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 |
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)
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).
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.