Hypomagnesemia

• Gastrointestinal

  • Decreased intestinal absorption

  • Decreased intake, though this is rare given relative abundance of magnesium in common foods

  • Increased losses (diarrhea, NG suction)

    • E.g., cystic fibrosis

• Kidney: 10-25% is absorbed in proximal tubule (PT), 50-70% absorbed in thick ascending limb (TAL), 10% in distal convoluted tubule (DCT)

  • Absorption in PT is relatively fixed, but absorption in TAL and DCT should increase as plasma magnesium level falls

  • Acquired tubular defects:

    • Post-ATN diuresis

    • Alcohol induced tubular injury

    • Drug induced tubular injury: thiazides, aminoglycosides, amphotericin B, cysplatin, pentamidine, tacrolimus, cyclosporine

    • Hypercalcemia

  • Genetic tubular defects:

    • Gitelman

    • Familial hypomagnesemia with hypercalciuria and nephrocalcinosis

      • NKCC2 and ROMK generate positive voltage gradient, and allow Mg to be reabsorbed passively

      • Mutations in claudins lead to magnesium and calcium losses in the urine

    • TRMP6 mutation

• Compartmental redistribution

  • Pancreatitis: loss of Mg into the fat

  • Refeeding syndrome

  • Hungry bone syndrome

  • Transcellular shift

• Usually asymptomatic when mild

• Neuromusuclar symptoms: muscle cramps, tremors, msucle weakness, fatigue

• Neurologic: seizures, delirium

• Cardiac: arrhythmias,

66% stored in bones, 1/3 in muscles, 1% in plasma

20-30% bound to plasma proteins and not filtered by kidneys

• Second most abundant intracellular cation

• Important for enzymatic and physiologic processes including glycolysis, DNA synthesis/transcription, and ATP generating