title: Glycyrrhetinic acid food supplementation lowers serum potassium concentration in chronic hemodialysis patients.
abstract: Hyperkalemia is a common life-threatening problem in hemodialysis patients. Because glycyrrhetinic acid (GA) inhibits the enzyme 11beta-hydroxy-steroid dehydrogenase II and thereby increases cortisol availability to the colonic mineralocorticoid receptor, it has the potential to lower serum potassium concentrations. To test this, 10 patients in a 6 month prospective, double-blind, placebo-controlled crossover study were given cookies or bread rolls supplemented with glycyrrhetinic acid or placebo. Twenty-four-hour blood pressure measurements were performed at baseline and week 6 and 12 of each treatment period. The ratio of plasma cortisol/cortisone was significantly increased in all patients on GA as compared to baseline or placebo, indicating appropriate enzyme inhibition. Nine of the 10 patients had a persistent decrease in predialysis serum potassium concentration. On GA, mean predialysis serum potassium was significantly lower than at baseline or on placebo. On placebo, serum potassium was significantly elevated above the upper limit of normal in 76% compared to 30% of measurements during GA treatment. Furthermore, on this treatment the frequency of severe hyperkalemia significantly decreased from 9% to 0.6%. No differences were found in parameters reflecting sodium retention. Although these studies show that prolonged GA supplementation persistently lowers serum potassium in dialysis patients, a long-term toxicity study will be mandatory before we recommend the routine use of this treatment.
authors.affiliation: Department of Nephrology and Hypertension, Inselspital, University of Berne, Switzerland.
authors.forename: Stefan
authors.initials: S
authors.lastname: Farese
authors.forename: Anja
authors.initials: A
authors.lastname: Kruse
authors.forename: Andreas
authors.initials: A
authors.lastname: Pasch
authors.forename: Bernhard
authors.initials: B
authors.lastname: Dick
authors.forename: Brigitte M
authors.initials: BM
authors.lastname: Frey
authors.forename: Dominik E
authors.initials: DE
authors.lastname: Uehlinger
authors.forename: Felix J
authors.initials: FJ
authors.lastname: Frey
mesh_terms: D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000368:Aged; D000369:Aged, 80 and over; D000450:Aldosterone / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D003348:Cortisone / Q000097:blood; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004791:Enzyme Inhibitors / Q000008:administration & dosage* / Q000009:adverse effects; D005260:Female; D005527:Food, Fortified; D006034:Glycyrrhetinic Acid / Q000008:administration & dosage* / Q000009:adverse effects; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006947:Hyperkalemia / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D007676:Kidney Failure, Chronic / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood* / Q000652:urine; D011446:Prospective Studies; D006435:Renal Dialysis / Q000009:adverse effects*; D012083:Renin / Q000097:blood; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D004791:Enzyme Inhibitors; D000450:Aldosterone; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2; C468387:HSD11B2 protein, human; D012083:Renin; D006034:Glycyrrhetinic Acid; D011188:Potassium; D003348:Cortisone; D006854:Hydrocortisone