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 magnesium 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 magnesium 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 magnesium) 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 magnesium and calcium) in the thick ascending limb of Henles loop of the kidney is impaired. This results in loss of magnesium 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 magnesium in the distal convoluted tubule.
Cuboid syndrome or cuboid subluxation describes a condition that results from subtle injury to the calcaneocuboid joint and ligaments in the vicinity of the cuboid bone, one of seven tarsal bones of the human foot. This condition often manifests in the form of lateral (little toe side) foot pain and sometimes general foot weakness. Cuboid syndrome, which is relatively common but not well defined or recognized, is known by many other names, including lateral plantar neuritis, cuboid fault syndrome, peroneal cuboid syndrome, dropped cuboid, locked cuboid and subluxed cuboid. Signs and symptoms
A patient with cuboid syndrome usually seeks medical advice and attention complaining of pain, discomfort, or weakness along the lateral aspect of the foot between the fourth and fifth metatarsals and the calcaneocuboid joint. The pain may radiate throughout the foot. Tenderness may be elicited over the tendon of the peroneus longus muscle and an antalgic gait may be observed. The pain may be observed in a controlled environment by standing on the toes or rolling the arches of the foot, as these motions tend to exercise the foots calcaneocuboid joint and ligament, which are characteristically strained in a patient suffering from cuboid syndrome. Also, the pain may come on suddenly or it may develop gradually and persist over time. Sometimes the pain is intermittent, subsiding partially or completely for a period of time before returning again. Causes
A patient may develop Cuboid syndrome through either a single traumatic event (e.g., ankle sprain) or insidiously with repetitive strain over time.