Hypernatremia Medication

  • Author: Ivo Lukitsch, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Apr 19, 2010
 

Medication Summary

Some patients with nephrogenic diabetes insipidus—particularly those in whom it is mild or incomplete—may benefit from diuretic therapy (ie, thiazides) 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.

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Diuretics

Class Summary

These drugs may be used to enhance sodium excretion.

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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.

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Vasopressin analogs

Class Summary

These agents may enhance sodium excretion.

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Desmopressin (DDAVP)

 

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

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Contributor Information and Disclosures
Author

Ivo Lukitsch, MD  Faculty, Department of Internal Medicine, Section of Nephrology, Tulane University School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

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

Disclosure: Nothing to disclose.

Specialty Editor Board

Anil Kumar Mandal, MD  Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School 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, and Central Society for Clinical Research

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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

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

Disclosure: Nothing to disclose.

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, 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, and International Society of Nephrology

Disclosure: Nothing to disclose.

References

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  2. Verbalis JG, Berl T. Disorders of water balance. In: Brenner BM, ed. Brenner and Rector's The Kidney. 8th ed. Philadelphia, Pa: Saunders Elsevier; 2008:Chapter 13.

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

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  16. 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. Dec 14 2009;[Medline].

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

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  19. 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. Nov 2008;23(11):3501-8. [Medline].

 
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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 hypernatremiaSymptoms related to the characteristics of hypernatremia
Cognitive dysfunction and symptoms associated with neuronal cell shrinkageLethargy, obtundation, confusion, abnormal speech, irritability, seizures, nystagmus, myoclonic jerks
Dehydration or clinical signs of volume depletionOrthostatic blood pressure changes, tachycardia, oliguria, dry oral mucosa, abnormal skin turgor, dry axillae,
Other clinical findingsWeight loss, generalized weakness
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