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Medication

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)

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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)

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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.

Class Summary

These agents may enhance sodium excretion.

Desmopressin (DDAVP)

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

Questions

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Media Gallery

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.

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Author

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, 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

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Society of Nephrology<br/>Received income in an amount equal to or greater than $250 from: Healthcare Quality Strategies, Inc.

Chief Editor

Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Interim Chair, Deming Department of Medicine, Tulane University School of Medicine

Vecihi Batuman, MD, 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, Southern Society for Clinical Investigation

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.

Acknowledgements

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

Disclosure: Nothing to disclose.

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

Hypernatremia Medication

Medication Summary

Diuretics

Class Summary

Hydrochlorothiazide (Esidrix, HydroDiuril, Microzide)

Hydrochlorothiazide (Esidrix, HydroDiuril, Microzide)

Furosemide (Lasix)

Furosemide (Lasix)

Vasopressin analogs

Class Summary

Desmopressin (DDAVP)

Desmopressin (DDAVP)

Hypernatremia Medication

Medication Summary

Diuretics

Class Summary

Hydrochlorothiazide (Esidrix, HydroDiuril, Microzide)

Hydrochlorothiazide (Esidrix, HydroDiuril, Microzide)

Furosemide (Lasix)

Furosemide (Lasix)

Vasopressin analogs

Class Summary

Desmopressin (DDAVP)

Desmopressin (DDAVP)

References

Tables

Contributor Information and Disclosures

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