Nephrol Dial Transplant (2002) 17: 201-203
© 2002 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
Inflammation, CRP, calcium overload and a high calcium–phosphate product: a ‘liaison dangereuse’
1 Department of Nephrology and Dialysis, Ospedale San Paolo, University Center, Milan, Italy, 2 Clinical and Laboratory Research Department at Bellco, Bellco SpA, Mirandola, Italy and 3 Department of Internal Medicine, University of Pisa, Pisa, Italy
Introduction
Ectopic calcifications are defined as a process of inappropriate biomineralization occurring in soft tissues [1]. They are typically composed of calcium salts. In uraemic patients such a condition—referred to as metastatic calcification—is associated with systemic mineral imbalance (hyperphosphataemia and increased calcium–phosphate ion product), which is claimed to be responsible for progressive cardiac and vascular damage, leading to invalidating clinical complications and increased mortality risk.
More specifically, Levin et al. [2] showed recently that the critical limit for plasma phosphate is 6.5 mg/dl. Patients with plasma levels above that limit have a 52% higher risk of death from coronary artery disease, compared with the patients whose serum phosphate is below it. Block et al. [3] demonstrated that serum phosphate levels >6.5 mg/dl and a calcium–phosphate ion product >72 mg2/dl2 are associated with an 18–39% higher risk of death, compared with normal reference
Calcium overload—how?
Soft-tissue calcium deposition—the cofactors
Assessing the risk
Again about vascular damage—the second part of the story
Inflammation and calcium—a ‘liaison dangereuse’
Conclusions
Notes
References
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