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

5.1mmol/L

3.5 - 5.0

Chloride

101 mmol/L

95 - 105

Bicarbonate

10 mmol/L

22 - 28

Creatinine

305 umol/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

y-Glutamyl transferase

30 U/L

< 40

Alanine transferase

27 U/L

< 35

Magnesium

0.83 mmol/L

0.75 -0.95

Interpret the biochemical results, giving underlying reasons to explain the abnormalities. 
(40% marks)

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College answer

• Chronic renal failure with secondary hyperparathyroidism

• Elevated urea and creatinine  

• Decreased calcium, raised ALP and phosphate

• Dehydration or GI bleed

• Raised U:Cr  

• Mixed HAGMA and NAGMA

• Low HCO3 and delta ratio >1

• Chronic renal failure (uraemia and RTA)

• Acute on chronic renal failure (sepsis, dehydration, GI bleed etc.) 
 
(Other reasonable explanations were accepted.) 

Discussion

Let us dissect these results systematically:

  1. There is no gas exchange parameters, and we can make no comment about compensation.
  2. The bicarbonate is low, suggesting metabolic acidosis.
  3. The anion gap is raised (130+5.1 - 101 - 10 = 24.1); the expected gap is around 9.5 (given that the albumin is 29)
  4. The delta ratio is very near to 1.0, suggesting that this is a pure high anion gap metabolic acidosis. This can be accounted for by the presence of lactate and non-volatile acids of renal failure (sulfate, phosphate, urate)
  5. The creatinine and urea are raised, with a very high urea but only a moderately raised creatinine, suggesting that there is either significant dehydration or a prolonged period of subnormal renal function (giving time for the urea to accumulate).
  6. The phosphate is raised (likely as a result of renal failure). The other potential reasons for a raised phosphate may include rhabdomyolysis or other causes of large-scale cell death, eg.  hepatic necrosis. In this case the latter is unlikely because of relatively normal LFTs.
  7. The total and ionised calcium are low, which is likely to be the consequence of hyperphosphataemia.
  8. Alkaline phpsphatase is raised, suggesting there is some bone destruction taking place, which may be the result of secondary hyperparathyroidism. This gives the impresison of chronicity; i.e. the renal failure is at least of subacute onset.

The college do not ask for a diagnosis.

References

References