A 28-year-old female presented to the Emergency Department with general malaise. The following results are obtained from blood and urine respectively:

Parameter

Patient Value

Adult Normal Range

Blood Results:

FiO2

0.21

pH

7.29*

7.35 – 7.45

pO2

106 mmHg (14 kPa)

pCO2

26.0 mmHg (3.5 kPa)*

35.0 – 45.0 (4.6 – 6.0)

SpO2

97%

Bicarbonate

12.0 mmol/L*

22.0 – 26.0

Base Excess

-13.0 mmol/L*

-2.0 – +2.0

Sodium

137 mmol/L

135 – 145

Potassium

0.9 mmol/L*

3.5 – 5.0

Chloride

119 mmol/L*

95 – 105

Glucose

8.1 mmol/L*

3.5 – 6.0

Phosphate

0.3 mmol/L*

0.8 – 1.5

Urine Results:

pH

7.50

Sodium

36 mmol/L*

10 – 20

Potassium

37 mmol/L*

5 – 15

Chloride

22 mmol/L

20 – 40

  1. Describe the acid base abnormality on the blood results. (10% marks)
  1. Give three potential causes of these findings with a rationale for your answer.
    (15% marks)

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College answer

a)    There is a non-anion gap metabolic acidosis.

b)    Likely causes
1.    Type 1 or 2 Renal Tubular Acidosis (High urinary pH)
2.    Salt wasting nephropathies (high urinary Na)
3.    Diuretic use/abuse (High urinary Na and K, low K and Phos)
4.    Conns (High urinary Na and K, low plasma K)
 

Discussion

Let us dissect these results systematically:

1)  The A-a gradient is essentially normal:
(0.21 x 713) - (26 x 1.25) - 106 = 11.23 mmHg

2) There is an acidaemia, which is mild.

3) The CO2 is appropriately low

4)  There is a metabolic acidosis (the SBE is -13)

5) The respiratory compensation is appropriate:  (1.5 × 12) + 8 = 26 mmHg, or (40 - 13) = 27 mmHg, depending on which formula you use.  

6) The anion gap is (137) - (119 + 12) = 6, or 6.9 when calculated using the absurdly low potassium value. To calculate the delta ratio would therefore be pointless.

7) The urinary anion gap is (36+37) - 22 = 51, i.e. it is a positive urinary anion gap.  This suggests a renal cause of the acidosis. A negative (neGUTive) anion gap would suggest that gastrointestinal causes of NAGMA are in play, as the kidneys are doing their job. However, the combination of low urinary chloride and a urinary pH higher than the serum pH suggests that clearly they are not. 

Additional findings include a low phosphate and a higher than expected glucose.

So, what are the possible renal-related reasons for a NAGMA?

The inclusion of Conn's syndrome, or primary aldosteronism, is somewhat unexpected, as the excess of aldosterone (and therefore the increased activity of sodium-reabsorbing eNaC channels in the collecting duct) is actually expected to cause a decrease in the urinary sodium concentration. So much so in fact that the change in the ratio of serum to urinary sodium has been used as a cheap tool to screen for Conn's syndrome (Willenberg et al, 2009). 

References

References

Willenberg, H. S., et al. "The serum sodium to urinary sodium to (serum potassium) 2 to urinary potassium (SUSPPUP) ratio in patients with primary aldosteronism.European journal of clinical investigation 39.1 (2009): 43-50.

Kraut, Jeffrey A., and Nicolaos E. Madias. "Metabolic acidosis: pathophysiology, diagnosis and management." Nature Reviews Nephrology 6.5 (2010): 274-285.

Fencl, Vladimir, et al. "Diagnosis of metabolic acid–base disturbances in critically ill patients." American journal of respiratory and critical care medicine162.6 (2000): 2246-2251.

Moviat, M. A. M., F. M. P. Van Haren, and J. G. Van Der Hoeven. "Conventional or physicochemical approach in intensive care unit patients with metabolic acidosis." Critical Care 7.3 (2003): R41.