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      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Individualization of dialysate calcium concentration according to baseline pre-dialysis serum calcium.

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          Abstract

          A positive calcium balance may contribute to vascular calcification, while a negative balance increases iPTH. We explored the impact of different dialysate calcium concentrations on bone and mineral metabolism parameters according to pre-dialysis serum calcium levels.

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          Elevated extracellular calcium levels induce smooth muscle cell matrix mineralization in vitro.

          Hsueh Yang, Gabrielle Curinga, Cecilia M. Giachelli (2004)
          Hyperphosphatemia, elevated calcium x phosphorus product (Ca x P), and calcium burden, major causes of vascular calcification, are correlated with increased cardiovascular morbidity and mortality in dialysis patients. To address the underlying mechanisms responsible for these findings, we have utilized an in vitro human smooth muscle cell (HSMC) model of vascular calcification. Previous studies using this system demonstrated enhanced calcification of HSMC cultures treated with phosphorus levels in the hyperphosphatemic range, and implicated a sodium-dependent phosphate cotransport-dependent mechanism in this effect. In the present study, we examine the effect of increasing calcium concentrations on HSMC calcification in vitro. Increasing calcium to levels observed in hypercalcemic individuals increased mineralization of HSMC cultures under normal phosphorus conditions. Importantly, at these total calcium concentrations, ionized calcium levels increased from 1.2 mmol/L to 1.7 mmol/L, consistent with levels observed physiologically in normocalcemic and hypercalcemic individuals, respectively. Furthermore, increasing both calcium and phosphorus levels led to accelerated and increased mineralization in the cultures. Calcium-induced mineralization was dependent on the function of a sodium-dependent phosphate cotransporter, since it was inhibited by phosphonoformic acid (PFA). While elevated calcium did not affect short-term phosphorus transport kinetics, long-term elevated calcium treatment of HSMCs induced expression of the sodium-dependent phosphate cotransporter, Pit-1. These studies suggest that elevated calcium may stimulate HSMC mineralization by elevating Ca x P product and enhancing the sodium-dependent phosphate cotransporter-dependent mineralization pathway previously observed in HSMCs.
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            Bone metabolism and disease in chronic kidney disease

            Garabed Eknoyan, Adeera Levin, Nathan W. Levin (2003)
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              Association of bone activity, calcium load, aortic stiffness, and calcifications in ESRD.

              F Metivier, G London, Christine de Peretti … (2008)
              An inverse relationship between arterial calcifications and bone activity has been documented in patients with ESRD. Calcium overload is associated with arterial calcification, which is associated with arterial stiffening. Whether bone activity interacts with calcium load, aortic stiffness, or arterial calcification is unknown. This study assessed the impact of bone activity on the relationships between the dosage of calcium-containing phosphate binders and aortic stiffness (measured by pulse wave velocity) or abdominal aorta calcification score. Aortic stiffness and calcification were both positively associated with calcium load and negatively associated with bone activity. A significant interaction was found between dosage of calcium-containing phosphate binders and bone activity such that calcium load had a significantly greater influence on aortic calcifications and stiffening in the presence of adynamic bone disease. Independent of any other factor, including dosage of calcium-containing phosphate binders, adynamic bone was associated with greater aortic stiffening, suggesting cross-talk between the bone and arterial walls.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Blood Purif.
                Title: Blood purification
                Publisher: S. Karger AG
                ISSN (Electronic): 1421-9735
                ISSN (Print): 0253-5068
                Publication date (Electronic): 2014
                Volume: 38
                Issue: 3-4
                Affiliations
                [1 ] Division of Nephrology and Hypertension, IIS-Fundación Jiménez Díaz, Madrid, Spain.
                Article
                Publisher Item ID: 000366126
                DOI: 10.1159/000366126
                PubMed ID: 25531119
                SO-VID: f859c981-b034-4455-b071-57182242bb33
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