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Updated: Jun 1, 2026
A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
Published on: June 2, 2022
Does any therapy exist for vascular calcifications in uremia?
Sandro Mazzaferro1, Marzia Pasquali, Silverio Rotondi
1Department of Cardiovascular, Respiratory, Nephrologic and Geriatric Sciences, Sapienza University of Rome, Rome, Italy. sandro.mazzaferro@uniroma1.it
Insights
Vascular calcifications in uremia are complex, influenced by ion imbalances and inhibitors like pyrophosphate. Current therapies focus on managing calcium, phosphate, and parathyroid hormone levels, but individualized strategies are crucial for effective treatment.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Biochemistry
Background:
- Vascular calcification in uremia is multifactorial, involving traditional and nontraditional risk factors.
- Divalent ion derangements are critical, alongside the role of physiological calcification inhibitors.
- Pyrophosphate is a potent inhibitor, but its instability limits clinical use; bisphosphonates are challenging in renal patients.
Purpose of the Study:
- To review the complex pathogenesis of vascular calcifications in uremia.
- To discuss potential therapeutic targets beyond current management strategies.
- To highlight the importance of individualized treatment approaches.
Main Methods:
- Review of current literature on uremic vascular calcification.
- Analysis of the roles of divalent ions and calcification inhibitors.
- Evaluation of experimental models and potential therapeutic agents.
Main Results:
- Multiple proteins (e.g., Matrix Gla protein, fetuin) are implicated in calcification.
- Metabolic acidosis induction is not recommended; sodium thiosulphate shows potential but requires safety confirmation.
- Current therapies aim to normalize calcium, phosphate, and parathyroid hormone, with uncertain efficacy.
Conclusions:
- Understanding uremic vascular calcification requires considering ion balance, inhibitors, and specific proteins.
- Novel therapeutic strategies are under investigation, but require further validation.
- Personalized treatment selection is essential for managing vascular calcifications in uremic patients.
Abstract:
The pathogenesis of vascular calcifications in uremia is not completely understood, but is regarded as multifactorial, involving traditional and nontraditional risk factors. In particular, derangements in divalent ions are considered of outmost importance, but also the role of physiologic inhibitors of calcification is now claimed. The most powerful physiologic inhibitor of calcification is pyrophosphate, but its biochemical instability precludes its clinical use to date. The pharmacologic analogs of pyrophosphate, bisphosphonates, cannot be easily tested for this purpose in renal patients, given their renal clearance. The list of proteins involved in calcification is a growing one, and experimental models point to the potential clinical relevance of matrix Gla protein, fetuin, osteopontin, osteoprotegerin and bone morphogenetic protein-7. Induction of metabolic acidosis, although theoretically useful, is not recommended, while administration of sodium thiosulphate could be beneficial, but its safety awaits confirmation. Actually, the only available therapies for vascular calcifications are those directed toward achievement of the biochemical targets for calcium, phosphate and parathyroid hormone with the hope, but not the certainty, that this will be efficacious. However, to this purpose, selection of the most appropriate strategy in the individual patient seems essential.
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