Interpretation of U&Es

Interpretation of U&Es can be broken into its two components i.e. Urea (Kidney function) and Electrolytes.  Note that the two should be interpreted in context of each other and the clinical scenario- many abnormalities seen in U&Es are not pathological (e.g. due to drugs, dehydration etc).

Renal Component (Urea and Creatinine)

  • Physiology
    • Creatinine is produced in the liver (energy store for fast twitch muscle fibres)- it can be phosphorylated to store phosphate to produce ATP, after which it is excreted by the kidneys
      • Amount in blood depends on kidney function, liver function (much less so) and muscle mass (this latter component can be very important when interpreting creatinine levels)
    • Urea is produced from the breakdown of amino acids in the liver and is excreted by the kidneys too.
      • Whilst urea levels can be an indication for kidney function, there are many other things that may affect urea levels e.g.
        • Increase: dehydration; GI bleed; increased protein breakdown (post-op; trauma; infection; malignancy); drugs; high protein diet
        • Decrease: malnutrition; liver disease; pregnancy
  • Normal values
    • Creatinine levels: typically 60-120μmol/l for men and 55-100μmol/l for women (NB labs will differ between reference ranges)
      • NB Creatinine can correlate with lean body mass (i.e. a cachexic old lady will have a significantly lower creatinine than a body builder but may still have an acute kidney injury)
        • it is important, where possible, to measure/estimate a baseline creatinine for the individual patient
    • Urea: around 2.5-8mmol/l
  • Interpretation
    • A rise in both urea and creatinine suggests renal dysfunction
      • A rise in creatinine >50% above baseline is indicative of AKI
      • Other tests should be carried out to further evaluate kidney function e.g. urinalysis, FBC, blood gases (if patient is unwell), other electrolytes e.g. PO4 and Ca2+; CK; Immunoglobulins/complement; urine output etc
    • A solitary rise in urea (as suggested above) may not be due to kidney function- important to check fluid status

Electrolyte Component

  • Sodium (135-145mEq/l or mmol/l)
    • Hyponatraemia
    • Hypernatraemia
      • Causes
        • In normovolaemic patients- commonly iatrogenic (e.g. excess IV saline or sodium containing drugs)
        • In dehydrated/hypovolaemic patients
          • can be due to sodium loss e.g. diarrhoea/vomiting, burns
          • or due to lack of reabsorption e.g. diabetes insipidus or osmotic diuresis (e.g. in DKA or hypoaldosteronism)
      • Investigations
        • Check serum and urine osmolarities +/- DDAVP (ADH) test +/- water deprivation (diabetes insipidus)
      • Treat cause and correct sodium (slowly- risk of osmotic demyelination)
        • if euvolaemic- give dextrose only rather than saline (and/or salt restrict)
        • if hypovolaemic- give saline (NB must replace fluid loss prior to sodium correction)
  • Potassium (3.5-5.5mmol/l)
  • Calcium (corrected calcium 2.05-2.6mmol/l)
  • Magnesium (0.75-1mmol/l)
    • Hypomagnesaemia
      • Causes
        • Excess loss e.g. diuretics, severe diarrhoea, DKA
        • Poor nutrition/alcoholism
          • NB most magnesium is found in bone and cells, so will reduce if calcium, phosphate and/or potassium are low (ALL OF THESE SHOULD BE CHECKED WITH MAGNESIUM)
      • Management
        • Replace Mg – 8-12g of magnesium sulphate (as an infusion) over first 24 hours then 4-6mg/day until Mg is normal
      • NB ALWAYS REPLACE MAGNESIUM PRIOR TO OTHER ELECTROLYTE DISTURBANCES (particularly hypocalcaemia, which will not correct itself without normalising Mg first)
  • Phosphate
    • Hypophosphataemia
      • Causes
        • Vit D deficiency
        • Refeeding syndrome
        • Primary hyperparathyroidism
        • Poor nutrition/alcoholism
      • Management
        • Often can be managed with oral phosphate supplements if necessary
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