This has been asked about indirectly in Question 11 from the first paper of 2008. A specific tabulated answer was called for in Question 25 from the second paper of 2007.  The college answer to Question 25 is quite good; the table presented below is virtually identical, with the (perhaps unhelpful) addition of a few more obscure indices.

A Comparison of Findings in Pre-Renal and Intra-Renal Failure

Intra-renal Failure

Pre-renal failure

Urine osmolality

Less than 400-450 mOsm/kg: concentrating ability is lost

More than 450-500 mOsm/kg: concentrated urine is being passed.

This demonstrated that concentrating capacity is preserved,
which is unlikely in ATN.

Urine sodium

High in ATN (>40 meq/L) due in part to the tubular injury. Injured tubules cannot concentrate urine or appropriately reabsorb sodium.

Low in prerenal disease (<20 meq/L) in a (sometimes) appropriate attempt to conserve sodium. Pre-renal failure may also include various low-output or decreased renal blood flow states such as cirrhosis and CCF. 

Urea/ creatinine ratio

Normal in ATN

May be greater. In dehydration, urea is disproportionately elevated (indicating a loss of total body water).

The ratio is calculated from US units, rather than the usual units. In the US, your creatinine is not 500μmol/L, its 0.5mmol/L. Urea remains in mmol/L. Thus, urea/creatinine gives you the ratio. Anything above 100 is considered abnormal (ie. too much urea and not enough creatinine).

Urine/serum creatinine ratio

More than 40

Less than 20

Urine/serum osmolality

More than 1.0

More than 1.5

Fractional excretion of urea

More than 25%

Less than 25%

Fractional excreton of sodium

More than 2% (demonstrating a failure of sodium resorption)

Less than 1% (demonstrating a tendency to conserve sodium, as if in a state of hypovolemia)

Urine microscopy


  • muddy brown granular casts
  • epithelial cell casts
  • free epithelial cells
  • Nothing, or hyaline casts (which are non-specific)


Obviously, these are imperfect. Bagshaw Langenberg and Bellomo took them apart in a 2006 article, which concluded that "the scientific basis for the use of urinary biochemistry, indices, and microscopy in patients with septic ARF is weak". For one, they are easily confounded. Urine and serum osmolality indices are confounded by the use of dopamine, mannitol, and other diuretic agents. In general, though one is expected to know about these parameters, one is also expected to know about their limited utility.

As for words from authority, in his excellent Case Presentations in Chemical Pathology (Elsevier, 2013) Martin Crook presents this table of comparison on page 32:

A table of biochemical tests helpful to distinguish ATN from pre-renal failure from a book by Martin Crook


Sanjay Subramanian, John A. Kellum, and Claudio Ronco "Oliguria" in: Critical Care Nephrology by Ronco, Bellomo and Kellum (2009) pp. 341

Crook, Martin. Case Presentations in Chemical Pathology. Elsevier, 2013.

Bagshaw, Sean M., Christoph Langenberg, and Rinaldo Bellomo. "Urinary biochemistry and microscopy in septic acute renal failure: a systematic review."American journal of kidney diseases 48.5 (2006): 695-705.