The Phosphorus and the Vascular Calcification in ESRD between Old Adventures and New Horizons
1Department of Medicine; UOC of Nephrology, “A. Landolfi” Hospital, Via Melito snc, 83029 Solofra, Italy
2Medizinische Klinik III, Klinikum Coburn, Ketschendorfer Straße 33, 96450 Koburg, Germany
3Department of Nephrology and Urology, Federico II University, 80138 Naples, Italy
4Prince of Wales Hospital, Faculty of Medicine, Chinese University of Hong Kong, Shatin, New Territories, Hong Kong
The Phosphorus and the Vascular Calcification in ESRD between Old Adventures and New Horizons
Description
Cardiovascular disease is the main cause of morbidity and mortality in patients with end-stage renal disease (ESRD). The mechanisms underlying this increased risk are not clearly understood. The mechanisms involved in the connection between chronic cardiovascular disease and chronic kidney disease (CKD) are probably numerous. Phosphorus and vascular calcification can be considered the causal link between them. The association between vascular calcifications, inflammation, and atherosclerosis seems to be not a simple passive precipitation but a complex problem of the mineral metabolism in CKD. It has already been shown that vascular calcifications produce an increase in the rigidity of the vascular wall with deceleration of the progression of the pulse wave and alteration of its morphology. Increasing arterial stiffness contributes to increasing ventricular afterload, decreased sub-endocardial perfusion, and increased mechanical fatigue of arteries, resulting in chronic low-grade cardiac ischemia due to increased oxygen consumption and reduced diastolic coronary flow. In fact, serum concentrations of calcium and phosphate exceed the calcium-phosphate solubility product, but precipitation in the vasculature does not normally take place because of VC inhibitors. Human and mouse studies have revealed multiple local and systemic inhibitors which are associated with reduced vascular calcification. But phosphate is probably the predominant inducer of vascular calcification, and elevated serum levels are strongly associated with increased vascular calcification and mortality. So, we are back to phosphorus, reevaluating the effects and observing, at the light of new evidence (such as the FGF and Kloto), its importance in determining the link between CKD and Chronic Heart Disease. Potential topics include, but are not limited to:
- Phosphate metabolism in CKD stages 3–5: dietary and pharmacological control
- Phosphorus, FGF-23 and Kloto
- Calcium-phosphorus and blood pressure in dialysis patients
- Vitamin D and paracalcitol for ESRD and dialysis patients
- Inflammation and vascular calcification
- The new guidelines on KDIGO chronic kidney disease-mineral and bone disorders (CKD-BMDs): expectations, novelty, and confirmation
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