{"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&hellip;<\/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"],"_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}]}}