Abstract
Phosphate is an important cardiovascular risk factor and lowering elevated blood phosphate concentrations is a main therapeutic target in kidney patients. Phosphate is subject to the blood mineral buffering system which controls the precipitation of calcium and phosphate. Calciprotein particles (CPP), self-assembling complexes of calcium phosphate and serum proteins, are the nanomorphological correlates of this system. CPP1 are spherical, 50-100 nm in diameter, and contain amorphous mineral. CPP2 are oblongated, 100-200nm in the long axis, and they contain a crystalline mineral core. The relative abundance and biological activity of these particles are a matter of intense research, because they can cause oxidative stress, inflammation, and calcification in cellular assay. Therapeutically reducing this endogenous stressor by prolonging crystal formation time might improve patient outcome. This concise review article summarizes our current knowledge about the blood mineral buffering system and proposes Mineral Stress as a novel modifiable cardiovascular risk factor. It furthermore outlines possible implications this might have for improving patient care.
Highlights
Phosphate is an important cardiovascular risk factor and lowering elevated blood phosphate concentrations is a main therapeutic target in kidney patients
Phosphate is subject to the blood mineral buffering system which controls the precipitation of calcium and phosphate
The relative abundance and biological activity of these particles are a matter of intense research, because they can cause oxidative stress, inflammation, and calcification in cellular assay. Reducing this endogenous stressor by prolonging crystal formation time might improve patient outcome. This concise review article summarizes our current knowledge about the blood mineral buffering system and proposes Mineral Stress as a novel modifiable cardiovascular risk factor
Summary
Patients suffering from chronic kidney disease (CKD), and even more so those with advanced disease already undergoing dialysis treatment, are at very high risk of cardiovascular morbidity and mortality [1]. The direction of causality for these relationships largely remains unresolved This is especially true for vascular calcification, where it is uncertain whether it is the functional or structural impact of calcium phosphate deposition (e.g., vessel stiffness, altered remodeling, and plaque instability) or the underlying processes leading to ectopic mineralization that are injurious and more directly related to outcome. Blood phosphate was identified by Block and colleagues as a major nontraditional cardiovascular risk factor in patients with kidney disease [4, 5]. Despite often aggressive attempts to address this important therapeutic target, International Journal of Nephrology concomitant reductions in cardiovascular prognosis have not been achieved This raises questions about our understanding of the pathophysiologic mechanism(s) underlying cardiovascular disease in kidney disease patients and whether the assumptions on which they are based are correct
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
