Derangements of magnesium and phosphate

Hypomagnesaemia

• Causes
  • • GI loss
    • Renal loss / Polyuria – consider renal tubular disorders
    • Starvation
    • Alcoholism (common)
    • Malabsorption
    • Refeeding syndrome
    • Drugs – especially PPIs, diuretics, cisplatin
• Can check the fractional excretion of magnesium to check for rare renal causes
• May present with tremors, ataxia, nystagmus, seizures, arrhythmias (classically torsades de pointes) and cardiac arrest.
• The ECG changes include
  • • Prolonged PR and QT intervals
    • ST segment depression
    • T wave inversion
    • Flattened P waves
    • Increased QRS duration
    • Torsades de pointes
• Treatment for severe or symptomatic hypomagnesaemia – 2g 50% magnesium sulphate (4 mL; 8 mmol) IV over 15 min
• For torsades de pointes – 2g 50% magnesium sulphate (4 mL; 8 mmol) IV over 1-2 min
• For seizures – 2g 50% magnesium sulphate (4 mL; 8 mmol) IV over 10 min
• Low magnesium can cause hypocalcaemia – treating hypocalcaemia in this setting won’t help much.. you need to replace the magnesium first
• Ensure vitamin D replete – magnesium helps convert vitamin D into its active form. Therefore low magnesium levels can render vitamin D supplements ineffective

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Hypermagnesaemia

• Typically due to renal failure or the administration of excessive magnesium in hospital
• ECG changes include
  • • Prolonged PR and QT intervals
    • Peaked T waves
    • Heart block
    • VF, VT, PEA and asystole
• Consider treating hypermagnesemia at levels above 1.75 mmol if the patient is symptomatic or develops ECG changes
• Treatment
  • • Calcium chloride 10% 5-10 mL, repeated if necessary
    • Saline diuresis with 0.9% sodium chloride
    • 1 mg /kg IV furosemide
    • Consider dialysis

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Hypophosphataemia

• Normal range 0.8-1.5 mmol/L
• Causes
  • • Redistribution – respiratory alkalosis, DKA, refeeding syndrome
    • Renal loss – primary hyperparathyroidism, diuretics, dialysis, renal tubular disease
    • Reduced supply – reduced intake/malnutrition, ETOH withdrawal, malabsorption, vitamin D deficiency (reduces phosphate absorption)
    • GI loss – vomiting or diarrhoea
• Investigation
  • • Always check the VBG first – it may appear low if the patient was hyperventiliating at the time of venesection
    • Serum pH, vitamin D level, bone profile, U&Es, CBG, parathyroid hormone level, uric acid (for Fanconi’s)
    • Urine pH, electrolytes
    • Consider retinol binding protein (RBP) if suspecting tubular disease (indicates proximal tubular damage). Some labs only do urine beta-2 macroglobulin instead
    • You can check fractional urinary phosphate excretion if you suspect renal loss
      • • Check paired urine and serum phosphate
        • Calculate the fractional excretion of phosphate (normal is <20%. Very high suggest a tubular problem).
        • Sometimes the tubular maximum reabsorption of phosphate calculated instead
• Causes of isolated renal phosphate wasting
  • • X linked hypophosphatemia rickets
    • Hereditary hypophosphatemia rickets (AD inherited)
    • Oncogenic osteomalacia (very rare, paraneoplastic)
• Other causes of renal phosphate wasting are tubular issues with other biochemical abnormalities
• Renal Fanconi syndrome (not related to Fanconi’s anaemia)
  • • Glycosuria, aminoaciduria (never really measured), phosphaturia, metabolic acidosis, hypouricemia
    • Due to proximal tubular failure
    • Can be genetic, but often due to drugs/toxins

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Hyperphosphataemia

• • Causes – as usual, it’s all about excretion, intake, distribution, as well as spurious causes
    • • The usual cause is reduced renal excretion of phosphate. This is
        • • Usually due to chronic kidney disease
          • Rarely due to hypoparathyroidism, pseudohypoparathyroidism and parathyroid suppression (eg vitamin A or D excess, granulomatous disease)
      • Sometimes the cause is transcellular shifts
        • • DKA, rhabdomyolysis, sepsis, tumour lysis syndrome
      • Rarely due to increased administration (including phosphaate enemas)
      • Spurious – multiple myeloma, macroglobulinaemia, dyslipidaemia, haemolysis
  • Effects
    • • Mostly asymptomatic
      • In CKD hyperphosphotaemia is part of secondary hypoparathyroidism and renal osteodystrophy
        • • Sometimes symptoms of associated hypocalacaemia (especially in CKD)
          • Calcium can precipitate into soft tissues (itching, subcutanoues nodules, vascular calcification)
  • Investigations
    • • Check all other electrolytes
      • Not much more to do if cause is obvious eg CKD, over-administration
      • Consider checking CK, PTH, vitamin D, myeloma screen, lipids, LFTs
  • Treatment
    • • In CKD / secondary hypoparathyroidism
        • • Restrict dietary phospahte
          • Phosphate binders (Sevelamer, calcium carbonate, calcium acetate)
          • More in CKD section
      • Acutely – IV fluids, consider dialysis