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      Low calcium dialysate combined with CaCO 3 in hyperphosphatemia in hemodialysis patients

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          Abstract

          This aim of this study was to observe the effects of the application of low calcium dialysate (LCD) combined with oral administration of CaCO 3 in the treatment of hyperphosphatemia, as well as blood Ca 2+, calcium-phosphate product (CPP), parathyroid hormone (PTH) and blood pressure in patients undergoing hemodialysis. Thirty-one maintenance hemodialysis (MHD) patients with hyperphosphatemia, but normal blood Ca 2+, underwent dialysis with an initial dialy-sate Ca 2+ concentration (DCa) of 1.50 mmol/l for six months and then with 1.25 mmol/l for six months. The patients who underwent dialysis with a DCa of 1.25 mmol/l were treated orally with 0.3 g CaCO 3 tablets three times a day. In the third and sixth months [observation end point (OEP)] of the dialysis, the concentrations of Ca 2+, phosphorus and intact PTH (iPTH) were measured; blood pressure and side-effects prior to and following dialysis were also observed. The Ca 2+, CPP and iPTH levels increased (P<0.05) in the sixth month of treatment with a DCa of 1.50 mmol/l. However, the Ca 2+ concentration declined to a certain degree, CPPs decreased significantly (P<0.05) and the iPTH concentration increased following treatment with a DCa of 1.25 mmol/l for six months. The incidence rate of adverse effects of LCD was 12.9% (4/31); the effects were mainly muscle spasms, hypotension and elevated PTH. The periodic application of LCD combined with the oral administration of CaCO 3 effectively reduced serum phosphorus and CPPs among MHD patients with hyperphosphatemia, indicating that the treatment may be used clinically.

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          Most cited references21

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          Association of Cumulatively Low or High Serum Calcium Levels with Mortality in Long-Term Hemodialysis Patients

          Background: The outcome-predictability of baseline and instantaneously changing serum calcium in hemodialysis patients has been examined. We investigated the mortality-predictability of time-averaged calcium values to reflect the ‘cumulative’ effect of calcium burden over time. Methods: We employed a Cox model using up-to-5-year (7/2001–6/2006) time-averaged values to examine the mortality-predictability of cumulative serum calcium levels in 107,200 hemodialysis patients prior to the use of calcimimetics, but during the time where other calcium-lowering interventions, including lower dialysate calcium, were employed. Results: Both low ( 10.0 mg/dl) calcium levels were associated with increased mortality (reference: 9.0 to 3.5 mg/dl) and PTH levels (>150 pg/ml). Higher paricalcitol doses shifted the calcium range associated with the greatest survival to the right, i.e. from 9.0 to <9.5 to 9.5 to <10.0 mg/dl. African-Americans exhibited the highest death hazard ratio of hypocalcemia <8.5 mg/dl, being 1.35 (95% CI: 1.22–1.49). Both a rise and drop in serum calcium over 6 months were associated with increased mortality compared to the stable group. Conclusions: Whereas in hemodialysis patients cumulatively high or low calcium levels are associated with higher death risk, subtle but meaningful interactions with phosphorus, PTH, paricalcitol dose and race exist.
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            QTc dispersion increases during hemodialysis with low-calcium dialysate.

            The risk of ventricular arrhythmias is known to increase during hemodialysis (HD) treatment, but the cause of this phenomenon has remained unidentified. QT dispersion (= QTmax - QTmin) reflects heterogeneity of cardiac repolarization, and increased dispersion is known to predispose the heart to ventricular arrhythmias and sudden cardiac death. We studied the effect of dialysate calcium concentration on cardiac electrical stability during HD treatment in 23 end-stage renal disease patients. Three HD treatments were applied with dialysate Ca++ concentrations of 1.25 mmol/L (dCa++1.25), 1.5 mmol/L (dCa++1.5), and 1.75 mmol/L (dCa++1.75). The QTc interval and QTc dispersion were measured before and after the three sessions. With the dCa++1.5 and dCa++1.75 dialyses, serum Ca++ increased and the QTc interval remained stable (dCa++1.5) or decreased (dCa++1.75), but no significant change was noted in QTc dispersion. With dCa++1.25 HD, serum Ca++ decreased (1.24 +/- 0.11 vs. 1.20 +/- 0.09 mmol/L, P < 0. 05), and both the QTc interval (403 +/- 27 vs. 419 +/- 33 ms, P < 0. 05) and QTc dispersion increased (38 +/- 19 vs. 49 +/- 18 ms, P < 0. 05). The change in the QTc interval correlated inversely with the change in serum Ca++ (r = -0.68, P < 0.0001). Except for serum Ca++ and plasma intact parathyroid hormone, predialysis and postdialysis values in other blood chemistry, blood pressure, heart rate, body weight, and total ultrafiltration were equal in the three dialysis sessions. This study is the first, to our knowledge, to demonstrate that HD increases QTc dispersion if a low-calcium (dCa++1.25) dialysate is used. This indicates that the use of low-calcium dialysate may predispose HD patients to ventricular arrhythmias and that perhaps it should be avoided, at least when treating patients with pre-existing cardiac disease.
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              Phosphate Elimination in Modalities of Hemodialysis and Peritoneal Dialysis

              Hyperphosphatemia is highly prevalent in hemodialysis (HD) and peritoneal dialysis (PD) patients and is a major risk factor for cardiovascular mortality. Elimination of inorganic phosphate by dialysis is a cornerstone of the management of hyperphosphatemia. Phosphate clearance during HD is affected by various factors of dialysis prescription, such as blood and dialysate flow rate, dialyzer membrane surface area and ultrafiltration volume. Phosphate mass removal can be improved by hemodiafiltration, increased dialysis frequencies and extended treatment times. Short daily or extended daily or 3 times weekly nocturnal HD allow higher phosphate mass removal and potentially complete discontinuation of phosphate binder medication. In PD, phosphate mass removal appears to be correlated with peritoneal creatinine but not urea clearance. In hyperphosphatemic PD patients, the decision on the optimal PD modality should be based on peritoneal creatinine and ideally also on peritoneal phosphate transport characteristics.
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                Author and article information

                Journal
                Exp Ther Med
                Exp Ther Med
                ETM
                Experimental and Therapeutic Medicine
                D.A. Spandidos
                1792-0981
                1792-1015
                June 2013
                17 April 2013
                17 April 2013
                : 5
                : 6
                : 1732-1736
                Affiliations
                Department of Nephrology, Air Force General Hospital, Beijing 100142, P.R. China
                Author notes
                Correspondence to: Professor Zhuo Gao, Department of Nephrology, Air Force General Hospital, 30 Fucheng Road, Haidian, Beijing 100142, P.R. China, E-mail: gaozhuocn@ 123456163.com
                Article
                etm-05-06-1732
                10.3892/etm.2013.1067
                3702715
                23837063
                deb61d26-2108-4603-a227-a9ed0ee11394
                Copyright © 2013, Spandidos Publications

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

                History
                : 10 January 2013
                : 20 March 2013
                Categories
                Articles

                Medicine
                low calcium dialysis,hyperphosphatemia,calcium-phosphate product,parathyroid hormone
                Medicine
                low calcium dialysis, hyperphosphatemia, calcium-phosphate product, parathyroid hormone

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