A 63 year old patient with a background of type II diabetes  had vascular surgery 24 hours previously. His post operative course has been uncomplicated except for consistently  elevated serum potassium measurements. He is not receiving supplemental potassium and vital recordings have been stable. His most recent arterial blood gases and plasma  biochemistry are presented below:

 Arterial blood Value Reference range pH 7.24 7.36-7.44 PCO2 24 mmHg  (3.2 kPa) 40 mmHg       (5.3-5.7 kPa) PO2 90 mmHg (12.0 kPa) 80-100 mmHg (10.5-13.0 kPa) HCO3 - 10 22-33 mmol/L Na+ 135 135 -145 mmol/L K+ 5.7 3.2-4.5 mmol/L Urea 15 3.0-8.0 mmol/L Creatinine 180 50-100 umol/L Cl - 120 100-110 mmol/L Albumin 35 35-50 G/L

a) Describe the acid base abnormality

b) List three causes of the acid-base  abnormality.

c)  What is the most likely cause of the abnormality in this patient?

a) Describe the acid base abnormality

This is a normal anion gap metabolic acidosis.

b) List three causes of the acid-base  abnormality.

The major causes are:
o   Loss of bicarbonate (eg diarrhoea, pancreatic biliary drainage and urinary diversions (ureterosigmoidostomy)
o   Renal tubular acidosis (RTA).

c)  What is the most likely cause of the abnormality in this patient?

Type 4 RTA.

## Discussion

Let us dissect these results systematically.

1. The A-a gradient cannot be calculated, as no FiO2 is supplied to us
2. There is acidaemia
3. The PaCO2 is compensatory
4. The SBE is not supplied, but the bicarbonate is 10, suggesting a severe metabolic acidosis
5. The respiratory compensation is adequate and lurks around the natural limits of human respiratory compensation for metabolic acidosis- the expected PaCO2(10 × 1.5) + 8 = 23mmHg
6. The anion gap is normal:
(135 + 5.7) - (120 + 10) = 10.7
7. Urinary pH and electrolytes are not supplied, but they would be interesting.

Three causes of normal anion gap metabolic acidosis?

The mnemonic PANDA RUSH comes to mind, even though it is not very good.

• Pancreatico-duodenal fistula
• Acetazolamide
• Normal saline intoxication (or any other sort of exogenous chloride excess)
• Diarrhoea
• Aldosterone antagonists
• Renal tubular acidosis Type 1 (distal)
• Ureteric diversion
• Small bowel fistula
• Hyperalimentation (TPN)

In the question text, the college harps on about the raised potassium. Truly, there is only one sort of normal anion gap acidosis which is stereotypically associated with hyperkalemia:  Type 4  renal tubular acidosis, or the use of spironolactone. Of all the other causes, none have any firm commitment to hyperkalemia.

### References

References

Laing, Christopher M., et al. "Renal tubular acidosis: developments in our understanding of the molecular basis." The international journal of biochemistry & cell biology 37.6 (2005): 1151-1161.

An excellent overview of the physicochemical approach to RTA can be found in this article from Critical Care.

Ring, Troels, Sebastian Frische, and Søren Nielsen. "Clinical review: Renal tubular acidosis–a physicochemical approach." Critical Care 9.6 (2005): 573.