{"id":"e65af50ca504","type":"article","url":"https://hartvaat.nl/2026/04/22/obesitas-en-primair-aldosteronisme-oorzaak-gevolg-of-beide/","title":"Obesitas en primair aldosteronisme: oorzaak, gevolg of beide?","title_en":"","category":"hypertensie","category_label":"Hypertensie","professions":["huisarts","internist"],"tags":["aldosteronsynthaseremmers","baxdrostat","cagrisema","lorundrostat","obesitas","resistente-hypertensie","resistente-hypertensie-aldosteronremmers","select-trial","semaglutide","tirzepatide"],"journal":"Hypertension","doi":"https://www.ahajournals.org/doi/abs/10.1161/HYPERTENSIONAHA.126.26227","source_url":"https://doi.org/https://www.ahajournals.org/doi/abs/10.1161/HYPERTENSIONAHA.126.26227","authors":[],"significance":5,"published":"2026-05-05","source_date":"2026-04-22","image":"","kennis":["https://hartvaat.nl/kennis/hypertensie/secundaire-hypertensie/","https://hartvaat.nl/kennis/hypertensie/eindorgaanschade-hypertensie/"],"congress":"","summary_en":"A review of the bi-directional relationship between obesity and aldosterone. Obesity correlates with higher circulating aldosterone and urinary excretion in normo- and hypertensive individuals without primary aldosteronism. Mineralocorticoid receptor activation in adipocytes can expand visceral fat, while adipocytes stimulate adrenal aldosterone production via leptin, CTRP-1 and resistin. Patients with idiopathic hyperaldosteronism are more obese than those with aldosterone-producing adenomas; aldosterone falls after weight loss. Mendelian randomisation partly supports causality. Clinical implication: weight loss should be a priority in PA patients.","created":"2026-07-03T10:32:51Z","updated":"2026-07-03T13:31:46Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Review over de bidirectionele relatie tussen obesitas en aldosteron. Obesitas correleert met hogere circulerende aldosteronspiegels en urine-uitscheiding bij normo- en hypertensieven zonder primair aldosteronisme. Mineralocorticoïdreceptoractivatie in adipocyten kan visceraal vetweefsel doen toenemen, terwijl adipocyten via leptine, CTRP-1 en resistine de bijnier stimuleren. Patiënten met idiopathisch hyperaldosteronisme zijn obeser dan die met aldosteron-producerend adenoom; aldosteronspiegels dalen na gewichtsverlies. Mendeliaanse randomisatie ondersteunt deels causaliteit. Klinische implicatie: gewichtsverlies bij patiënten met PA verdient prioriteit.","abstract_original":"Hypertension, Volume 83, Issue 6, Page e26227, June 1, 2026. 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, C1q/TNF-related proteins 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-sample Mendelian randomization analysis suggested that peri-renal adipose tissue, a form of visceral adipose tissue encompassing the adrenal glands, was causally linked to idiopathic hyperaldosteronism but not to other forms of hypertension. These observations support the speculation that at least a portion of idiopathic hyperaldosteronism cases represent adipocyte-driven hyperaldosteronism that might be effectively treated by weight loss. This review will provide the trans-disciplinary rationale for the hypothesis supporting a causal relationship between obesity and idiopathic hyperaldosteronism. This unproven hypothesis is eminently testable given the powerful pharmacological and surgical weight loss strategies currently available."}