title: Pseudoaldosteronism with increased serum cortisol associated with pneumonia, hypouricemia, hypocalcemia, and hypophosphatemia.
abstract: We describe here the interesting case of a 73-year-old hypertensive man with pseudoaldosteronism. He had been taking glycyrrhizin at a dose of 75 mg/day for 12 years because of mild liver damage, but had never experienced any previous symptoms associated with hypokalemia. He was referred to our hospital because of hypokalemic tetraparesis and rhabdomyolysis. At that time, we noted mineralocorticoid excess characterized by hypokalemia due to urinary K loss, exacerbation of hypertension due to increased tubular Na reabsorption, metabolic alkalosis, and suppression of both plasma renin activity and plasma aldosterone concentration. His urinary free cortisol excretion rate and the urinary ratio of free cortisol to free cortisone were markedly elevated. Thus we diagnosed pseudoaldosteronism that was related to the long-term use of glycyrrhizin. When he developed pseudoaldosteronism, he also contracted pneumonia, and exhibited elevated levels of serum cortisol and creatinine clearance (CCr) as well as hypouricemia, hypocalcemia, and hypophosphatemia. All normalized after the recovery from pneumonia and the administration of spironolactone. The extracellular volume expansion associated with increased tubular Na reabsorption by the aldosterone-sensitive distal nephron and the resulting increase in CCr caused an inhibition of proximal tubular reabsorption of uric acid, Ca, and inorganic phosphate, leading to their renal loss and therefore hypouricemia, hypocalcemia, and hypophosphatemia, respectively. In this patient, the increased circulating cortisol associated with the stress of inflammation caused by pneumonia triggered the development of pseudoaldosteronism.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Onishi
authors.forename: S
authors.initials: S
authors.lastname: Muto
authors.forename: S
authors.initials: S
authors.lastname: Homma
authors.forename: T
authors.initials: T
authors.lastname: Inaba
authors.forename: R
authors.initials: R
authors.lastname: Shuto
authors.forename: E
authors.initials: E
authors.lastname: Kusano
authors.forename: Y
authors.initials: Y
authors.lastname: Asano
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000652:urine; D019695:Glycyrrhizic Acid / Q000009:adverse effects*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood* / Q000652:urine; D006996:Hypocalcemia / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D017674:Hypophosphatemia / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D056929:Liddle Syndrome / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D008297:Male; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D011014:Pneumonia / Q000150:complications*; D015499:Renal Tubular Transport, Inborn Errors / Q000097:blood / Q000188:drug therapy / Q000209:etiology; D012307:Risk Factors; D013148:Spironolactone / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome; D015854:Up-Regulation; D014545:Urinary Calculi / Q000097:blood / Q000188:drug therapy / Q000209:etiology
chemical_list: D015415:Biomarkers; D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone; D019695:Glycyrrhizic Acid; D006854:Hydrocortisone