{"id":4422403,"date":"2025-01-11T16:39:05","date_gmt":"2025-01-11T22:39:05","guid":{"rendered":"https:\/\/myendoconsult.com\/learn\/topics\/aldosteronism\/"},"modified":"2025-01-12T17:54:46","modified_gmt":"2025-01-12T23:54:46","slug":"aldosteronism","status":"publish","type":"oen_topic","link":"https:\/\/myendoconsult.com\/learn\/topics\/aldosteronism\/","title":{"rendered":"Aldosteronism"},"content":{"rendered":"\n<h2 class=\"wp-block-heading\">PRIMARY ALDOSTERONISM (PA)<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Definition and Subtypes<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Primary Aldosteronism (PA)<\/strong>: Characterized by <strong>hypertension, suppressed renin, and increased aldosterone secretion<\/strong> (Conn, 1955).<\/li>\n\n\n\n<li><strong>Main Subtypes<\/strong>:\n<ol class=\"wp-block-list\">\n<li><strong>Bilateral Idiopathic <a href=\"https:\/\/myendoconsult.com\/learn\/hyperaldosteronism\/\" data-wpil-monitor-id=\"180\">Hyperaldosteronism<\/a> (IHA)<\/strong>: Most common.<\/li>\n\n\n\n<li><strong>Aldosterone-Producing Adenoma (APA)<\/strong>: Also common.<\/li>\n\n\n\n<li><strong>Unilateral <a href=\"https:\/\/myendoconsult.com\/learn\/non-classical-adrenal-hyperplasia\/\" data-wpil-monitor-id=\"181\">Adrenal Hyperplasia<\/a> (UAH)<\/strong>: Rare, unilateral zona glomerulosa hyperplasia.<\/li>\n\n\n\n<li><strong>Familial Hyperaldosteronism (FH)<\/strong>:\n<ul class=\"wp-block-list\">\n<li><strong>Type I (Glucocorticoid-Remediable Aldosteronism, GRA)<\/strong>: Autosomal dominant, suppressed by exogenous glucocorticoids.<\/li>\n\n\n\n<li><strong>Type II<\/strong>: Familial occurrence of APA and\/or IHA.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Ectopic Aldosterone Secretion<\/strong> (very rare, e.g., ovarian tumor).<\/li>\n<\/ol>\n<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Clinical Presentation<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Prevalence<\/strong>: ~5% of all hypertension cases (most common identifiable secondary HTN).<\/li>\n\n\n\n<li><strong>Many Patients<\/strong>: Normal serum potassium (no hypokalemia).<\/li>\n\n\n\n<li><strong>Hypokalemia (if present)<\/strong>: May cause alkalosis, nocturia, polyuria, muscle cramps, palpitations, <a href=\"https:\/\/myendoconsult.com\/learn\/positive-chvostek-sign\/\" data-wpil-monitor-id=\"184\">positive Chvostek\/Trousseau signs<\/a>.<\/li>\n\n\n\n<li><strong>Suspect PA<\/strong>:\n<ul class=\"wp-block-list\">\n<li>Hypertension + Hypokalemia.<\/li>\n\n\n\n<li>Resistant (treatment-refractory) hypertension.<\/li>\n\n\n\n<li>Hypertension + Adrenal incidentaloma.<\/li>\n\n\n\n<li>Onset of hypertension &lt;20 years old.<\/li>\n\n\n\n<li>Severe hypertension.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Case-Finding and Confirmation<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Screening Test<\/strong>: Morning (8\u201310 am) ratio of <strong>Plasma Aldosterone Concentration (PAC)<\/strong> to <strong>Plasma Renin Activity (PRA)<\/strong>.\n<ul class=\"wp-block-list\">\n<li>Avoid MR antagonists or high-dose amiloride.<\/li>\n\n\n\n<li>Correct hypokalemia first to avoid false negatives.<\/li>\n\n\n\n<li>PAC:PRA ratio has ~75% sensitivity\/specificity.<\/li>\n\n\n\n<li>Elevated ratio \u2192 proceed to <strong>confirmatory<\/strong> aldosterone-suppression testing (oral sodium loading, saline infusion, captopril test, or fludrocortisone test).<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Subtyping<\/strong>\n<ul class=\"wp-block-list\">\n<li><strong>Imaging<\/strong> (CT) of adrenals is done, but non-diagnostic in many cases.<\/li>\n\n\n\n<li><strong><a data-wpil-monitor-id=\"182\" href=\"https:\/\/myendoconsult.com\/learn\/adrenal-vein-sampling-interpretation\/\">Adrenal Venous Sampling<\/a> (AVS)<\/strong> is usually necessary if a surgical cure is desired.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<h3 class=\"wp-block-heading\">Treatment Options<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Unilateral Aldosterone Excess<\/strong> (APA or UAH): <strong>Unilateral laparoscopic adrenalectomy<\/strong> \u2192 corrects hypokalemia, improves HTN (30\u201360% cured).<\/li>\n\n\n\n<li><strong>Bilateral Idiopathic Hyperaldosteronism (IHA)<\/strong> or <strong>Familial Hyperaldosteronism Type I (GRA)<\/strong>:\n<ul class=\"wp-block-list\">\n<li><strong>Medical therapy<\/strong> with <strong>Mineralocorticoid Receptor (MR) antagonist<\/strong> (e.g., spironolactone, eplerenone).<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Goal<\/strong>: Not only lower BP but also <strong>block\/minimize<\/strong> aldosterone\u2019s harmful cardiovascular effects.<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">THE BIOLOGIC ACTIONS OF ALDOSTERONE<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Regulation of Aldosterone Secretion<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Stimulators<\/strong>:\n<ul class=\"wp-block-list\">\n<li><strong>Angiotensin II<\/strong> (RAAS)<\/li>\n\n\n\n<li><strong>Hyperkalemia<\/strong><\/li>\n\n\n\n<li><strong>ACTH<\/strong> (minor)<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Inhibitors<\/strong>:\n<ul class=\"wp-block-list\">\n<li><strong>Atrial Natriuretic Factor<\/strong> (ANF)<\/li>\n\n\n\n<li><strong>Hypokalemia<\/strong><\/li>\n<\/ul>\n<\/li>\n\n\n\n<li>About 50\u201370% of aldosterone is bound (to albumin, CBG); 30\u201350% free.<\/li>\n\n\n\n<li>Half-life: ~15\u201320 min. Normal blood aldosterone: 0\u201321 ng\/dL.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Classic Roles<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Regulation of ECF Volume<\/strong> &amp; <strong>Potassium Homeostasis<\/strong>.<\/li>\n\n\n\n<li>Binds <strong>mineralocorticoid receptor (MR)<\/strong> in distal <a href=\"https:\/\/myendoconsult.com\/learn\/nephron\/\" data-wpil-monitor-id=\"185\">nephron<\/a> \u2192 promotes Na\u207a reabsorption in exchange for K\u207a\/H\u207a excretion.<\/li>\n\n\n\n<li><strong>Angiotensin II<\/strong> \u2192 negative <a href=\"https:\/\/myendoconsult.com\/learn\/endocrine-feedback-loops\/\" data-wpil-monitor-id=\"186\">feedback loop<\/a> with ECF volume.<\/li>\n\n\n\n<li><strong>MR Tissue Distribution<\/strong>: Highest in kidney (distal tubule), colon, hippocampus. Lower in heart, GI tract, etc.<\/li>\n\n\n\n<li><strong>Mechanism<\/strong>: Increases expression of aldosterone-regulated kinase \u2192 modifies apical Na\u207a channels \u2192 \u2191Na\u207a reabsorption \u2192 negative luminal charge \u2192 \u2191K\u207a &amp; H\u207a excretion.<\/li>\n<\/ul>\n\n\n\n<figure class=\"wp-block-image size-full\"><img loading=\"lazy\" decoding=\"async\" width=\"2400\" height=\"1941\" src=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-INTRACELLULAR-PROCESSES.png\" alt=\"\" class=\"wp-image-4422808\" srcset=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-INTRACELLULAR-PROCESSES.png 2400w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-INTRACELLULAR-PROCESSES-300x243.png 300w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-INTRACELLULAR-PROCESSES-768x621.png 768w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-INTRACELLULAR-PROCESSES-1536x1242.png 1536w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-INTRACELLULAR-PROCESSES-2048x1656.png 2048w\" sizes=\"auto, (max-width: 2400px) 100vw, 2400px\" \/><figcaption class=\"wp-element-caption\">Intracellular processes (mechanism of action of aldosterone)<\/figcaption><\/figure>\n\n\n\n<h3 class=\"wp-block-heading\">Mineralocorticoid Escape<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>After 3\u20135 days of high mineralocorticoid exposure, <strong>escape<\/strong> phenomenon occurs: various counterregulatory mechanisms (renal hemodynamics, ANP, etc.) limit continued volume expansion.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Nonclassic Effects<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Nongenomic Actions<\/strong>: Rapid cell surface receptor (likely G protein\u2013coupled) modifies sodium-hydrogen exchange.<\/li>\n\n\n\n<li><strong>Tissue Fibrosis and Injury<\/strong>: Aldosterone can induce collagen gene expression, TGF-\u03b2, PAI-1 \u2192 possible microangiopathy, fibrosis in heart, vessels, kidney. Imbalance between volume state &amp; aldosterone is key.<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">ADRENAL VENOUS SAMPLING (AVS) FOR PRIMARY ALDOSTERONISM<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Rationale<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Distinguish<\/strong> unilateral aldosterone-producing adenoma (APA) vs. bilateral hyperaldosteronism (IHA).<\/li>\n\n\n\n<li><strong>Imaging<\/strong> (CT) is only ~50% accurate. AVS is gold standard for subtyping if surgical cure is pursued.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Protocol<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Patient Preparation<\/strong>\n<ul class=\"wp-block-list\">\n<li>Control BP but hold MR antagonists (spironolactone) a few weeks prior.<\/li>\n\n\n\n<li>Some centers use continuous cosyntropin (ACTH) infusion to stabilize aldosterone secretion.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Procedure<\/strong>\n<ul class=\"wp-block-list\">\n<li>Femoral vein approach \u2192 selective catheterization of <strong>both <a href=\"https:\/\/myendoconsult.com\/learn\/localization-of-source-of-hyperaldosteronism-adrenal-vein-sampling\/\" data-wpil-monitor-id=\"183\">adrenal<\/a> veins<\/strong> + a reference vein (IVC or external iliac).<\/li>\n\n\n\n<li>Radiographic contrast to confirm correct catheter tip position.<\/li>\n\n\n\n<li>Blood sampling for aldosterone &amp; cortisol from each adrenal vein + reference site.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Interpretation<\/strong>\n<ul class=\"wp-block-list\">\n<li>Cortisol levels confirm correct catheterization.<\/li>\n\n\n\n<li>Compare aldosterone\/cortisol ratios from each side to reference.<\/li>\n\n\n\n<li><strong>Unilateral<\/strong> disease: Markedly elevated ratio on one side, suppressed on contralateral.<\/li>\n\n\n\n<li><strong>Bilateral<\/strong> disease: Similar ratios both sides.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<h3 class=\"wp-block-heading\">Complications<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>~2.5% rate in experienced centers: groin hematoma, adrenal hemorrhage, vein dissection.<\/li>\n<\/ul>\n\n\n\n<figure class=\"wp-block-image size-full\"><img loading=\"lazy\" decoding=\"async\" width=\"1433\" height=\"902\" src=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/AVS-interpretation-simplified-min-1.jpg\" alt=\"AVS interpretation simplified\" class=\"wp-image-661752\" srcset=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/AVS-interpretation-simplified-min-1.jpg 1433w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/AVS-interpretation-simplified-min-1-300x189.jpg 300w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/AVS-interpretation-simplified-min-1-768x483.jpg 768w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/AVS-interpretation-simplified-min-1-624x393.jpg 624w\" sizes=\"auto, (max-width: 1433px) 100vw, 1433px\" \/><figcaption class=\"wp-element-caption\">Interpretation of AVS<\/figcaption><\/figure>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">RENIN\u2013ANGIOTENSIN\u2013ALDOSTERONE SYSTEM (RAAS) AND RENOVASCULAR HYPERTENSION<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">RAAS Basics<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Renin<\/strong>:\n<ul class=\"wp-block-list\">\n<li>Produced by juxtaglomerular cells in kidney.<\/li>\n\n\n\n<li>Rate-limiting step converting angiotensinogen \u2192 angiotensin I.<\/li>\n\n\n\n<li>Stimulated by low renal perfusion, low tubule NaCl (macula densa), sympathetic tone.<\/li>\n\n\n\n<li>Suppressed by high BP, high sodium, etc.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Angiotensin I \u2192 II<\/strong>\n<ul class=\"wp-block-list\">\n<li>Via <strong>angiotensin-converting enzyme (ACE)<\/strong>.<\/li>\n\n\n\n<li>Angiotensin II \u2192 vasoconstriction, aldosterone secretion, increased sympathetic outflow, vasopressin release, etc.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Aldosterone<\/strong>\n<ul class=\"wp-block-list\">\n<li>Final effector in Na\u207a reabsorption, K\u207a excretion.<\/li>\n\n\n\n<li>ECF volume &amp; BP regulation.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n\n\n\n<figure class=\"wp-block-image size-full\"><img loading=\"lazy\" decoding=\"async\" width=\"3000\" height=\"2100\" src=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-Pathway.png\" alt=\"\" class=\"wp-image-4422803\" srcset=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-Pathway.png 3000w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-Pathway-300x210.png 300w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-Pathway-768x538.png 768w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-Pathway-1536x1075.png 1536w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/RAAS-Pathway-2048x1434.png 2048w\" sizes=\"auto, (max-width: 3000px) 100vw, 3000px\" \/><figcaption class=\"wp-element-caption\">RAAS Pathway<\/figcaption><\/figure>\n\n\n\n<h3 class=\"wp-block-heading\">Renovascular Hypertension<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Cause<\/strong>: Renal artery stenosis (atherosclerosis or fibromuscular dysplasia) \u2192 decreased perfusion \u2192 \u2191renin \u2192 \u2191angiotensin II \u2192 \u2191aldosterone \u2192 HTN.<\/li>\n\n\n\n<li><strong>Suspicion<\/strong>:\n<ul class=\"wp-block-list\">\n<li>Onset &lt;30 years or &gt;55 years with no risk factors\/family history.<\/li>\n\n\n\n<li>Sudden severe or treatment-resistant HTN.<\/li>\n\n\n\n<li>Unexplained atrophic kidney, rise in creatinine after ACE inhibitor, etc.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Diagnosis<\/strong>:\n<ul class=\"wp-block-list\">\n<li>Gold standard: <strong>Renal arteriography<\/strong>.<\/li>\n\n\n\n<li>Less invasive: <strong>MR angiography<\/strong>, <strong>CT angiography<\/strong>, <strong>Duplex Doppler US<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"<p>PRIMARY ALDOSTERONISM (PA) Definition and Subtypes Clinical Presentation Case-Finding and Confirmation Treatment Options THE BIOLOGIC ACTIONS OF ALDOSTERONE Regulation of Aldosterone Secretion Classic Roles Mineralocorticoid Escape Nonclassic Effects ADRENAL VENOUS SAMPLING (AVS) FOR PRIMARY ALDOSTERONISM Rationale Protocol Complications RENIN\u2013ANGIOTENSIN\u2013ALDOSTERONE SYSTEM (RAAS) AND RENOVASCULAR HYPERTENSION RAAS Basics Renovascular Hypertension<\/p>\n","protected":false},"featured_media":0,"template":"","oen_topic_chapter":[684],"class_list":["post-4422403","oen_topic","type-oen_topic","status-publish","hentry","oen_topic_chapter-adrenal-gland","post-wrapper","thrv_wrapper"],"_links":{"self":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic\/4422403","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic"}],"about":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/types\/oen_topic"}],"version-history":[{"count":7,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic\/4422403\/revisions"}],"predecessor-version":[{"id":4422809,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic\/4422403\/revisions\/4422809"}],"wp:attachment":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/media?parent=4422403"}],"wp:term":[{"taxonomy":"oen_topic_chapter","embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/oen_topic_chapter?post=4422403"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}