Cerebral Salt-Wasting Syndrome Medication

  • Author: Sudha Garimella-Krovi, MBBS; Chief Editor: Stephen Kemp, MD, PhD   more...
 
Updated: Mar 29, 2012
 

Medication Summary

IV hypertonic saline solutions are employed to correct intravascular volume depletion and hyponatremia and to replace ongoing urinary sodium loss.[9]

As previously mentioned, some clinicians have reported a favorable response to mineralocorticoid therapy in cerebral salt-wasting syndrome (renal salt wasting). Mineralocorticoids, such as fludrocortisone, promote increased sodium reabsorption, as well as potassium loss, from the renal distal tubules.

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Mineralocorticoids

Class Summary

Mineralocorticoids enhance sodium reabsorption in the kidney by direct action on distal tubule cells, resulting in expanded extracellular fluid volume. They increase renal excretion of potassium and hydrogen ion.

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Fludrocortisone

 

Fludrocortisone promotes the increased reabsorption of sodium and the loss of potassium by the renal distal tubules.

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Contributor Information and Disclosures
Author

Sudha Garimella-Krovi, MBBS  Clinical Assistant Professor of Pediatrics, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences

Sudha Garimella-Krovi, MBBS is a member of the following medical societies: American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Coauthor(s)

James E Springate, MD  Associate Professor of Pediatrics, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Attending Physician, Department of Pediatrics, Division of Pediatric Nephrology, Women and Children's Hospital of Buffalo

James E Springate, MD is a member of the following medical societies: American Academy of Pediatrics, American Physiological Society, American Society of Pediatric Nephrology, International Pediatric Transplant Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Erawati V Bawle, MD, FAAP, FACMG Division of Genetic and Metabolic Disorders, Children's Hospital of Michigan; Professor (Clinician-Educator), Department of Pediatrics, Wayne State University School of Medicine

Erawati V Bawle, MD, FAAP, FACMG is a member of the following medical societies: American Academy of Pediatrics, American College of Medical Genetics, American Medical Association, and American Society of Human Genetics

Disclosure: Nothing to disclose.

Barry B Bercu, MD Professor, Departments of Pediatrics, Molecular Pharmacology and Physiology, University of South Florida College of Medicine, All Children's Hospital

Barry B Bercu, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Federation for Clinical Research, American Medical Association, American Pediatric Society, Association of Clinical Scientists, Endocrine Society, Florida Medical Association, Lawson-Wilkins Pediatric Endocrine Society, Pituitary Society, Society for Pediatric Research, Society for the Study of Reproduction, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

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.

References

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Possible mechanisms for cerebral salt-wasting syndrome. The injured brain may release natriuretic proteins that act directly on the kidney. In addition, cerebral injury may increase sympathetic nervous system activity, elevating renal perfusion pressure and releasing dopamine.
 
 
 
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