Question 20.1

The following venous blood results are from a 56-year-old patient presenting with abdominal pain.

Parameter

Patient Value

Adult Normal Range

Sodium

130 mmol/L*

135 – 145

Potassium

5.1 mmol/L*

3.5 – 5.0

Chloride

101 mmol/L

95 – 105

Bicarbonate

10 mmol/L*

22 – 28

Creatinine

305 mmol/L*

50 – 100

Urea

75.6 mmol/L*

3.5 – 7.2

Glucose

5.2 mmol/L

3.5 – 6.0

Calcium corrected

2.05 mmol/L*

2.12 – 2.62

Ionized Calcium

0.97 mmol/L*

1.14 – 1.30

Phosphate

3.97 mmol/L*

0.73 – 1.37

Protein

66 g/L

61 – 83

Albumin

29 g/L*

35 – 50

Alkaline phosphatase

220 U/L*

30 – 110

g-Glutamyl transferase

30 U/L

< 40

Alanine transferase

27 U/L

< 35

Magnesium

0.83 mmol/L

0.75 – 0.95

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College answer

Not available.

Discussion

That's not a lot of history, and therefore for the candidates the real struggle would have been to fight the natural urge to spend a few minutes connecting these abnormalities into a single grand unifying diagnosis. Fortunately, one immediately presents itself.

So: the abnormalities are:

  • Hyponatremia: which is only very mild
  • Hyperkalemia: which is again only mild
  • Metabolic acidosis which appears to be mainly NAGMA:
    the anion gap is slightly raised (19), and therefore the delta ratio is 0.5
  • Creatinine is rather elevated
  • Urea is wildly elevated, much more than the rise in creatinine
  • Calcium is low, including both the total and ionised
  • Phosphate is raised
  • Albumin is low, which is incredibly non-specific
  • Of the LFTs, only the alk phos is raised.

What could have caused all this, AND abdominal pain? The mind boggles. However, even the boggling mind would agree that the urea of 76 (!) is the most profoundly disturbed value here. Renal failure is also present, and any kind of renal failure could be to blame for the creatinine rise, but only one kind of renal failure can give rise to a urea/creatinine ratio so heavily skewed in favour of urea.  The abdominal pain here, therefore, must clearly be the pain of a humongously overdistended (if not ruptured) bladder. This is obstructive uropathy. Marshall (1964) explained this phenomenon as the result of increased hydrostatic pressure in the tubule which slows tubular transport and increases the transport of urea out of the tubule lumen.

Thus:

  • Raised urea and creatinine due to obstructive uropathy
  • Metabolic acidosis and raised phosphate due to renal failure
  • Depressed calcium due to raised phosphate
  • Elevated alk. phos. due to hypocalcemia-induced PTH release
  • Hyponatremia due to inadequate water excretion 
  • Hyperkalemia due to renal failure and acidosis


 

References