# Question 18.2

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)

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

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.