Urinary Anion Gap

OVERVIEW

Urinary Anion Gap = [Na+]+ [K+] – [Cl]

  • the cations normally present in urine are Na+, K+, NH4+, Ca2+,and Mg2+.
  • the anions normally present are Cl, HCO3, sulphate, phosphate and some organic anions.
  • only Na+, K+ and Cl are commonly measured in urine so the other charged species are the unmeasured anions (UA) and cations (UC).

CLINICAL USE

  • the urinary anion gap can help to differentiate between GIT and renal causes of a hyperchloraemic metabolic acidosis.
  • it has been found experimentally that the Urinary Anion Gap (UAG) provides a rough index of urinary ammonium excretion.
  • ammonium is positively charged so a rise in its urinary concentration (ie increased unmeasured cations) will cause a fall in UAG

PATHOPHYSIOLOGY

  • hyperchloraemic acidosis can be caused by:
    • (i) Loss of base via the kidney (eg renal tubular acidosis)
    • (ii) Loss of base via the bowel (eg diarrhoea)
    • (iii) Gain of mineral acid (eg HCl infusion)
  • if the acidosis is due to loss of base via the bowel then the kidneys can respond appropriately by increasing ammonium excretion to cause a net loss of H+ from the body -> the UAG would tend to be decreased -> increased NH4+ (with presumably increased Cl-) => increased urinary cations => decreased UAG.
  • if the acidosis is due to loss of base via the kidney, then as the problem is with the kidney it is not able to increase ammonium excretion and the UAG will not be increased.
  • experimentally, it has been found that patients with diarrhoea severe enough to cause hyperchloraemic acidosis have a negative UAG (average value -27 +/- 10 mmol/l) and patients with acidosis due to altered urinary acidification had a positive UAG.

SUMMARY

  • low urinary AG = GI loss of base
  • no change in urinary AG = renal loss of base
  • negative urinary AG = severe diarrhea
  • positive urinary AG = altered urinary acidification

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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