• Visual inspection
  • Dipstick
  • Microscopy – cells, casts and crystals
  • Electrolytes – Na, K, Ca
  • Osmolality
  • Urinary Cystatin C


  • yellow: normal
  • pale/clear: diuretics, diabetes insipidus
  • milky: lipiduria, UTI
  • pink/opalescent: haemoglobinuria
  • pink/cloudy -> red: haematuria
  • tea coloured: myoglobinuria, metronidazole, porphyria
  • blue: methylene blue administration
  • green: high dose propofol
  • orange: rifampicin, conjugated bilirubin
  • grey/black: homogentisic acid in alkaptonuria, melanogens in disseminated melanoma, Addisons disease


  • specific gravity: normal 1.003-1.030, increased: hyperglycaemia, proteinuria, SIADH, intravascular dehydration, radiocontrast, deceased: DI, GN, pyelonephritis, renal failure
  • pH: normal 4.5-8, < 6: acidosis and pre-renal failure, >7: alkalosis and alkalinising agents, RTA
  • glucose: hyperglycaemia or renal glycosuria
  • blood: positive in haematuria, haemoglobinuria, myoglobinuria
  • protein: albuminuria (requires further investigation – GN, MM, malignancy, pyelo)
  • BHCG: pregnancy status
  • WCC: pyuria
  • nitrites: bacterial infection (most convert nitrates to nitrite)
  • ketones: starvation, diabetic or alcoholic ketoacidosis, carbohydrate free and high fat+protein diet
  • bilirubin and urobilinogen: conjugated -> excess production or biliary obstruction, urobilinogen -> absent in biliary obstruction



  • RBC: renal disease (low specificity), dysmorphic cells -> GN
  • WCC: infection (low specificity), renal calculi, interstitial nephritis, GN, vasculitis, infarction
  • tubular cells: tubular disease
  • eosinophils: interstitial nephritis


  • hyaline: can be normal
  • red cell casts: glomerular disease (GN), endocarditis
  • white cell casts: pyelonephritis, interstitial nephritis, vasculitis, infarction
  • granular: non-specific to many renal parenchymal disease
  • fatty: diabetic nephropathy and nephrotic syndrome
  • epithelial: recovery phase of ATN
  • eosinophilia: interstitial nephritis and atheroembolism


  • oxalate crystals: ethylene glycol poisoning
  • calculi: calcium, magnesium-ammonium-phosphate, urate, cysteine
  • drugs: sulphonamides, methotrexate, acyclovir, radiocontrast



  • increased loss: hypoadrenalism, salt-losing nephropathy, ATN, excess salt loads, SIADH
  • decreased loss: hyperaldosteronism, Cushing syndrome, intravascular dehydration, pre-renal failure, hepatorenal syndrome


  • helps clarify whether loss is renal or extra-renal
  • increased loss: hypomagnesaemia, ATN, loop and thiazide diuretics, hyperaldosteronism, Cushing syndrome, amphotericin B


  • may help clarify the mechanism of metabolic alkalosis
  • UrCl- <10mmol/L: intravascular volume depletion (diuretics, vomiting)
  • UrCl- >10mmol/L: intravascular volume expansion + hypokalaemia (hyperaldosteronism)


  • may clarify deranged calcium homeostasis
  • increased loss: loop diuretics, idiopathic hypercalcuria, hypoparathyroidism, vitamin D intoxication, renal failure, RTA, sarcoidosis
  • decreased excretion: hyperparathyroidism, malabsorption syndromes, vitamin D deficiency, thiazide diuretics


  • like Na+ is a marker of hydration and concentration ability but also reflects excreted osmotically active substances (ie. mannitol, radiocontrast, glucose)


  • predictor of severity of acute tubular dysfunction in a range of renal pathologies.

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a 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 three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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