Physiological Changes in Conn Syndrome (Primary Aldosteronism)

Pathophysiology of Conn Syndrome

The American College of Cardiology notes that elevated aldosterone levels with suppressed renin activity, typically resulting in an aldosterone-to-renin ratio greater than 30, are characteristic of Conn syndrome 2, 3
Sodium retention and potassium excretion due to excessive aldosterone production occur in patients with Conn syndrome 2
Hypertension is a classic presentation of Conn syndrome, as seen in a 25-year-old woman with high blood pressure 1, 3
Hypokalemia is often present, causing weakness and metabolic alkalosis in patients with Conn syndrome 2, 4

Increased extracellular fluid volume due to sodium retention mediated by aldosterone's action on the distal tubule occurs in Conn syndrome 2
Increased effective circulating volume as a result of sodium and water retention is a physiological change in Conn syndrome 2
Decreased proximal tubule Na+ reabsorption occurs as a compensatory response to the volume expansion in Conn syndrome 2

A patient with Conn syndrome typically presents with hypertension, high aldosterone level, and an adrenal mass on imaging 1, 2, 3

Measuring plasma aldosterone and renin activity is involved in the diagnosis of primary aldosteronism 2
Confirmatory testing with saline suppression or salt loading tests is used to diagnose primary aldosteronism 2
Imaging of the adrenal glands to identify adenomas is a diagnostic step for primary aldosteronism 2
Adrenal vein sampling to confirm lateralization, especially in patients over 40 years, is a diagnostic consideration for primary aldosteronism 2

Laparoscopic adrenalectomy is the treatment of choice for unilateral aldosterone-producing adenomas 2
Medical management with mineralocorticoid receptor antagonists, such as spironolactone or eplerenone, is used for bilateral disease or non-surgical candidates 2