Hypermagnesemia is an uncommon laboratory finding and symptomatic hypermagnesemia is even less common. This disorder has a low incidence of occurrence, because the kidney is able to eliminate excess magnesium by rapidly reducing its tubular reabsorption to almost negligible amounts.
In healthy adults, plasma magnesium ranges from 1.7-2.3 mg/dL. Approximately 30% of total plasma magnesium is protein-bound and approximately 70% is filterable through artificial membranes (15% complexed, 55% free Mg2+ ions). With a glomerular filtration rate (GFR) of approximately 150 L per day and an ultrafiltrable magnesium concentration of 14 mg/L, the filtered magnesium load is approximately 2,100 mg per day. Normally, only 3% of filtered magnesium appears in urine; thus, 97% is reabsorbed by the renal tubules. In contrast to sodium and calcium, only approximately 25-30% of filtered magnesium is reabsorbed in the proximal tubule. Approximately 60-65% of filtered magnesium is reabsorbed in the thick ascending loop of Henle and 5% is reabsorbed in the distal nephron.  Relatively little is known about cellular magnesium transport mechanisms. 
Familial hypocalciuric hypercalcemia
Milk alkali syndrome
Patients with end-stage renal disease often have mild hypermagnesemia, and the ingestion of magnesium-containing medications (eg, antacids, cathartics) can exacerbate the condition.  In patients undergoing regular dialysis, the serum magnesium level directly relates to the dialysate magnesium concentration. 
In patients with acute renal failure, hypermagnesemia usually presents during the oliguric phase; the serum magnesium level returns to normal during the polyuric phase. If a patient receives exogenous magnesium during the oliguric phase, severe hypermagnesemia can result, especially if the patient is acidotic.
People often take magnesium-containing medications (eg, antacids,  laxatives,  rectal enemas). Hypermagnesemia can develop after treatment of drug overdoses with magnesium-containing cathartics,  and it also occurs in patients taking magnesium-containing medications for therapeutic purposes [10, 11] ; however, most of these patients have normal renal function.  If the patient does not ingest a large amount of magnesium but has a gastrointestinal disorder (eg, gastritis, colitis, gastric dilation), absorption may increase. [13, 14] In any case, monitoring serum magnesium levels in patients taking magnesium-containing medications is prudent.
Excessive tissue breakdown (sepsis, shock, large burns), especially with concurrent renal failure, can deliver a large amount of magnesium from the intracellular space, along with a massive elevation of phosphorus and potassium. 
In the treatment of eclampsia, hypermagnesemia is induced deliberately and sometimes can be symptomatic. [10, 15, 16] Occasionally, hypermagnesemia also can occur in the newborn infant. [17, 18] Maternal magnesium therapy can increase the need for feeding and respiratory support  and may cause neurobehavioral disorders in the newborn. 
Lithium therapy causes hypermagnesemia by decreasing urinary excretion, although the mechanism for this is not completely clear.
Familial hypocalciuric hypercalcemia may cause modest elevations in serum magnesium.  This autosomal dominant disorder is characterized by very low excretion of calcium and magnesium and by a normal parathyroid hormone level. Abnormalities of calcium and magnesium handling are due to mutations in the calcium-sensing receptor,  resulting in increased magnesium reabsorption in the loop of Henle.
There has been some interest in the use of magnesium in the treatment and prevention of cardiac arrhythmias and in the treatment of subarachnoid hemorrhage [25, 26] ; however, significant hypermagnesemia has not been reported in these settings.
Effects of Hypermagnesemia
Symptoms of hypermagnesemia usually are not apparent unless the serum magnesium level is greater than 2 mmol/L. Concomitant hypocalcemia, hyperkalemia, or uremia exaggerate the symptoms of hypermagnesemia at any given level.
These are the most common presenting problems. Hypermagnesemia causes blockage of neuromuscular transmission by preventing presynaptic acetylcholine release and by competitively inhibiting calcium influx into the presynaptic nerve channels via the voltage-dependent calcium channel. 
One of the earliest symptoms of hypermagnesemia is deep-tendon reflex attenuation. Facial paresthesias also may occur at moderate serum levels.
Muscle weakness is a more severe manifestation, occurring at levels greater than 5 mmol/L. This manifestation can result in flaccid muscle paralysis and depressed respiration and can eventually progress to apnea.
Conduction system symptoms
Hypermagnesemia depresses the conduction system of the heart and sympathetic ganglia.  A moderate increase in serum magnesium can lead to a mild decrease in blood pressure, and a greater concentration may cause severe symptomatic hypotension. Magnesium is also cardiotoxic and, in high concentrations, can cause bradycardia. Occasionally, complete heart block and cardiac arrest may occur at levels greater than 7 mmol/L.
Apparently, hypocalcemia results from a decrease in the secretion of parathyroid hormone (PTH) or from end-organ resistance to PTH.  Paralytic ileus develops from smooth-muscle paralysis,  and mothers being treated with magnesium for preterm labor suppression are at risk. 
Hypermagnesemia may interfere with blood clotting through interference with platelet adhesiveness, thrombin generation time, and clotting time.
These symptoms include nausea, vomiting, and cutaneous flushing.
Diagnosis and Summary
Hypermagnesemia usually results from a combination of excess magnesium intake and a coexisting impairment of renal function. Diagnosis is usually straightforward and involves measuring serum magnesium levels, as many cases are unsuspected.  If a magnesium level is not immediately available, a clue to the existence of hypermagnesemia would be the disease context (preeclampsia, renal failure), the presence of magnesium-containing preparations, or a decreased anion gap.
Prevention and Treatment of Hypermagnesemia
Prevention of hypermagnesemia is usually possible. Anticipate hypermagnesemia in patients who are receiving magnesium treatment, especially those with reduced renal function. Initially, withdraw magnesium therapy, which often is enough to correct mild to moderate hypermagnesemia.
In patients with symptomatic hypermagnesemia that is causing cardiac effects or respiratory distress, antagonize the effects by infusing calcium gluconate. Calcium antagonizes the toxic effect of magnesium, and these ions electrically oppose each other at their sites of action. This treatment usually leads to immediate symptomatic improvement. In subjects with frankly impaired ability to excrete magnesium (eg, end-stage renal disease), renal replacement therapy may also be necessary.
Drug Category: Diuretics
Agents that promote magnesium excretion are effective in treating hypermagnesemia.
Furosemide (Lasix) may promote excretion of magnesium. It increases excretion of water by interfering with the chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.
Drug Category: Calcium salts
Calcium may moderate nerve and muscle performance in hypermagnesemia.
Calcium gluconate (Kalcinate) directly antagonizes neuromuscular and cardiovascular effects of magnesium. Use in patients with symptomatic hypermagnesemia that is causing cardiac effects or respiratory distress.
Drug Category: Antidiabetic agents
Agents that shift magnesium ions into cells are helpful in treating hypermagnesemia.
Glucose and insulin may help promote magnesium entry into cells. Glucose should be administered with insulin to prevent hypoglycemia. Monitor blood sugar levels frequently.