Magnesium metabolism

Walser, Mackenzie

doi:10.1007/bf02269144

Cited by 114 publications

(51 citation statements)

References 562 publications

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“…The magnesium concentration in health is closely maintained within a normal range that varies between laboratories, but is roughly 1.50–2.3 mEq/l (1.8–2.8 mg/dl). Only about 1–2% of total body magnesium is present in the extracellular fluid [4] of which about 20% is protein bound. The principal stores of the body’s 21–28 g (1,750–2,400 mEq) of magnesium are bone (67%) and muscle (20%).…”

Section: Normal Magnesium Homeostasismentioning

confidence: 99%

Magnesium in Chronic Kidney Disease: Unanswered Questions

Spiegel

2011

Blood Purif

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Background: Magnesium ion is critical for life and is integrally involved in cellular function and a key component of normal bone mineral. In health, the kidneys, gastrointestinal tract and bone are responsible for maintaining serum magnesium concentrations in the normal range and magnesium balance. Most clinical disorders involving magnesium, other than chronic kidney disease (CKD), result in hypomagnesemia, either from gastrointestinal or kidney losses. CKD and particularly end-stage kidney disease is the only clinical condition where sustained hypermagnesemia may occur and net magnesium balance may be positive. Methods: This review will focus on normal magnesium homeostasis and review the literature in CKD with a particular focus on end-stage kidney disease and the potential role of magnesium as a phosphate binder and in cardiovascular and bone health. Results: A number of small to medium-size interventional trials have shown that magnesium-based compounds can serve as effective phosphate binders. Observational studies suggest that higher serum magnesium concentrations in dialysis patients may improve survival and may slow the progression of vascular calcification. While a few small prospective trials support these findings, no large or long-term studies are available. Conclusions: Magnesium balance remains poorly understood in patients with end-stage kidney disease. While observational and small randomized trials suggest that exogenous administration may be useful as a phosphate binder and may have protective cardiovascular effects in terms of both arrhythmias and vascular calcification, large randomized trials are needed to test these hypotheses.

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Section: Normal Magnesium Homeostasismentioning

confidence: 99%

Magnesium in Chronic Kidney Disease: Unanswered Questions

Spiegel

2011

Blood Purif

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“…INTRODUCTION 60% of total bdoy magnesium resides in the skeleton; however, few studies have been carried out to characterize bone magnesium pools (1). Based on the studies of Blaxter (2) and Neuman and Mulryan (3) it has been felt that magnesium is largely a surface limited ion (hydration shell and/or crystal surface) and is incapable of Received for publication 9 April 1973 and in revised form 16 July 1973. penetrating into the lattice structure (3).…”

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confidence: 99%

Bone Magnesium Pools in Uremia

Alfrey¹,

Miller²

1973

J. Clin. Invest.

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A B S T R A C T Bone magnesium pools were studied in vitro in bone specimens obtained from control subjects, from patients with chronic renal failure before and after renal transplantation, and in a patient with chronic hypomagnesemia. 30% of bone magnesium is in a surface limited pool present either within the hydration shell or else on the crystal surface. The larger fraction of bone magnesium was shown not to be associated with bone matrix but rather to be an integral part of the bone crystal. With incineration this pool was mobilized at the same temperature that sudden enlargement of bone crystal size occurred. It is suggested that heating causes surface calcium to displace magnesium from the apatite crystal. Both magnesium pools are increased in patients with chronic renal failure.The major factor determining magnesium concentration in bone would appear to be the serum magnesium level. Following renal transplantation, in association with the fall in serum magnesium, surface magnesium was within the normal range; whereas, residual magnesium was not different from the other uremic bones. Both magnesium pools were significantly reduced in a patient with chronic hypomagnesemia. The in vitro studies would suggest that surface magnesium should rapidly reflect changes in serum magnesium levels, whereas, the deeper magnesium pool is probably deposited at time of bone formation with mobilization being dependent upon the resorptive processes. Since magnesium can influence crystal size and stability it seems possible that excess bone magnesium may play a role in renal osteodystrophy.

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“…To simplify the presentation, concentrations are expressed in floating point style, i.e. 4 00, -1 3.43, -3 1.15, -3 4.25, - 40, -1 1.32, -3 1.76, -3 1.92, -3 8.12, -1 1.68, -3 1.29, -3 4.00, -1 1.13, - mammalian cell membrane is probably rigidly controlled, as there is complete equilibration of the magnesium in soft tissues with isotopic magnesium within a few hours [19], and yet the intra-cellular magnesium concentration appears to be largely independent of the circulating concentration [20]. The molecular species subject to homeostasis is not known; if it is Mg2+, then [Mgz+] is unlikely to be a feedback signal, except possibly on a short term basis.…”

Section: Magnesium and The Composition Of An Adeninementioning

confidence: 99%

Magnesium, Potassium, and the Adenylate Kinase Equilibrium

Blair

1970

European Journal of Biochemistry

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The influence of magnesium and potassium on the equilibrium catalysed by adenylate kinase has been studied. An equation has been derived which describes the effect of these ions on the equilibrium; values for the metal‐nucleotide stability constants, and for the “true” equilibrium constant, [AMP2−] · [ATP4−]/([ADP3−])2, have been calculated, which give the best fit of this equation to the experimental data. Using these constants, the concentrations of all significant species in an adenine nucleotide pool equilibrated by adenylate kinase can be calculated, for any specified total concentrations of magnesium, potassium, and adenine nucleotide pool, at any pH and any pyrophosphate bond content of the adenine nucleotide pool. Magnesium emerges as a significant feedback signal from an adenine nucleotide pool considered as an isolated system. The possible significance of this data with respect to the control of metabolic flux in general and of phosphofructokinase in particular is discussed.

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Magnesium metabolism

Cited by 114 publications

References 562 publications

Magnesium in Chronic Kidney Disease: Unanswered Questions

Magnesium in Chronic Kidney Disease: Unanswered Questions

Bone Magnesium Pools in Uremia

Magnesium, Potassium, and the Adenylate Kinase Equilibrium

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