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Volume 29, Issue 3, Pages 196-215 (May 2009)


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The Brain in Hyponatremia: Both Culprit and Victim

David B. Mount, MDCorresponding Author Informationemail addressemail address

Summary 

Abnormalities in thirst and vasopressin (AVP) release play key roles in the genesis of hyponatremia; both processes are under the control of osmoreceptive neurons in the central nervous system (CNS). The acute development of hyponatremia in turn leads to profound cerebral edema, whereas treatment of chronic hyponatremia can be associated with osmotic demyelination syndrome (ODS). The brain is thus both “culprit” and “victim” in hyponatremia. This review summarizes recent advances in the understanding of osmoreception in the brain, the CNS response to acute and chronic hyponatremia, and the pathophysiology of ODS.

Renal Division, Brigham and Women's Hospital, Boston, MA; Renal Division, VA Boston Healthcare System, Harvard Medical School, Boston, MA

Corresponding Author InformationAddress reprint requests to David B. Mount, MD, Renal Division, Brigham and Women's Hospital, Room 540, 4 Blackfan Circle, Boston, MA 02115

 Supported by National Institutes of Health grants (DK57708 and DK070756), the American Heart Association, and the Veterans Administration.

PII: S0270-9295(09)00058-8

doi:10.1016/j.semnephrol.2009.03.021


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