Newly Published
Review Article  |   June 2020
Mineralocorticoid Dysfunction during Critical Illness: A Review of the Evidence
Author Notes
  • From the School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa (G.D.N., C.F.); the Department of Anaesthesia and Perioperative Medicine, Royal Brisbane and Women’s Hospital, Queensland, Australia (G.D.N.); the Faculty of Medicine, University of Queensland, Brisbane, Queensland, Australia (G.D.N., J.C., J.L.); The George Institute, Sydney, New South Wales, Australia (J.C.); The Wesley Hospital, Brisbane, Queensland, Australia (J.C.); Intensive Care Services, Royal Brisbane and Women’s Hospital, Herston, Brisbane, Queensland, Australia (J.C., J.L.); Nimes University Hospital, University of Montpellier, Nimes, France (J.L.); and the Institute for Cellular and Molecular Medicine, Department of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria, South Africa (R.A.).
  • Submitted for publication August 16, 2019. Accepted for publication April 17, 2020.
    Submitted for publication August 16, 2019. Accepted for publication April 17, 2020.×
  • Correspondence: Address correspondence to Dr. Nethathe: Level 4, Ned Hanlon Building, Royal Brisbane and Women’s Hospital, Butterfield Street, Herston, Brisbane, 4029 Queensland, Australia. gladness.nethathe@wits.ac.za. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Review Article / Critical Care / Endocrine and Metabolic Systems / Renal and Urinary Systems / Electrolyte Balance
Review Article   |   June 2020
Mineralocorticoid Dysfunction during Critical Illness: A Review of the Evidence
Anesthesiology Newly Published on June 3, 2020. doi:https://doi.org/10.1097/ALN.0000000000003365
Anesthesiology Newly Published on June 3, 2020. doi:https://doi.org/10.1097/ALN.0000000000003365
Abstract

The recent demonstration of the significant reduction in mortality in patients with septic shock treated with adjunctive glucocorticoids combined with fludrocortisone and the effectiveness of angiotensin II in treating vasodilatory shock have renewed interest in the role of the mineralocorticoid axis in critical illness. Glucocorticoids have variable interactions at the mineralocorticoid receptor. Similarly, mineralocorticoid receptor–aldosterone interactions differ from mineralocorticoid receptor–glucocorticoid interactions and predicate receptor–ligand interactions that differ with respect to cellular effects. Hyperreninemic hypoaldosteronism or selective hypoaldosteronism, an impaired adrenal response to increasing renin levels, occurs in a subgroup of hemodynamically unstable critically ill patients. The suggestion is that there is a defect at the level of the adrenal zona glomerulosa associated with a high mortality rate that may represent an adaptive response aimed at increasing cortisol levels. Furthermore, cross-talk exists between angiotensin II and aldosterone, which needs to be considered when employing therapeutic strategies.