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- W2017013072 abstract "To the Editor: Matsui et al.1 have nicely demonstrated a fetuin-containing mineral complex in adenine-treated rats with renal failure that is prevented by alendronate treatment. However, the conclusion that this is related to, or is a marker of vascular calcification is premature. The presence of this complex is not surprising considering the extremely high circulating phosphate levels that occur in this model. In addition, the failure to control pH during the preparation of the serum almost certainly increased these complexes because of the reduced solubility in alkaline solution. We routinely dilute our plasma samples immediately after they are obtained in order to prevent precipitation of calcium and phosphate. The absence of the complexes in alendronate-treated rats can easily be explained by the significantly lower calcium concentration, which, as was shown by the authors, has a major impact on complex formation. The inhibition of vascular calcification is probably due to a direct inhibition as we have shown for bisphosphonates in cultured aortas.2 The formation of the mineral complexes is probably just a physicochemical phenomenon related to ambient phosphate and calcium levels. Their correlation with vascular calcification can be explained by the fact that calcium and phosphate levels also affect vascular calcification, rather than by a direct pathophysiological link." @default.
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- W2017013072 date "2009-10-01" @default.
- W2017013072 modified "2023-09-30" @default.
- W2017013072 title "Mineral complexes and vascular calcification" @default.
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- W2017013072 doi "https://doi.org/10.1038/ki.2009.273" @default.
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