A comparison of calcium acetate/magnesium carbonate and sevelamer-hydrochloride effects on fibroblast growth factor-23 and bone markers: post hoc evaluation from a controlled, randomized study

Covic, Adrian; Passlick–Deetjen, Jutta; M, Kroczak; Büschges-Seraphin, Beatrix; Ghenu, Adrian; Ponce, Pedro; Marzell, Barbara; Francisco, A.L.M. de

doi:10.1093/ndt/gft203

Cited by 57 publications

(49 citation statements)

References 49 publications

(51 reference statements)

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“…CALMAG randomized controlled trial using CaMg versus sevelamer-HCl in a population of dialysis patients has demonstrated the effectiveness of CaMg complex in lowering serum phosphorus [105]. In rodent CKD models, CaMg reduced arterial calcification, comparable to the effects of sevelamer-HCL, without over-suppression of bone turnover or skeletal Mg accumulation [106,107,108]. CaMg could potentially be an effective alternative to treat hyperphosphatemia.…”

Section: Derangements Of Bone Mineral Metabolismmentioning

confidence: 99%

Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure

Dhondup

Qian²

2017

Blood Purif

133

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The kidneys play a pivotal role in the regulation of electrolyte and acid-base balance. With progressive loss of kidney function, derangements in electrolytes and acid-base inevitably occur and contribute to poor patient outcomes. As chronic kidney disease (CKD) has become a worldwide epidemic, medical providers are increasingly confronted with such problems. Adequate diagnosis and treatment will minimize complications and can potentially be lifesaving. In this review, we discuss the current understanding of the disease process, clinical presentation, diagnosis and treatment strategies, integrating up-to-date knowledge in the field. Although electrolyte and acid-base derangements are significant causes of morbidity and mortality in CKD and end-stage renal disease patients, they can be effectively managed through a timely institution of combined preventive measures and pharmacological therapy. Exciting advances and several upcoming outcome trials will provide further information to guide treatment and improve patient outcomes.

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Section: Derangements Of Bone Mineral Metabolismmentioning

confidence: 99%

Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure

Dhondup

Qian²

2017

Blood Purif

133

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“…24,25 The introduction of a new oral phosphate binder formulation for patients receiving dialysis that combines a magnesium salt with a calcium salt has also led to increased interest in the effects of magnesium. 26,27 In this Review, we examine evidence from experimen tal studies and clinical investigations that suggest a role of magnesium in the high frequency of cardiovascular disease in patients with CKD.…”

Section: Introductionmentioning

confidence: 99%

Magnesium and cardiovascular complications of chronic kidney disease

Massy

Drüeke

2015

Nat Rev Nephrol

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Cardiovascular complications are the leading cause of death in patients with chronic kidney disease (CKD). Abundant experimental evidence suggests a physiological role of magnesium in cardiovascular function, and clinical evidence suggests a role of the cation in cardiovascular disease in the general population. The role of magnesium in CKD-mineral and bone disorder, and in particular its impact on cardiovascular morbidity and mortality in patients with CKD, is however not well understood. Experimental studies have shown that magnesium inhibits vascular calcification, both by direct effects on the vessel wall and by indirect, systemic effects. Moreover, an increasing number of epidemiologic studies in patients with CKD have shown associations of serum magnesium levels with intermediate and hard outcomes, including vascular calcification, cardiovascular events and mortality. Intervention trials in these patients conducted to date have had small sample sizes and have been limited to the study of surrogate parameters, such as arterial stiffness, vascular calcification and atherosclerosis. Randomized controlled trials are clearly needed to determine the effects of magnesium supplementation on hard outcomes in patients with CKD.

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“…Both treatments turned out to be comparably effective and well tolerated. This outcome was confirmed by investigating the effects of both phosphate binders on fibroblast growth factor-23, an important marker for outcome and severity of disease in CKD [36] that is inversely associated with serum Mg concentration in HD patients [37]. Here, again, CaMg and sevelamer turned out to have comparable efficacy.…”

Section: Discussionmentioning

confidence: 81%

Calcium Acetate/Magnesium Carbonate and Cardiovascular Risk Factors in Chronic Hemodialysis Patients

Matias¹,

Jorge²,

Azevedo³

et al. 2016

Nephron

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Background/Aim: Calcium acetate/magnesium carbonate (CaMg) is a recent phosphate binder that has been shown to have protective cardiovascular (CV) effects in animal models. The aim of this study was to evaluate the relationship between CaMg therapy and CV risk markers like pulse pressure (PP), left ventricular mass index (LVMI) and valvular calcifications compared to sevelamer or no phosphate binder (NPB) therapy in chronic hemodialysis (HD) patients. Methods: We performed a 48-month prospective study in 138 HD patients under hemodiafiltration with a dialysate Mg concentration of 0.5 mmol/l. Patients underwent treatment with CaMg or sevelamer for at least 36 months or NPB therapy. Demographic, clinical, biochemical and echocardiographic parameters were evaluated at baseline and after a 48-month period. Results: At the end of the study, patients who had taken CaMg showed a significant reduction in PP (p < 0.001), LVMI (p = 0.003), aortic (p = 0.004) and mitral valve calcifications (p = 0.03) compared with NPB patients. Patients under CaMg showed a significant reduction of PP (p < 0.001), LVMI (p = 0.01) and aortic valve calcifications (p = 0.02) compared to sevelamer patients. In a multivariable analysis, CaMg therapy was negatively associated with progression of LVMI (p = 0.02) and aortic valve calcifications (p = 0.01). Patients under CaMg showed higher serum Mg levels (0.93 ± 0.14 mmol/l) compared to patients under sevelamer (0.87 ± 0.13) or NPB patients (0.82 ± 0.12; p < 0.001). Conclusions: In prevalent HD patients, the use of CaMg over 48 months was associated with a reduction of PP and LVMI and with a stabilization of aortic valve calcifications. These protective and promising results of this new phosphate binder need to be confirmed in randomized controlled studies.

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A comparison of calcium acetate/magnesium carbonate and sevelamer-hydrochloride effects on fibroblast growth factor-23 and bone markers: post hoc evaluation from a controlled, randomized study

Cited by 57 publications

References 49 publications

Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure

Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure

Magnesium and cardiovascular complications of chronic kidney disease

Calcium Acetate/Magnesium Carbonate and Cardiovascular Risk Factors in Chronic Hemodialysis Patients

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