<unk>  may result from gastrointestinal or kidney causes. Gastrointestinal causes include low dietary intake of<unk> , reduced gastrointestinal absorption or increased gastrointestinal loss due to rapid gastrointestinal transits. Kidney causes involve increased excretion of<unk> . Poor dietary intake of<unk>  has become an increasingly important factor – many people consume diets high in refined foods such as white bread and polished rice which have been stripped of<unk> -rich plant fiber.<unk>  is not uncommon in hospitalized patients. Up to 12% of all people admitted to hospital, and as high as 60–65% of people in an intensive care unit, have hypomagnesemia. About 57% of the US population does not meet the US RDA for dietary intake of<unk> . The kidneys are very efficient at maintaining body levels; however, if the diet is deficient, or certain medications such as diuretics or proton pump inhibitors are used, or in chronic alcoholism, levels may drop. Low levels of<unk>  in blood may be due to not enough<unk>  in the diet, the intestines not absorbing enough<unk> , or the kidneys excreting too much<unk> . Deficiencies may be due to the following conditions: Medications * Loop and thiazide diuretic use (the most common cause of hypomagnesemia) * Antibiotics (i.e. aminoglycoside, amphotericin, pentamidine, gentamicin, tobramycin, viomycin) block resorption in the loop of Henle. 30% of patients using these antibiotics have hypomagnesemia. * Long term, high dosage use of proton-pump inhibitors such as omeprazole * Other drugs * Digitalis, displaces<unk>  into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively increasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect. * Adrenergics, displace<unk>  into the cell * Cisplatin, stimulates kidney excretion * Ciclosporin, stimulates kidney excretion * Mycophenolate mofetil Genetics * Gitelman-like diseases, which include the syndromes caused by genetic mutations in SLC12A3, CLNCKB, BSND, KCNJ10, FXYD2, HNF1B or PCBD1. In these diseases, the hypomagnesemia is accompanied by other defects in electrolyte handling such as hypocalciuria and hypokalemia. The genes involved in this group of diseases all encode proteins that are involved in reabsorbing electrolytes (including<unk>  in the distal convoluted tubule of the kidney. * Hypercalciuric hypomagnesemic syndromes, which encompass the syndromes caused by mutations in CLDN16, CLDN19, CASR or CLCNKB. In these diseases, reabsorption of divalent cations (such as<unk>  and calcium) in the thick ascending limb of Henle's loop of the kidney is impaired. This results in loss of<unk>  and calcium in the urine. * Mitochondriopathies, such as caused by mutations in SARS2, MT-TI or as seen with Kearns-Sayre syndrome. * Other genetic causes of hypomagnesemia, such as mutations in TRPM6, CNNM2, EGF, EGFR, KCNA1 or FAM111A. Many of the proteins encoded by these genes play a role in the transcellular absorption of<unk>  in the distal convoluted tubule. Metabolic abnormalities * Insufficient selenium, vitamin D or sunlight exposure, or vitamin B6. * Gastrointestinal causes: the distal digestive tract secretes high levels of<unk> . Therefore, secretory diarrhea can cause hypomagnesemia. Thus, Crohn's disease, ulcerative colitis, Whipple's disease and celiac sprue can all cause hypomagnesemia. * Postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and kidney transplant. Other * Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines. * Malabsorption * Acute pancreatitis * Fluoride poisoning * Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications.
Magnesium deficiency
Fluorine deficiency
Boron deficiency 
Fluoride toxicity
Selenium deficiency
Thiamine deficiency
Copper deficiency
Vitamin D toxicity