1. By defining a model for control of potassium homoeostasis, patients with unexplained hypokalaemia may then be described as fitting or not fitting the model. Fitting the model implies an abnormality of known control mechanisms (e.g. aldosterone); by contrast, not fitting the model suggests other unknown factors responsible for the hypokalaemia and, possibly, hypertension.

2. In the presence of normal acid-base status, potassium excretion (Uκ+. V) is regulated by plasma potassium (Pκ+), delivery of sodium to the distal tubule and aldosterone secretion. A linear relationship (correlation coefficient of 0.72) was defined by:

Uκ+V/Pκ+ = 5.1 × log(UAldoV) × log(Uκ+V) + 1.4

based on a 24 h urine collection and plasma sample, in 16 normal subjects, 50 hypertensive normokalaemic subjects and 11 patients with hyperaldosteronism.

3. The relationship was robust and held true for variations in dietary sodium and potassium intake (5–300 and 20–100 mmol/day respectively) and variations in aldosterone excretion produced by enalapril. Patients with abnormal renal potassium wasting due to known extraneous factors (n = 11) all fell outside the 95% confidence limits.

4. Twelve patients with hypertension and hypokalaemia and renal potassium wasting all fitted within the confidence limits, being no different from 22 controls selected on the basis of age and urinary potassium excretion (30–50 mmol/day). This suggests that in these 12 patients the hypokalaemia (but not necessarily the hypertension) was not due to ‘unknown’ steroids but rather lack of regulation of the controlling variable, aldosterone.

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