Posaconazole-Induced Apparent Mineralocorticoid Excess| High Yield Nephrology Board Review.

💥 Hypertension + hypokalemic metabolic alkalosis + suppressed renin AND aldosterone? Think apparent mineralocorticoid excess (AME)—and don't forget POSACONAZOLE! 🧠 HIGH-YIELD BOARD REVIEW ⚡ MECHANISM: Posaconazole inhibits 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), reducing conversion of active cortisol to cortisone in mineralocorticoid-sensitive tissues. 🔥 WHY IT MATTERS: Cortisol can activate mineralocorticoid receptors → increased ENaC-mediated sodium reabsorption and increased potassium and hydrogen ion secretion in the collecting duct. 🎯 CLINICAL PRESENTATION: New or worsening hypertension, hypokalemia, metabolic alkalosis, and suppressed renin and aldosterone. 🔬 DIAGNOSIS: Review medication exposure, check blood pressure and electrolytes, and measure renin and aldosterone. Consider other causes of low-renin, low-aldosterone hypertension, including licorice exposure, inherited AME, Liddle syndrome, and other drug effects. 💊 MANAGEMENT: Coordinate with the prescribing clinician to reduce the dose, discontinue, or switch posaconazole when clinically appropriate. Correct potassium and manage blood pressure; mineralocorticoid receptor blockade or ENaC blockade may be considered with close monitoring. ⚠️ IMPORTANT DISTINCTION: Posaconazole can also inhibit adrenal steroid synthesis, including 11β-hydroxylase, and may cause a related mineralocorticoid phenotype. Its effects are not always explained by 11β-HSD2 inhibition alone. 🏆 BOARD EXAM PEARL: Posaconazole + hypertension + hypokalemia + metabolic alkalosis + low renin/low aldosterone = suspect drug-induced pseudohyperaldosteronism / AME-like state. 🔥 Know the mechanism, recognize the biochemical pattern, and identify the medication trigger! #Posaconazole #AME #Pseudohyperaldosteronism #Hypokalemia #Hypertension #Nephrology #Electrolytes #NephrologyBoardReview #MedicalEducation