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Hypermagnesemia occurs rarely because the kidney is very effective in excreting excess magnesium. It usually develops only in people with kidney failure who are given magnesium salts or who take drugs that contain magnesium (e.g. some antacids and laxatives). It is usually concurrent with hypocalcemia and/or hyperkalemia.
- Weakness, nausea and vomiting
- Impaired breathing
- Decreased respirations
- Arrhythmia and Asystole
- Decreased or absent deep tendon reflexes
Arrhythmia and asystole are possible cardiac complications of hypermagnesemia. Magnesium acts as physiologic calcium blocker, which results in electrical conduction abnormalities.
Clinical consequences related to serum concentration:
- 4.0 mEq/l hyporeflexia
- >5.0 mEq/l Prolonged atrioventricular conduction
- >10.0 mEq/l Complete heart block
- >13.0 mEq/l Cardiac arrest
Note that the therapeutic range for the prevention of the pre-eclampsic uterine contractions is: 4.0-7.0 mEq/L. As per Lu and Nightingale, serum Mg2+ concentrations associated with maternal toxicity (also neonate depression - hypotonia and low Apgar scores) are:
- 7.0-10.0 mEq/L - loss of patellar reflex
- 10.0-13.0 mEq/L - respiratory depression
- 15.0-25.0 mEq/L - altered atrioventricular conduction and (further) complete heart block
- >25.0 mEq/L - cardiac arrest
Hypermagnesemia in renal failure
An evaluation of 515 patients on hemodialysis demonstrated that serum magnesium concentration lower than 2.77 mg/dL (1.14 mmol/L) is a significant predictor for increased all-cause mortality. While the mean serum magnesium concentration of this study population (2.77 mg/dL or 1.14 mmol/L) would be considered indicative of mild hypermagnesemia in the healthy population, serum magnesium concentrations in hemodialysis patients may be optimal at a higher concentration, in view of better survival under hemodialysis conditions, without causing severe and symptomatic hypermagnesemia. Consistently, lower magnesium levels were significantly associated with the presence of vascular calcification of the hand arteries in a study investigating 390 nondiabetic hemodialysis patients. These results suggest that higher serum magnesium concentrations may play an important protective role in the development of vascular calcification in hemodialysis patients. Results from a longitudinal study with end-stage renal disease patients suggest that hypermagnesemia may retard the development of arterial calcifications in end-stage renal disease. Significantly lower values of carotid intima-media thickness and aortic pulse wave velocity values, which are surrogate markers for vascular calcification, were observed in chronic kidney disease patients with high serum magnesium levels (0.90-1.32 mmol/L or 2.18-3.21 mg/dL) indicating a lower arteriosclerotic burden associated with a lower risk of cardiovascular events and mortality. Consequently, CKD patients with mildly elevated magnesium levels could have a survival advantage over those with lower magnesium levels.
Magnesium status depends on three organs: uptake in the intestine, storage in the bone and excretion in the kidneys. Hypermagnesemia is therefore often due to problems in these organs, mostly intestine or kidney.
- Haemolysis, magnesium concentration in erythrocytes is approximately three times greater than in serum, therefore hemolysis can increase plasma magnesium. Hypermagnesemia is expected only in massive hemolysis.
- Renal insufficiency, excretion of magnesium becomes impaired when creatinine clearance falls below 30 ml/min. However, hypermagnesemia is not a prominent feature of renal insufficiency unless magnesium intake is increased.
- Other conditions that can predispose to mild hypermagnesemia are diabetic ketoacidosis, adrenal insufficiency, hyperparathyroidism and lithium intoxication.
Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium supplementation is often sufficient. In more severe cases the following treatments are used:
- Intravenous calcium gluconate, because the actions of magnesium in neuromuscular and cardiac function are antagonized by calcium.
Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:
- Intravenous diuretics, in the presence of normal renal function
- Dialysis, when kidney function is impaired and the patient is symptomatic from hypermagnesemia
- Pritchard JA. The use of the magnesium ion in the management of eclamptogenic toxemias. Surg Gynecol Obstet. 1955; 100:131–140
- Lu JF,Nightingale CH. Magnesium sulfate in eclampsia and pre-eclampsia. Clin Pharmacokinet. 2000; 38:305–314
- Ishimura E, Okuno S, Yamakawa T et al. (2007). Serum magnesium concentration is a significant predictor of mortality in maintenance hemodialysis patients. Magnes Res 20: 237–244.
- Ishimura E, Okuno S, Kitatani K et al. (2007). Significant association between the presence of peripheral vascular calcification and lower serum magnesium in hemodialysis patients. Clin Nephrol 68: 222–227.
- Meema HE, Oreopoulos DG, Rapoport A. (1987). Serum magnesium level and arterial calcification in end-stage renal disease. Kidney Int 32: 388–394.
- Salem S, Bruck H, Bahlmann FH et al. (2012). Relationship between magnesium and clinical biomarkers on inhibition of vascular calcification. Am J Nephrol 35: 31–39.
- Massy ZA, Drüeke TB (2012). Magnesium and outcomes in patients with chronic kidney disease: focus on vascular calcification, atherosclerosis, and survival. Clin Kidney J 5 (Suppl 1): i52–i61.
- Jahnen-Dechent W, Ketteler M (2012). Magnesium basics. Clin Kidney J 5 (Suppl 1): i3–i14.
- BJMU: Causes and treatment of hypermagnesemia
- Magnesium – a versatile and often overlooked element: new perspectives with a focus on chronic kidney disease
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