Although serum Mg may not accurately reflect the overall body Mg balance, clinical symptoms of Mg deficiency correlate well with serum Mg. Levels < 1.0 mEq/L usually indicate significant total body Mg depletion. However, the severity of the symptoms among patients with similar degrees of hypomagnesemia vary widely. The so-called Mg retention test should not be used in patients with renal impairment or in transplant patients receiving cyclosporine or tacrolimus which cause urinary Mg wasting.
Mg balance is primarily a renal function (Mg intake does not appear to be regulated). The average diet provides 20 - 30 mEq daily, but the net absorption is only about 7 mEq. The kidneys normally excrete an equal amount in order to maintain Mg balance. However, in the presence of Mg deficiency urinary Mg excretion can be reduced to a minimum of about 2 mEq/day. Renal Mg reabsorption takes place primarily in the proximal tubule (30% of the filtered load) and the thick ascending limb of Henle's loop (65%). Overall renal reabsorption appears to be saturable, so that a higher Mg intake results in a proportional increase urinary excretion. For this reason, it is difficult for patients with normal renal function to develop hypermagnesemia.

1. GI problems
   • Diarrhea, NG suction, fistulas, etc
   • Poor intake (as in alcoholics)
   • Poor absorption (malabsorption, ileal bypass, etc]
2. Renal Losses
   • Acute alcohol consumption.
   • Osmotic or saline diuresis
   • Primary hyperaldosteronism
   • Hypercalciuric disorders
   • Tubulo-interstitial nephropathies
   • Drugs: diuretics, aminoglycosides,
     cyclosporine A, tacrolimus, cis-platinum, etc.
   • Primary Renal Mg Wasting
3. Internal Redistribution (from ECF to ICF)
   • IV administration of glucose or aminoacids (TPN)
   • Treatment of diabetic ketoacidosis (DKA)
   • Pancreatitis

1. Neural and Neuromuscular:
   Neural and neuromuscular abnormalities are the most common clinical signs of hypomagnesemia. Lowered excitability threshold may be manifested as irritability, psychosis, esophageal spasms (leading to dysphagia), and convulsions. Neuromuscular manifestations include tremor, fasciculations, and tetany. The latter occurs almost exclusively in presence of hypocalcemia.
   Chronic, whole-body Mg depletion may be associated with lethargy, poor appetite, nausea, muscle cramps, paresthesias, and mental abnormalities (irritability, confusion, disorientation, etc.).
2. Cardiovascular
   • ECG changes: Prolonged PR & QT intervals and flattening of the T waves.
   • Ventricular dysrhythmias: Premature contractions, tachycardia, and fibrillation. These occur almost exclusively in patients receiving digoxin therapy because both digoxin and hypomagnesemia promote the loss of K from myocardial cells. Thus, hypomagnesemia, like hypokalemia, predisposes patients to digitalis toxicity.
3. Metabolic
   Although an acute fall in plasma Mg tends to stimulate the release of parathormone (PTH), chronic hypomagnesemia has the opposite effect, resulting in hypoparathyroidism and hypocalcemia. Also, hypomagnesemia is associated with target-tissue resistance to the actions of PTH. Correction of the hypocalcemia induced by Mg deficiency requires the repletion of Mg stores as an essential first step.

   Because Mg⁺⁺ is necessary for the activation of the Na-K-ATPase, Mg deficiency is almost always associated with intracellular K⁺ depletion. Also, Mg depletion induces renal K ⁺ loss possibly by inhibiting K ⁺ reabsorption in the proximal tubules. The hypokalemia associated with Mg deficiency can be corrected only through the administration of both ions.

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