Hyperaldosteronism, Primary

Responsible for up to 20% of moderate to severe systemic arterial Htn.

End organ damage from long-standing Htn (e.g., chronic kidney disease, cardiomyopathy).

Abnormal glucose tolerance in up to 50% of pts with hyperaldosteronism.

Hypernatremia and hypervolemia with high total body sodium.

Htn may be refractory to treatment, with increased risk of cardiovascular complications, including malignant hypertensive crisis.

Hypokalemia and hypomagnesaemia with low intracellular potassium and magnesium may cause cardiac arrhythmia and general muscle weakness.

Hypertensive response to intubation or surgical incision

Hypokalemia and associated muscle weakness or potential for arrhythmia

Metabolic alkalosis

Also known as Conn syndrome; described by Jerome W. Conn, University of Michigan, in 1955.

Characterized by Htn, hypernatremia, hypokalemia, metabolic alkalosis, and low plasma renin level.

Classically caused by a unilateral aldosterone producing adrenal adenoma.

Primary hyperaldosteronism is a renin-independent and incompletely suppressible over secretion of the mineralocorticoid aldosterone secreted from the zona glomerulosa of the adrenal cortex.

Aldosterone acts on the mineralocorticoid receptor in the distal convoluted tubule of the nephron and the collecting ducts to enhance sodium and water reabsorption, at the expense of potassium. Excess loss of potassium leads to loss of hydrogen ions to maintain electroneutrality.

Usually aldosterone secretion is controlled by the renin-angiotensin feedback system in response to thirst, hypovolemia, reduced renal juxtaglomerular apparatus perfusion pressure, and reduced tubular sodium concentration.

Aldosterone promotes restoration of circulating volume by correcting water and sodium depletion.

Dx is by combination of clinical suspicion of persistent Htn, hypernatremia and spontaneous hypokalemia, and metabolic alkalosis in the absence of diuretics. Dx is confirmed by measuring the plasma aldosterone to renin ratio—a value over 35 ng/dL per ng/mL/h has sensitivity of 100% and specificity of 92%. Post test specificity can be improved by measuring post-sodium infusion aldosterone. Values above 7 ng/dL showed specificity of 100%.