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Magnesium as a Phosphate Binder

The safe and effective use of magnesium carbonate as a phosphate binder has been reported by O'Donovan1 in 1986 and Delmez et al in 19962. Delmez et al, demonstrated that magnesium carbonate was an effective binder which allowed for the reduction by more than one half the dose of calcium carbonate. The mean daily dose of magnesium and calcium was 465mg and 1200mg, respectively.

The use of magnesium carbonate as a phosphate binder should not result in magnesium accumulation. Kelber et al3, demonstrated that magnesium is readily dialyzed. Regarding magnesium and it's impact on bone, Moriniere et al4 reported no significant changes in bone histomorphology after 8 to 20 months of treatment with Mg(OH)2. Serum magnesium levels averaged 3.6 mg/dL during this time.

Critics have stated that serum magnesium levels over 3.0 mg/dL are too high. However, the literature clearly states that to find significant symptomatic hypermagnesemia, serum levels will be at least 6.0 mg/dL. More importantly, cardio-protective properties of magnesium have been reported with slight hypermagnesemia.

Meema et al, demonstrated by microradioscopic method, a clear reduction in arterial calcification. They found a significant correlation between the elevation of serum magnesium from 2.69 ± 0.52 to 3.29 ± 0.83mg/dL and the reversal of arterial calcification. They summarize their work by stating that in end-stage renal disease the elevation of serum magnesium may retard the development of arterial calcification5. In 1997, Tzanakis et al, reported similar results in patients on hemodialysis and the occurrence of mitral annular calcification (MAC). They found that patients with serum magnesium levels below 3 mg/dL were twice as likely to develop MAC as compared to those above 3 mg/dL6.

By combining magnesium carbonate with calcium carbonate, MagneBind® 300 and MagneBind® 400 Rx allow for a significant reduction in calcium intake and enhanced phosphate binding. Patients appreciate the improved motility afforded by the addition of magnesium and the reduction of calcium. MagneBind® 300 is an excellent choice for patients who have to pay out of pocket for their binders.

If increasing folic acid intake is indicated, or when a prescription is required for third party coverage, MagneBind® 400 Rx would be an appropriate choice. MagneBind® 400 Rx contains 1 mg of folic acid per tablet and is usually dosed 3-4 tablets p/day, as an adjunct. MagneBind® 400 Rx provides an economical way to provide substantial phosphate binding activity and additional folic acid.

1 O'Donovan R, Baldwin D, Hammer M, Moniz C, Parsons V: Substitution of aluminum salts by magnesium salts in control of dialysis hyperphosphataemia. Lancet 1:880-882, 1986.
2 Delmez JA, Kelber J, Norwood KY, Giles KS and Slatopolsky E: Magnesium carbonate as a phosphate binder: A prospective, controlled, crossover study. Kidney Int., Vol 49, 163-167, 1996.
3 Kelber J, Slatopolsky E and Delmez J: Acute Effects of Different Concentrations of Dialysate Magnesium During High-Efficiency Dialysis. Amer. J. of Kid. D. Vol. 24, No 3, 453-460; 1994.
4 Moriniere P, Vinatier I, Westeel PF: Magnesium hydroxide as a complementary aluminum-free phosphate binder to moderate doses of oral calcium in uraemic patients on chronic haemodialysis. Nephrol Dial Transplant 3: 651-656, 1988.
5 Meema HE, Oreopoulos DG and Rapoport A: Serum magnesium level and arterial calcification in end-stage renal disease. Kidney Int. Vol. 32, 388-394, 1987.
6 Tzanakis I, Pras A, Kounali D, Mamali V, Kartsonakis V, Mayopoulou-Symvoulidou D, Kallivretakis N: Mitral annular calcifications in haemodialysis patients: a possible protective role of magnesium. Nephrol Dial Transplant 12: 2036-2037, 1997.



Magnesium Abstracts

Kidney Int. 1996 Jan;49(1):163-7.

Magnesium carbonate as a phosphorus binder: a prospective, controlled, crossover study.Delmez JA, Kelber J, Norword KY, Giles KS, Slatopolsky E.
Renal Division, Washington University School of Medicine, Saint Louis, Missouri, USA.

The use of calcium carbonate (CaCO3) to bind phosphorus (P) in chronic hemodialysis patients has been a popular tactic in the past decade. Nonetheless, problems with hypercalcemia decrease its usefulness, particularly in patients treated with calcitriol. A P binder not containing calcium (Ca) would be of value in these circumstances. In short-term studies, we showed that magnesium carbonate (MgCO3) was well-tolerated and controlled P and Mg levels when given in conjunction with a dialysate Mg of 0.6 mg/dl. We, therefore, performed a prospective, randomized, crossover study to evaluate if the chronic use of MgCO3 would allow a reduction in the dose of CaCO3 and yet achieve acceptable levels of Ca, P, and Mg. We also assessed whether the lower dose of CaCO3 would facilitate the use of larger doses of calcitriol. The two phases were MgCO3 plus half the usual dose of CaCO3 and CaCO3 alone given in the usual dose. It was found that MgCO3 (dose, 465 +/- 52 mg/day elemental Mg) allowed a decrease in the amount of elemental Ca ingested from 2.9 +/- 0.4 to 1.2 +/- 0.2 g/day (P < 0.0001). The Ca, P, Mg levels were the same in the two phases. The maximum dose of i.v. calcitriol without causing hypercalcemia was 1.5 +/- 0.3 micrograms/treatment during the MgCO3 phase and 0.8 +/- micrograms/treatment during the Ca phase (P < 0.02). If these studies are confirmed, the use of MgCO3 and a dialysate Mg of 0.6 mg/dl may be considered in selected patients who develop hypercalcemia during treatment with i.v. calcitriol and CaCO3.

http://www.ncbi.nlm.nih.gov/pubmed/8770963?ordinalpos=19&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Am J Kidney Dis. 1994 Sep;24(3):453-60.

Acute effects of different concentrations of dialysate magnesium during high-efficiency dialysis. Kelber J, Slatopolsky E, Delmez JA.
Department of Internal Medicine, Washington University School of Medicine, St Louis, MO 63110.

It has been suggested that magnesium carbonate (MgCO3) may be an effective and safe alternative to calcium carbonate in binding phosphorus in dialysis patients. In these studies, the concentration of magnesium in the dialysate was either very low or zero. To date, only patients undergoing conventional dialysis have been reported. The primary purpose of the present study was to determine the fluxes of magnesium using dialysate magnesium concentrations of 0 mg/dL, 0.6 mg/dL, and 1.8 mg/dL in eight patients undergoing high-efficiency hemodialysis. The net removal of magnesium was 486 +/- 44 mg, 306 +/- 69 mg, and 56 +/- 50 mg, with the use of dialysate magnesium concentrations of 0 mg/dL, 0.6 mg/dL, and 1.8 mg/dL, respectively (P = 0.001). Plasma magnesium levels significantly decreased from 3.3 +/- 0.2 mg/dL to 1.6 +/- 0.2 mg/dL and from 3.4 +/- 0.3 mg/dL to 2.1 +/- 0.2 mg/dL during the dialysis sessions using 0 mg/dL and 0.6 mg/dL magnesium dialysates, respectively. Plasma magnesium remained unchanged when 1.8 mg/dL dialysate magnesium was used. A significant independent correlation was found between the total magnesium removed and both the dialysate concentration used (P < 0.001) and the predialysis plasma magnesium level (P < 0.001). The measured magnesium removal exceeded the estimated predialysis extracellular fluid (ECF) magnesium pool with the use of magnesium-free dialysate. This was not found with dialysate magnesium concentrations of either 0.6 mg/dL or 1.8 mg/dL. A secondary purpose of the study was to determine the acute clinical tolerance of the low and magnesium-free dialysates.

http://www.ncbi.nlm.nih.gov/pubmed/8079970?ordinalpos=81&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Nephron. 1993;63(4):379-83.

Successful control of hyperparathyroidism in patients on continuous ambulatory peritoneal dialysis using magnesium carbonate and calcium carbonate as phosphate binders. Parsons V, Baldwin D, Moniz C, Marsden J, Ball E, Rifkin I.
Department of Renal Medicine, King's College, London, UK.

To avoid the use of aluminium as a phosphate binder, patients on CAPD who were stable were dialysed against a peritoneal dialysis fluid which was magnesium free. A mixture of calcium and magnesium carbonate was used as a phosphate binder over a period in excess of 1 year. Vitamin D analogues were used in the majority. Results show satisfactory control of hyperparathyroidism with mean parathyroid hormone concentration for the group of 121 pg/ml (normal < 100 pg/ml), calcium concentration of 2.41 mmol/l, magnesium 0.97 mmol/l, phosphate 1.36 mmol/l and aluminium 0.35 mmol/l (normal < 0.2 mumol/l). These results were as good as and better in some respects than a minority using calcium carbonate alone or remaining on aluminium hydroxide, the latter remaining on Mg-containing CAPD fluid.

http://www.ncbi.nlm.nih.gov/pubmed/8459870?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


J Ren Nutr. 2007 Nov;17(6):416-22.

Magnesium carbonate is an effective phosphate binder for chronic hemodialysis patients: a pilot study. Spiegel DM, Farmer B, Smits G, Chonchol M.
University of Colorado Health Sciences Center, Denver, Colorado, USA. david.spiegel@uchsc.edu

OBJECTIVE: This study was designed to evaluate the efficacy of magnesium carbonate as a phosphate binder in hemodialysis patients. DESIGN: This study was a prospective, randomized, open-label trial comparing magnesium carbonate/calcium carbonate versus calcium acetate as a sole phosphate binder. SETTING: This study involved outpatient hemodialysis. PARTICIPANTS: We recruited 30 stable hemodialysis patients without a history of frequent diarrhea. INTERVENTION: After receiving informed consent, we randomized patients 2:1 to magnesium carbonate versus calcium acetate. The dose of each binder was titrated to achieve the Kidney Disease Outcomes Quality Initiative (K/DOQI) phosphate target of <5.5 mg/dL. MAIN OUTCOME MEASURE: The efficacy-phase serum phosphorus concentration and the percentage of patients meeting K-DOQI targets for phosphorus, along with the daily elemental calcium intake, were the primary outcome measures. RESULTS: Magnesium carbonate provided equal control of serum phosphorus (70.6% of the magnebind group and 62.5% of the calcium acetate group had their average serum phosphorus within the K-DOQI target during the efficacy phase), while significantly reducing daily elemental calcium ingestion from phosphate binders (908 +/- 24 vs. 1743 +/- 37 mg/day, P < .0001). CONCLUSION: Magnesium carbonate was generally well-tolerated in this selected patient population, and was effective in controlling serum phosphorus while reducing elemental calcium ingestion.

http://www.ncbi.nlm.nih.gov/pubmed/17971314?ordinalpos=16&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Semin Dial. 2007 Jul-Aug;20(4):333-6.

The role of magnesium binders in chronic kidney disease. Spiegel DM.
Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Health Sciences Center, Denver, Colorado 80111, USA. david.spiegel@uchsc.edu

Magnesium is predominantly an intracellular cation that plays a critical role in cellular physiology. Serum levels are often slightly elevated in patients on chronic hemodialysis and older reports suggests that total body stores may also be increased, based on bone biopsies in patients treated with higher dialysate magnesium levels than are currently in use today. Several studies have shown that magnesium, particularly in the form of magnesium carbonate, is an effective phosphate binder and can decrease patients' exposure to calcium. Retrospective studies suggest that magnesium may prevent vascular calcification in dialysis patients, although this remains controversial and has not been evaluated prospectively. Magnesium may reduce arrhythmias postoperatively and, while it may theoretically reduce arrhythmic death in dialysis patients, this hypothesis has never been tested. While short-term or adjuvant use of magnesium carbonate appears safe and effective as a phosphate binder, more studies are needed to evaluate the long-term effects on vascular calcification, bone histology, and mortality.

http://www.ncbi.nlm.nih.gov/pubmed/17635824?ordinalpos=28&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Int Urol Nephrol. 2008;40(1):193-201. Epub 2008 Jan 10.

Magnesium carbonate for phosphate control in patients on hemodialysis. A randomized controlled trial. Tzanakis IP, Papadaki AN, Wei M, Kagia S, Spadidakis VV, Kallivretakis NE, Oreopoulos DG.
Department of Nephrology, General Hospital of Chania, 18, Michali Mefa St, Chania-Crete, PC 73100, Greece, ioatza@otenet.gr.

BACKGROUND: Magnesium salts bind dietary phosphorus, but their use in renal patients is limited due to their potential for causing side effects. The aim of this study was to evaluate the efficacy and safety of magnesium carbonate (MgCO(3)) as a phosphate-binder in hemodialysis patients. METHODS: Forty-six stable hemodialysis patients were randomly allocated to receive either MgCO(3) (n = 25) or calcium carbonate (CaCO(3)), (n = 21) for 6 months. The concentration of Mg in the dialysate bath was 0.30 mmol/l in the MgCO(3) group and 0.48 mmol/l in the CaCO(3) group. RESULTS: Only two of 25 patients (8%) discontinued ingestion of MgCO(3) due to complications: one (4%) because of persistent diarrhea, and the other (4%) because of recurrent hypermagnesemia. In the MgCO(3) and CaCO(3) groups, respectively, time-averaged (months 1-6) serum concentrations were: phosphate (P), 5.47 vs. 5.29 mg/dl, P = ns; Ca, 9.13 vs. 9.60 mg/dl, P < 0.001; Ca x P product, 50.35 vs. 50.70 (mg/dl)(2), P = ns; Mg, 2.57 vs. 2.41 mg/dl, P = ns; intact parathyroid hormone (iPTH), 285 vs. 235 pg/ml, P < 0.01. At month 6, iPTH levels did not differ between groups: 251 vs. 212 pg/ml, P = ns. At month 6 the percentages of patients with serum levels of phosphate, Ca x P product and iPTH that fell within the Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines were similar in both groups, whereas more patients in the MgCO(3) group (17/23; 73.91%) than in the CaCO(3) group (5/20, 25%) had serum Ca levels that fell within these guidelines, with the difference being significant at P < 0.01. CONCLUSION: Our study shows that MgCO(3) administered for a period of 6 months is an effective and inexpensive agent to control serum phosphate levels in hemodialysis patients. The administration of MgCO(3) in combination with a low dialysate Mg concentration avoids the risk of severe hypermagnesemia.

http://www.ncbi.nlm.nih.gov/pubmed/18193489?ordinalpos=24&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Perit Dial Int. 2006 May-Jun;26(3):366-73.

Relationship between serum magnesium, parathyroid hormone, and vascular calcification in patients on dialysis: a literature review. Wei M, Esbaei K, Bargman J, Oreopoulos DG.
Home Peritoneal Dialysis Unit, University Health Network and University of Toronto, Toronto, Ontario, Canada.

Secondary hyperparathyroidism is present in most patients with end-stage renal disease and has been linked to uremic bone disease, vascular calcification, and mortality. Current literature suggests an association between hypomagnesemia and cardiovascular disease in the general population. We reviewed all published studies on the relationship between serum magnesium and parathyroid hormone and the relationship between serum Mg and vascular calcification in dialysis patients. Of these, 10 of 12 studies of patients on hemodialysis and 4 of 5 studies of patients on peritoneal dialysis showed a significantinverse relationship between serum Mg and serum intact parathyroid hormone. Hyperparathyroidism develops in peritoneal dialysis patients dialyzed with a solution containing normal calcium (1.25 mmol/L) and low Mg (0.25 mmol/L), even though serum calcium is maintained at a normal level. Four of the hemodialysis studies and one of the peritoneal dialysis studies indicated that there is an inverse relationship between serum Mg and vascular calcification in these patients. Potential benefits have been attributed to magnesium carbonate as a phosphate binder and it may possibly be an effective, less toxic, less expensive phosphate binder. We believe that the role of Mg in secondary hyperparathyroidism and vascular calcification merits further investigation.

http://www.ncbi.nlm.nih.gov/pubmed/16722031?ordinalpos=160&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Magnes Res. 2004 Jun;17(2):102-8.

Intra- and extracellular magnesium levels and atheromatosis in haemodialysis patients. Tzanakis I, Virvidakis K, Tsomi A, Mantakas E, Girousis N, Karefyllakis N, Papadaki A, Kallivretakis N, Mountokalakis T.
Department of Nephrology, General Hospital of Chania, Chania, Greece. ioatza@otenet.gr

Traditional risk factors do not adequately explain the high prevalence of cardiovascular disease in patients with chronic renal insufficiency. Currently, there is a lot of evidence that hypomagnesaemia may play a significant role in the pathogenesis of cardiovascular diseases in general population. The aim of this study was to test the hypothesis that magnesium status in haemodialysis patients is related to the degree of atheromatosis of carotid arteries, as assessed by B-mode ultrasound. Intima-media thickness of both common carotids was assessed by B-mode ultrasound in 93 stable chronic haemodialysis patients and in 182 age- and sex-matched healthy controls. Intracellular magnesium as well as serum magnesium levels were obtained in the haemodialysis patients. Intracellular magnesium was estimated by determination of this ion in isolated peripheral lymphocytes. Haemodialysis patients had also a significantly higher mean common carotid intima-media thickness than controls (0.87+/-0.16 vs 0.76+/-0.13 mm, p < 0.001). Multivariate analysis revealed that in haemodialysis patients both serum magnesium and intracellular magnesium were negatively associated with common carotid intima-media thickness (p = 0.001 and p = 0.003 respectively). Significant associations between the age of the haemodialysis patients, the existence of diabetes mellitus as well as the serum calcium x serum phosphate product with common carotid intima-media thickness of haemodialysis patients were also observed. A strong negative association of both extracellular and intracellular magnesium with common carotid intima-media thickness exists in haemodialysis patients. The above finding suggests that magnesium may play an important protective role in the development and/or acceleration of arterial atherosclerosis in patients with chronic renal insufficiency.

http://www.ncbi.nlm.nih.gov/pubmed/15319142?ordinalpos=46&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Kidney Int. 1987 Sep;32(3):388-94.

Serum magnesium level and arterial calcification in end-stage renal disease. Meema HE, Oreopoulos DG, Rapoport A.
Department of Radiology, Toronto Western Hospital, Ontario, Canada.

In this paper we examine the relationship of serum levels of Ca, P, Ca X P, P/Mg, Ca X P/Mg, alkaline phosphatase, and iPTH to the development or regression of peripheral arterial calcifications (AC) in 44 patients with end-stage renal disease being treated by continuous ambulatory peritoneal dialysis (CAPD). The average follow-up time of this longitudinal study was 27 months (range 6-67 months). The patients were divided into two groups: Group A, those showing one or more increases of AC; and Group B, patients in whom AC either did not develop or decreased during the follow-up. There was no significant difference in serum Ca, P, Ca X P, alkaline phosphatase of iPTH between the two groups. However, serum Mg was significantly lower in Group A than in Group B (2.69 +/- 0.52 and 3.02 +/- 0.51 mg/dl, respectively, P less than 0.001), while the ratios P/Mg and Ca X P/Mg were significantly higher. Our observations suggest that in end-stage renal disease hypermagnesemia may retard the development of arterial calcifications.

http://www.ncbi.nlm.nih.gov/pubmed/3669498?ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Hemodial Int. 2009 May 12. [Epub ahead of print]

Long-term effects of magnesium carbonate on coronary artery calcification and bone mineral density in hemodialysis patients: A pilot study. Spiegel DM, Farmer B.
Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Health Sciences Center, Denver, Colorado, USA.

Observational data suggest that elevated magnesium levels in dialysis patients may prevent vascular calcification and in vitro magnesium can prevent hydroxyapatite crystal growth. However, the effects of magnesium on vascular calcification and bone mineral density have not been studied prospectively. Seven chronic hemodialysis patients participated in this open label, prospective pilot study to evaluate the effects of a magnesium-based phosphate binder on coronary artery calcification (CAC) scores and vertebral bone mineral density (V-BMD) in patients with baseline CAC scores >30. Magnesium carbonate/calcium carbonate (elemental Mg: 86 mg/elemental Ca 100 mg) was administered as the principal phosphate binder for a period of 18 months and changes in CAC and V-BMD were measured at baseline, 6, 12, and 18 months. Serum magnesium levels averaged 2.2+/-0.4 mEq/L (range: 1.3-3.9 mEq/L). Phosphorus levels (4.5+/-0.6 mg/dL) were well controlled throughout the 18 months study. Electron beam computed tomography results demonstrated a small not statically significant increase in absolute CAC scores, no significant change in median percent change, and a small none significant change in V-BMD. Magnesium may have a favorable effect on CAC. The long-term effect on bone mineral density remains unclear. Larger studies are needed to confirm these findings.

http://www.ncbi.nlm.nih.gov/pubmed/19469885?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum



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