify associates with mortality and cardiovascular events in CKD patients. Calcification propensity is known to increase with CKD stage. We investigated whether the T50 readout is directly dependent on excretory kidney function (eGFR) or rather explained by deranged parameters of bone and mineral metabolism in the course of CKD. T50, along with markers implicated in calcification and mineral metabolism, were measured in a cross-sectional cohort of 118 patients with CKD stage 1–5. Associations of T50 with measured parameters were analysed and partial correlations performed to test to which extent the association of T50 with eGFR can be attributed to variation of these parameters. T50 correlates with eGFR, but serum levels of phosphate and calcium largely explain this association. Phosphate, magnesium, fetuin A, albumin, bicarbonate, and serum cross-laps but not Parathyroid Hormone or Fibroblast Growth Factor 23 are associated with T50 in multivariate adjusted models. These findings indicate that T50 values depend mainly on the concentration of promoters and inhibitors of calcification in serum, but not excretory kidney function. Nature Publishing Group UK 2017-12-20 /pmc/articles/PMC5738386/ /pubmed/29263429 http://dx.doi.org/10.1038/s41598-017-18336-4 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Bielesz, Bernhard Reiter, Thomas Marculescu, Rodrig Gleiss, Andreas Bojic, Marija Kieweg, Heidi Cejka, Daniel Calcification Propensity of Serum is Independent of Excretory Renal Function |
title | Calcification Propensity of Serum is Independent of Excretory Renal Function |
title_full | Calcification Propensity of Serum is Independent of Excretory Renal Function |
title_fullStr | Calcification Propensity of Serum is Independent of Excretory Renal Function |
title_full_unstemmed | Calcification Propensity of Serum is Independent of Excretory Renal Function |
title_short | Calcification Propensity of Serum is Independent of Excretory Renal Function |
title_sort | calcification propensity of serum is independent of excretory renal function |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5738386/ https://www.ncbi.nlm.nih.gov/pubmed/29263429 http://dx.doi.org/10.1038/s41598-017-18336-4 |
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