Abstract for presentation at Australia and New Zealand Society of Nephrology Annual Scientific Conference

Purpose: Many patients with hyperkalaemia have a readily identifiable cause, which leads to appropriate management. In other patients, particularly with a reduced GFR, differentiating between hypoaldosteronism and pseudohypoaldosteronism is problematic.
The aim of this study was to see if a plasma aldosterone to potassium algorithm could be defined which would help identify patients with hyperkalaemia due to sub optimal levels of aldosterone; thereby validating treatment with 9-alpha-fluhydrocortisone, rather than sodium polystyrene sulfonate and/or dietary potassium restriction.
Methods: A literature search for studies providing details of plasma aldosterone and plasma potassium in normals (made hyperkalaemic)and patients with hypoaldosteronism, pseudohypoaldosteronism and renal failure with hyperkalaemia.
Results: Only one study was found in which normals were made significantly hyperkalaemic (to 6.3 mmol/l)¹. These subjects, while on a high sodium, low potassium (western) diet (n=5) allowed an arbitrary definition of a simple aldosterone to potassium algorithm for hypoaldosteronism (plasma aldosterone (ng/dl)< 10*(plasma potassium -4.2)).
Plasma aldosterone and potassium levels, in reported patients with a plasma potassium >5.5 and confirmed hypoaldosteronism (n=30) and pseudohypoaldosteronism (n=29, supported the use of the algorithm. Reported patients with hyperkalaemia and a reduced GFR (n=42)had values consistent with either hypoaldosteronism or pseudohypoaldosteronism, not predicted by their plasma renin activity.
Clinical application of this ratio, in two patients with moderate renal impairment and hyperkalaemia, has been helpful.
Conclusion: In hyperkalaemic patients a plasma aldosterone to potassium algorithm helps distinguish hypoaldosteronism from pseudohypoaldosteronism. Further clinical experience will define its general utility.

Reference: ¹ Dluhy R.G. et al.1972 J. Clin. Invest.51:1950