9
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Osteopontin protects against high phosphate-induced nephrocalcinosis and vascular calcification

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Pathologic calcification is a significant cause of increased morbidity and mortality in patients with chronic kidney disease (CKD). The precise mechanisms of ectopic calcification are not fully elucidated, but it is known to be caused by an imbalance of pro-calcific and anti-calcific factors. In the CKD population, an elevated phosphate burden is both highly prevalent and a known risk factor for ectopic calcification. Here we tested whether osteopontin, an inhibitor of calcification, protects against high phosphate load-induced nephrocalcinosis and vascular calcification. Osteopontin knockout mice were placed on a high phosphate diet for eleven weeks. Osteopontin deficiency together with phosphate overload caused uremia, nephrocalcinosis characterized by substantial renal tubular and interstitial calcium deposition, and marked vascular calcification when compared to controls. While the osteopontin-deficient mice did not exhibit hypercalcemia or hyperphosphatemia, they did show abnormalities in the mineral metabolism hormone fibroblast growth factor 23. Thus, endogenous osteopontin plays a critical role in the prevention of phosphate induced nephrocalcinosis and vascular calcification in response to high phosphate load. A better understanding of osteopontin’s role in phosphate induced calcification will hopefully lead to better biomarkers and therapies for this disease, especially in patients with CKD and other at risk populations.

          Related collections

          Author and article information

          Journal
          0323470
          5428
          Kidney Int
          Kidney Int.
          Kidney international
          0085-2538
          1523-1755
          10 February 2016
          09 March 2016
          May 2016
          01 May 2017
          : 89
          : 5
          : 1027-1036
          Affiliations
          [1 ]Pediatrics, University of Wisconsin School of Medicine and Public Health
          [2 ]Bioengineering, University of Washington
          Author notes
          Address for Correspondence: Cecilia Giachelli, Department of Bioengineering, University of Washington, 3720 15th Ave NE, Foege N330L, Box 355061, Seattle, WA 98195, phone: 206-543-0205, fax: 206-616-9763, ceci@ 123456uw.edu
          Article
          PMC4834144 PMC4834144 4834144 nihpa758318
          10.1016/j.kint.2015.12.046
          4834144
          27083280
          329c479e-c327-4615-8a8e-19ec3f729151
          Categories
          Article

          Comments

          Comment on this article