Vigil D, Ganta K, Sun Y, Dorin RI, Tzamaloukas AH, Servilla KS. Prolonged hypernatremia triggered by hyperglycemic hyperosmolar state with coma: A case report. World J Nephrol 2015; 4(2): 319-323 [PMID: 25949947 DOI: 10.5527/wjn.v4.i2.319]
Corresponding Author of This Article
Karen S Servilla, MD, Professor of Medicine, Nephrologist, Nephrology Section, Medicine Service, Raymond G Murphy Veterans Affairs Medical Center, 1501 San Pedro SE, Albuquerque, NM 87108, United States. karen.servilla@va.gov
Research Domain of This Article
Medicine, General & Internal
Article-Type of This Article
Case Report
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Nephrol. May 6, 2015; 4(2): 319-323 Published online May 6, 2015. doi: 10.5527/wjn.v4.i2.319
Prolonged hypernatremia triggered by hyperglycemic hyperosmolar state with coma: A case report
Darlene Vigil, Kavitha Ganta, Yijuan Sun, Richard I Dorin, Antonios H Tzamaloukas, Karen S Servilla
Darlene Vigil, Yijuan Sun, Antonios H Tzamaloukas, Karen S Servilla, Nephrology Section, Medicine Service, Raymond G Murphy Veterans Affairs Medical Center, Albuquerque, NM 87108, United States
Kavitha Ganta, Yijuan Sun, Richard I Dorin, Antonios H Tzamaloukas, Karen S Servilla, Nephrology Division, Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131, United States
Richard I Dorin, Endocrinology Section, Medicine Service, Raymond G Murphy Veterans Affairs Medical Center, Albuquerque, NM 87108, United States
Author contributions: Vigil D and Ganta K contributed equally to this work; Vigil D and Ganta K were responsible for parts of the bibliographic search and of the first draft of the report; Sun Y and Dorin RI made critical changes in the manuscript; Tzamaloukas AH assisted in the bibliographic search and wrote parts of the original report; Servilla KS conceived the work and made critical changes in the manuscript.
Ethics approval: NA.
Informed consent: Approval for this case report was obtained from the human research committee of the Raymond G Murphy VA Medical Center.
Conflict-of-interest: The authors have no conflicts of interest to declare.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Karen S Servilla, MD, Professor of Medicine, Nephrologist, Nephrology Section, Medicine Service, Raymond G Murphy Veterans Affairs Medical Center, 1501 San Pedro SE, Albuquerque, NM 87108, United States. karen.servilla@va.gov
Received: August 2, 2014 Peer-review started: August 2, 2014 First decision: October 14, 2014 Revised: January 7, 2015 Accepted: February 9, 2015 Article in press: February 11, 2015 Published online: May 6, 2015 Processing time: 279 Days and 10.3 Hours
Abstract
A man with past lithium use for more than 15 years, but off lithium for two years and not carrying the diagnosis of diabetes mellitus or nephrogenic diabetes insipidus (NDI), presented with coma and hyperglycemic hyperosmolar state (HHS). Following correction of HHS, he developed persistent hypernatremia accompanied by large volumes of urine with low osmolality and no response to desmopressin injections. Urine osmolality remained < 300 mOsm/kg after injection of vasopressin. Improvement in serum sodium concentration followed the intake of large volumes of water plus administration of amiloride and hydrochlorothiazide. Severe hyperglycemia may trigger symptomatic lithium-induced NDI years after cessation of lithium therapy. Patients with new-onset diabetes mellitus who had been on prolonged lithium therapy in the past require monitoring of their serum sodium concentration after hyperglycemic episodes regardless of whether they do or do not carry the diagnosis of NDI.
Core tip: Hyperglycemic coma with large losses of body water may aggravate lithium-induced nephrogenic diabetes insipidus (NDI) which had been asymptomatic and undiagnosed for years after cessation of lithium therapy. The development of conditions leading to loss of water and consciousness in patients who were on long term lithium therapy should trigger surveillance for NDI even when they were asymptomatic in the past.
