Medscape is available in 5 Language Editions – Choose your Edition here.


Hypernatremia Medication

  • Author: Ivo Lukitsch, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
Updated: Jul 14, 2016

Medication Summary

Some patients with nephrogenic diabetes insipidus—particularly those in whom it is mild or incomplete—may benefit from diuretic therapy (eg, thiazides, loop-diuretics) in an effort to increase proximal tubular reabsorption and decrease delivery to diluting segments where water may be lost. Inhibition of cyclooxygenase by nonsteroidal anti-inflammatory drugs (NSAIDs) may attenuate the polyuria in these patients. In addition, any medications that may cause nephrogenic diabetes insipidus (such as lithium) may require discontinuation.

In patients with central diabetes insipidus, desmopressin administered orally or intranasally may be used. Pharmacologic agents can be used in partial central diabetes insipidus to increase circulating AVP. These drugs include chlorpropamide, clofibrate, and carbamazepine.



Class Summary

These drugs may be used to enhance sodium excretion.

Hydrochlorothiazide (Esidrix, HydroDiuril, Microzide)


Inhibits the reabsorption of sodium in the distal tubules, causing increased excretion of sodium and water, as well as of potassium and hydrogen ions.

Furosemide (Lasix)


Loop diuretic that increases excretion of water by interfering with chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Increases renal blood flow without increasing filtration rate. Onset of action generally is within 1-h. Increases potassium, sodium, calcium, and magnesium excretion.


Vasopressin analogs

Class Summary

These agents may enhance sodium excretion.

Desmopressin (DDAVP)


Increases cellular permeability of collecting ducts, resulting in the reabsorption of water by the kidneys.

Contributor Information and Disclosures

Ivo Lukitsch, MD Consulting Staff/Faculty, Department of Nephrology, Ochsner Medical Center

Ivo Lukitsch, MD is a member of the following medical societies: American Society of Nephrology, American Society of Transplantation

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

Anil Kumar Mandal, MD Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida College of Medicine

Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, Central Society for Clinical and Translational Research

Disclosure: Nothing to disclose.


Trung Q Pham, MD Consulting Staff, Department of Internal Medicine, Kayenta Health Center

Disclosure: Nothing to disclose.

  1. Muhsin SA, Mount DB. Diagnosis and treatment of hypernatremia. Best Pract Res Clin Endocrinol Metab. 2016 Mar. 30 (2):189-203. [Medline].

  2. Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med. 2000 May 18. 342(20):1493-9. [Medline].

  3. Verbalis JG. Disorders of Water Balance. In:. Skorecki K, Chertow GM, Marsden PA, Yu ASL, Taal MW, eds. Brenner and Rector's The Kidney. 10th ed. Philadelphia, PA: Elsevier; 2016. 460-510.

  4. Chumlea WC, Guo SS, Zeller CM, et al. Total body water data for white adults 18 to 64 years of age: the Fels Longitudinal Study. Kidney Int. 1999 Jul. 56(1):244-52. [Medline].

  5. Bhave G, Neilson EG. Body fluid dynamics: back to the future. J Am Soc Nephrol. 2011 Dec. 22(12):2166-81. [Medline].

  6. Sterns HR. Renal function and disorders of water and sodium balance. ACP Medicine: A Publication of the American College of Physicians. New York, NY: WebMD; 2005. 10.1-10.19.

  7. Boone M, Deen PM. Physiology and pathophysiology of the vasopressin-regulated renal water reabsorption. Pflugers Arch. 2008 Sep. 456(6):1005-24. [Medline]. [Full Text].

  8. Loh JA, Verbalis JG. Disorders of water and salt metabolism associated with pituitary disease. Endocrinol Metab Clin North Am. 2008 Mar. 37(1):213-34, x. [Medline].

  9. Thornton SN. Thirst and hydration: Physiology and consequences of dysfunction. Physiol Behav. 2010. 100:15-20. [Medline].

  10. Kumar S, Berl T. Sodium. Lancet. 1998 Jul 18. 352(9123):220-8. [Medline].

  11. Darmon M, Timsit JF, Francais A, et al. Association between hypernatraemia acquired in the ICU and mortality: a cohort study. Nephrol Dial Transplant. 2010 Feb 17. [Medline].

  12. Lindner G, Funk GC, Schwarz C, et al. Hypernatremia in the critically ill is an independent risk factor for mortality. Am J Kidney Dis. Dec 2007. 50(6):952-7. [Medline].

  13. Stelfox HT, Ahmed SB, Khandwala F, et al. The epidemiology of intensive care unit acquired hyponatremia and hypernatremia in medical-surgical intensive care units. Crit Care. 2008 Dec 18. 12(6):R162. [Medline]. [Full Text].

  14. Funk GC, Lindner G, Druml W, et al. Incidence and prognosis of dysnatremias present on ICU admission. Intensive Care Med. 2010 Feb. 36(2):304-11. [Medline].

  15. Ates I, Özkayar N, Toprak G, Yılmaz N, Dede F. Factors associated with mortality in patients presenting to the emergency department with severe hypernatremia. Intern Emerg Med. 2016 Apr. 11 (3):451-9. [Medline].

  16. Kumar AB, Shi Y, Shotwell MS, Richards J, Ehrenfeld JM. Hypernatremia is a Significant Risk Factor for Acute Kidney Injury After Subarachnoid Hemorrhage: A Retrospective Analysis. Neurocrit Care. 2014 Sep 18. [Medline].

  17. VAN DE Louw A, Shaffer C, Schaefer E. Early intensive care unit-acquired hypernatremia in severe sepsis patients receiving 0.9% saline fluid resuscitation. Acta Anaesthesiol Scand. 2014 Sep. 58(8):1007-14. [Medline].

  18. Leung AA, McAlister FA, Finlayson SR, Bates DW. Preoperative hypernatremia predicts increased perioperative morbidity and mortality. Am J Med. 2013 Oct. 126(10):877-86. [Medline].

  19. Hawkins RC. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta. 2003 Nov. 337(1-2):169-72. [Medline].

  20. Lavagno C, Camozzi P, Renzi S, Lava SA, Simonetti GD, Bianchetti MG, et al. Breastfeeding-Associated Hypernatremia: A Systematic Review of the Literature. J Hum Lact. 2016 Feb. 32 (1):67-74. [Medline].

  21. Herrod PJ, Awad S, Redfern A, et al. Hypo- and hypernatraemia in surgical patients: is there room for improvement?. World J Surg. 2010 Mar. 34(3):495-9. [Medline].

  22. Chassagne P, Druesne L, Capet C, et al. Clinical presentation of hypernatremia in elderly patients: a case control study. J Am Geriatr Soc. Aug 2006. 54(8):1225-30. [Medline].

  23. Palevsky PM. Hypernatremia. Semin Nephrol. 1998 Jan. 18(1):20-30. [Medline].

  24. Hoefer D, Ruttmann-Ulmer E, Smits JM, et al. Donor hypo- and hypernatremia are predictors for increased 1-year mortality after cardiac transplantation. Transpl Int. 2009 Dec 14. [Medline].

  25. Hiyama TY, Matsuda S, Fujikawa A, et al. Autoimmunity to the sodium-level sensor in the brain causes essential hypernatremia. Neuron. 2010 May 27. 66(4):508-22. [Medline].

  26. Lin JJ, Lin KL, Hsia SH, et al. Combined central diabetes insipidus and cerebral salt wasting syndrome in children. Pediatr Neurol. 2009 Feb. 40(2):84-7. [Medline].

  27. Bockenhauer D, van't Hoff W, Dattani M, et al. Secondary nephrogenic diabetes insipidus as a complication of inherited renal diseases. Nephron Physiol. 2010. 116(4):p23-9. [Medline].

  28. Mavrakis AN, Tritos NA. Diabetes insipidus with deficient thirst: report of a patient and review of the literature. Am J Kidney Dis. 2008 May. 51(5):851-9. [Medline].

  29. Fried LF, Palevsky PM. Hyponatremia and hypernatremia. Med Clin North Am. 1997 May. 81(3):585-609. [Medline].

  30. Lindner G, Schwarz C, Kneidinger N, et al. Can we really predict the change in serum sodium levels? An analysis of currently proposed formulae in hypernatraemic patients. Nephrol Dial Transplant. 2008 Nov. 23(11):3501-8. [Medline].

  31. Lindner G, Funk GC. Hypernatremia in critically ill patients. J Crit Care. 2012 Jul 2. [Medline].

  32. Lindner G, Schwarz C, Funk GC. Osmotic diuresis due to urea as the cause of hypernatraemia in critically ill patients. Nephrol Dial Transplant. 2012 Mar. 27(3):962-7. [Medline].

Figure A: Normal cell. Figure B: Cell initially responds to extracellular hypertonicity through passive osmosis of water extracellularly, resulting in cell shrinkage. Figure C: Cell actively responds to extracellular hypertonicity and cell shrinkage in order to limit water loss through transport of organic osmolytes across the cell membrane, as well as through intracellular production of these osmolytes. Figure D: Rapid correction of extracellular hypertonicity results in passive movement of water molecules into the relatively hypertonic intracellular space, causing cellular swelling, damage, and ultimately death.
Table 1. Characteristics and symptoms of hypernatremia
Characteristics of hypernatremia Symptoms related to the characteristics of hypernatremia
Cognitive dysfunction and symptoms associated with neuronal cell shrinkage Lethargy, obtundation, confusion, abnormal speech, irritability, seizures, nystagmus, myoclonic jerks
Dehydration or clinical signs of volume depletion Orthostatic blood pressure changes, tachycardia, oliguria, dry oral mucosa, abnormal skin turgor, dry axillae,
Other clinical findings Weight loss, generalized weakness
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.