Table 3.

Factors that alter renal regulation of magnesium

Increase Magnesium Absorption	Decrease Magnesium Absorption
Dietary magnesium restriction	Hypermagnesemia
Parathyroid hormone	Metabolic acidosis
Glucagon	Hypercalcemia
Calcitonin	Phosphate depletion
Vasopressin	Potassium depletion
Aldosterone	Diuretics (loop and thiazide)
Insulin	Antibiotics (aminoglycosides)
Amiloride	Antifungals (amphotericin B)
Metabolic alkalosis	Antivirals (foscarnet)
EGF	Chemotherapy agents (cisplatin)
	Immunosuppressants (tacrolimus, cyclosporine, rapamycin)
	EGF receptor antagonists
	FHHNC caused by mutations in claudin-16 and claudin-19
	HSH caused by mutations in TRPM6
	Bartter’s syndrome caused by mutations in NKCC2 (type 1), ROMK (type II), ClC-Kb (type III), or CaSR (type V)
	Dominant hypomagnesemia caused by mutations of the FXYD2 gene, HNF1B, or CNNM2
	Isolated dominant hypomagnesemia caused by mutations of Kv1.1
	Isolated recessive hypomagnesemia caused by mutations of pro-EGF
	Gitelman’s syndrome caused by mutations of NCC
	EAST/SeSAME caused by mutations in Kir4.1

FHHNC, familial hypomagnesemia with hypercalciuria and nephrocalcinosis; HSH, hypomagnesemia with secondary hypocalcemia; TRPM6, transient receptor potential melastatin 6; NKCC2, Na⁺-K⁺-2Cl⁻ cotransporter; ROMK, renal outer medullary potassium K⁺; CLC-Kb, Cl channel Kb; CaSR, calcium-sensing receptor; FXYD2, sodium/potassium-transporting ATPase gamma chain (a protein that in humans is encoded by the FXYD2 gene); HFN1B, hepatocyte nuclear factor 1 beta; CNNM2, cyclin M2; NCC, thiazide-sensitive Na-Cl Cotransporter; EAST (epilepsy, ataxia, sensorineural deafness, and tubulopathy)/SeSAME (seizures, sensineural deafness, ataxia, mental retardation, and electrolyte imbalance).