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      Individualization of Dialysate Calcium Concentration According to Baseline Pre-Dialysis Serum Calcium

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          Background: 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. Results: Fifty-six hemodialysis patients were dialyzed with 3.0 or 2.5 mEq/l dialysate [calcium] in a crossover study of two weeks. Bone mineral metabolites were measured prior to and following the hemodialysis session. A 3.0 mEq/l dialysate [calcium] increased more post-dialysis total calcium and ionized calcium than 2.5 mEq/l dialysate [calcium]. The mildest dialysis-induced changes in calcium and PTH were observed in patients with pre-dialysis serum calcium <8.75 mg/dl dialyzed with 2.5 mEq/l dialysate [calcium] and in patients with pre-dialysis serum calcium >9.15 mg/dl dialyzed with 3.0 mEq/l calcium dialysate. Conclusion: In conclusion, the individualization of dialysate calcium concentration according to baseline pre-dialysis serum calcium may prevent major excursions in post-dialysis serum calcium and iPTH levels. Short Summary: High calcium dialysate may increase serum calcium in hemodialysis patients, while low dialysate calcium may increase PTH. Individualization of dialysate calcium according to predialysis serum calcium levels may prevent or decrease unwanted excursions of both serum calcium and PTH.

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

          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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            Association of bone activity, calcium load, aortic stiffness, and calcifications in ESRD.

            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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              Progression of aortic calcification is associated with disorders of mineral metabolism and mortality in chronic dialysis patients.

              Previous studies have shown that simple imaging methods may be useful for detection of vascular calcifications in dialysis patients. Based on annual, plain chest X-rays during follow-up on dialysis, we studied the associations of mineral metabolism with the presence and progression of aortic calcification. In addition, we assessed the impact of aortic calcification on mortality. Three hundred and eighty-four patients who started haemodialysis or peritoneal dialysis between 1997 and 2007 were included (age 61 ± 15 years, 64% male, 61% haemodialysis). Annual chest X-rays were screened for calcification in the aortic arch, and patients were categorized as having no, moderate or severe calcification. Progression was defined as an increase in calcification category during follow-up on dialysis. At baseline, 96 (25%) patients had severe, 205 (53%) patients had moderate and 83 (22%) patients had no aortic calcification. For 237 of the 288 patients with no or moderate calcifications at baseline, X-rays were available for follow-up. During follow-up (mean 2.3 years), aortic calcification progressed in 71 patients (30%). We found that baseline plasma calcium > 9.5 mg/dL and iPTH > 300 pg/mL were associated with progression [odds ratios of 3.1, 95% confidence interval (1.2-8.2) and 4.4 (1.4-14.1), respectively]. Progression of aortic calcification was significantly associated with increased risk of all-cause mortality (hazard ratio: 1.9; 95% CI: 1.2-3.1) and cardiovascular mortality (hazard ratio: 2.7; 95% CI: 1.3-5.6). Aortic calcification progressed in almost a third of the patients during dialysis. Hypercalcaemia and hyperparathyroidism were associated with an increased risk of progression. Progression of aortic calcification was significantly related to an increased mortality risk.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                February 2015
                19 December 2014
                : 38
                : 3-4
                : 224-233
                aDivision of Nephrology and Hypertension, IIS-Fundación Jiménez Díaz, Madrid, bUniversidad Autónoma de Madrid, Madrid, cInstituto ‘Reina Sofía' de Investigación Nefrológica, Madrid, dREDINREN, Madrid, eDivision of Medical Biochemistry, Hospital Gomez Ulla, Madrid, and fDivision of Nephrology, Hospital Perpetuo Socorro, Alicante, Spain
                Author notes
                *Emilio Gonzalez Parra, Unidad de Diálisis, IIS-Fundación Jiménez Díaz, Av Reyes Católicos 2, ES-28040 Madrid (Spain), E-Mail
                366126 Blood Purif 2014;38:224-233
                © 2014 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 3, References: 33, Pages: 10
                Original Paper


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