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Published on: May 31, 2016
Novel insights into uremic vascular calcification: role of matrix Gla protein and alpha-2-Heremans Schmid
Markus Ketteler1, Cees Vermeer, Christoph Wanner
1Department of Nephrology and Clinical Immunology, University Hospital Aachen, Germany. mketteler@ukaachen.de
Insights
Cardiovascular mortality is high in dialysis patients due to vascular calcifications. Novel evidence suggests deficiencies in calcification inhibitors, like matrix Gla protein, contribute to this condition.
Area of Science:
- Nephrology
- Cardiology
- Biochemistry
Background:
- Dialysis patients exhibit significantly higher cardiovascular mortality than non-uremic individuals.
- Vascular and valvular calcifications are prevalent in dialysis patients and predict cardiovascular death.
Purpose of the Study:
- To explore the role of calcium-regulatory proteins in the pathogenesis of cardiovascular calcifications in dialysis patients.
- To investigate novel mechanisms beyond hyperphosphatemia contributing to calcification.
Main Methods:
- Review of recent studies on knockout mice.
- Analysis of evidence linking deficiencies in specific proteins to calcification in uremic subjects.
Main Results:
- Hyperphosphatemia and high calcium x phosphate product were traditionally linked to calcification.
- Deficiencies in calcium-regulatory proteins, such as alpha(2)-Heremans Schmid glycoprotein and matrix Gla protein, are implicated in extraosseous calcifications.
Conclusions:
- Deficiencies in key calcification inhibitors may directly contribute to cardiovascular calcifications in dialysis patients.
- This finding offers new therapeutic targets for reducing cardiovascular risk in this population.
Abstract:
Cardiovascular mortality is markedly increased in the dialysis population when compared to non-uremic subjects. Vascular and valvular calcifications are most frequently found in dialysis patients at risk and are independent predictors of cardiovascular death in this population. Traditionally, the presence of hyperphosphatemia and an increased calcium x phosphate product was considered a major pathomechanistic condition leading to excessive vascular and soft-tissue calcifications in uremic subjects. Recent studies in knockout mice, however, revealed that deficiencies in calcium-regulatory proteins may also directly contribute to the development of extraosseus calcifications. alpha(2)-Heremans Schmid glycoprotein and matrix Gla protein are important inhibitors of calcification in vivo and there is novel evidence available that a deficiency in such proteins is involved in the pathogenesis of cardiovascular calcifications in dialysis patients.
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