Obesitas en primair aldosteronisme: oorzaak, gevolg of beide?

Obesity has been shown to correlate directly with circulating aldosterone levels and urinary aldosterone excretion in normotensive and hypertensive individuals without primary aldosteronism (PA). This relationship may be bi-directional, though it is probably not symmetrical. Activation of the mineralocorticoid receptor in adipocytes may cause expansion of visceral fat mass. Conversely, adipocytes have been shown to augment the adrenal production of aldosterone by their release of aldosterone secretagogues—leptin, CTRP-1, and resistin—into the circulation. Patients with PA are more obese (idiopathic hyperaldosteronism>aldosterone-producing adenoma) than those with essential or no hypertension (women>men). The stronger association of obesity with idiopathic hyperaldosteronism than with the more metabolically severe unilateral PA, and the reductions in aldosterone levels after weight loss, suggest a substantive role for adipocytes in circulating aldosterone levels. A 2-sampl