Abstract:Sixteen end-stage renal disease patients who received hemodialysis for 2.9 years with no magnesium in the dialysate were evaluated for serum calcium, magnesium and parathyroid hormone (PTH) status. Eleven of these patients became hypomagnesemic with subnormal total and ultrafiltrable serum Mg concentrations (low-Mg group). The five remaining patients had consistently normal serum Mg concentrations (normal-Mg group). All had normal total and ionized serum Ca. However, the total and ionized serum Ca levels in th… Show more
“…Kenny et al. (72) suggested that a low Mg dialysate might be expected to have a suppressive effect on parathyroid gland function; however, most studies failed to confirm this hypothesis. Several trials on the successful use of Mg salts to control hyperphosphatemia and hypeparathyroidism (73–76) support the hypothesis that hypermagnesemia may have a suppressive effect on PTH secretion in dialysis patients (77,78).…”
Section: Magnesium Parathyroid Hormone and Bone Diseasementioning
Magnesium (Mg) is the fourth most abundant cation in the body, mainly located within bone and skeletal muscle. The normal total plasma Mg concentration varies in a narrow range, with approximately 60% present as free Mg ions, the biologically active form. The kidney plays a principal role in Mg balance. Approximately 70-80% of plasma Mg is ultrafilterable, and under normal circumstances, 95% of the filtered load of Mg is reabsorbed. As chronic renal failure (CRF) progresses, urinary Mg excretion may be insufficient to balance intestinal Mg absorption and dietary Mg intake becomes a major determinant of serum and total body Mg levels. Until severe reductions in glomerular filtration rate (<30 ml/min), serum Mg levels are usually normal; with lower rates of renal function, serum Mg is increased. Concerning dialysis patients, dialysate Mg plays a critical role in maintaining Mg homeostasis, with serum Mg being largely dependent on the concentration of the ion in the dialysis solution. Magnesium has been implicated in diverse consequences, both beneficial and deleterious, in patients with CRF and dialysis. Potential harmful effects of elevated Mg include altered nerve conduction velocity, increased pruritus, and alterations to osseous metabolism and parathyroid gland function (mineralization defects, contribution to osteomalacic renal osteodystrophy, and adynamic bone disease). Hypermagnesemia also may retard vascular calcification. Low Mg levels have been associated with impairment of myocardial contractility, intradialytic hemodynamic instability, and hypotension. In addition, low Mg has been also linked to carotid intima-media thickness, a marker of atherosclerotic vascular disease and a predictor of vascular events.
“…Kenny et al. (72) suggested that a low Mg dialysate might be expected to have a suppressive effect on parathyroid gland function; however, most studies failed to confirm this hypothesis. Several trials on the successful use of Mg salts to control hyperphosphatemia and hypeparathyroidism (73–76) support the hypothesis that hypermagnesemia may have a suppressive effect on PTH secretion in dialysis patients (77,78).…”
Section: Magnesium Parathyroid Hormone and Bone Diseasementioning
Magnesium (Mg) is the fourth most abundant cation in the body, mainly located within bone and skeletal muscle. The normal total plasma Mg concentration varies in a narrow range, with approximately 60% present as free Mg ions, the biologically active form. The kidney plays a principal role in Mg balance. Approximately 70-80% of plasma Mg is ultrafilterable, and under normal circumstances, 95% of the filtered load of Mg is reabsorbed. As chronic renal failure (CRF) progresses, urinary Mg excretion may be insufficient to balance intestinal Mg absorption and dietary Mg intake becomes a major determinant of serum and total body Mg levels. Until severe reductions in glomerular filtration rate (<30 ml/min), serum Mg levels are usually normal; with lower rates of renal function, serum Mg is increased. Concerning dialysis patients, dialysate Mg plays a critical role in maintaining Mg homeostasis, with serum Mg being largely dependent on the concentration of the ion in the dialysis solution. Magnesium has been implicated in diverse consequences, both beneficial and deleterious, in patients with CRF and dialysis. Potential harmful effects of elevated Mg include altered nerve conduction velocity, increased pruritus, and alterations to osseous metabolism and parathyroid gland function (mineralization defects, contribution to osteomalacic renal osteodystrophy, and adynamic bone disease). Hypermagnesemia also may retard vascular calcification. Low Mg levels have been associated with impairment of myocardial contractility, intradialytic hemodynamic instability, and hypotension. In addition, low Mg has been also linked to carotid intima-media thickness, a marker of atherosclerotic vascular disease and a predictor of vascular events.
“…Some studies [48,50] indicated that serum Mg level did not influence PTH in patients on regular HD. Other studies reported a highly significant inverse correlation between Mg and PTH in HD patients [46,47,49,51,52,[55][56][57]65] . Table 1 summarizes data from clinical trials addressing the effect of Mg on serum PTH level in HD patients.…”
Cardiovascular disease is the leading cause of mortality and morbidity in patients with chronic kidney disease, which is partly explained by the fact that 40–70% of patients receiving dialysis have significant coronary artery disease. Recent clinical studies have shown that lower serum magnesium (Mg) levels are associated with vascular calcification and cardiovascular mortality among patients with end-stage renal disease (ESRD). On the other hand, hypermagnesemia inhibits parathyroid hormone secretion, which is considered an important independent risk factor for vascular calcification, left ventricular hypertrophy and mortality in ESRD patients. Finally, increasing evidence points towards a link between Mg and cardiovascular disease, even in subjects without chronic kidney disease. The purpose of this review was to critically review the current literature examining the effects of plasma Mg levels on cardiovascular disease and parathyroid hormone homeostasis in ESRD, and renal transplant patients.
“…In patients on HD, there is rapid equilibration between dialysate Mg and the ultrafilterable (nonprotein bound) Mg fraction in the blood; dialysate Mg is thus a major determinant of serum levels . Magnesium‐free dialysate is associated with high rates of hypomagnesemia . Hypomagnesemia can also be induced with dialysate Mg concentrations as high as 0.5 mmol/L .…”
Section: Magnesium Homeostasis In Health and On Dialysismentioning
Magnesium balance is infrequently discussed in the dialysis population, and the clinical consequences of derangements in magnesium homeostasis are incompletely understood. There is an association between hypomagnesemia and adverse outcomes including increases in cardiovascular disease and mortality, while elevated magnesium levels have also been linked with complications such as osteomalacia. In this review, we discuss the features of magnesium physiology relevant to dialysis patients and provide an updated summary of the literature linking magnesium derangements with bone disease, cardiovascular disease, sudden cardiac death, and mortality.
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