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Kidney Week

Abstract: FR-PO0898

A Deceptive Duo: Alcohol and Cannabis Mimicking Apparent Mineralocorticoid Excess

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Goycochea, Carlos J., Methodist Dallas Medical Center, Dallas, Texas, United States
  • Rodriguez Rivera, Carolina Isabel, Methodist Dallas Medical Center, Dallas, Texas, United States
  • Gandhi, Nisarg, Methodist Dallas Medical Center, Dallas, Texas, United States
  • Sebastian, Lisa M., Methodist Dallas Medical Center, Dallas, Texas, United States
Introduction

Apparent mineralocorticoid excess (AME) is a rare disorder of impaired 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2)activity, causing inappropriately activated mineralocorticoid receptors (MCR) leading to hypertension, low renin, low aldosterone and hypokalemic alkalosis. We present a case of substance use-associated hypokalemic metabolic alkalosis mimicking AME.

Case Description

A 46 year-old black woman was consulted to the nephrology service due to severe hypokalemia, hypomagnesemia, metabolic alkalosis and hypertension. Her history includes hypertension, hyperlipidemia, and mild hypokalemia but was not compliant with medications. The patient presented to the ED at the request of her PCP due to abnormal lab findings. Our patient was asymptomatic. Further questioning revealed alcohol use disorder and daily use of cannabis multiple times a day. Due to concerns for hyperaldosteronism work up demonstrated a serum aldosterone < 0.3, serum renin was <0.1, unable to calculate PRA ratio due to undetectable levels of both. Urine potassium-to-creatinine ratio was 8.57 mmol K/gram cr (reference: <22 mmol L/gram cr indicates extrarenal losses). Fractional excretion of potassium 1.6 (reference FKE < 9 suggests extrarenal origin). Improvement was achieved after electrolyte replacement and abstinence of marijuana and alcohol.

Discussion

This case presents a unique complex diagnostic challenge; the simultaneous use of alcohol and suggested licorice-infused cannabis creates a perfect biochemical storm that mimicked AME in its entirety. When 11β-HSD2 is inhibited, cortisol circulating higher than aldosterone aberrantly activates the MCR. Alcohol compounds this by driving hypercortisolemia directly suppressing 11β-HSD2. Licorice, a recognized cannabis flavoring agent, further inhibits 11β-HSD2 through glycyrrhizin. This case highlights that in any patient with low renin, low aldosterone hypertension and refractory hypokalemia, acquired AME must be considered and a thorough substance and dietary history is as diagnostically essential as genetic testing.