RT Book, Section
A1 Mount, David B.
A2 Jameson, J. Larry
A2 Fauci, Anthony S.
A2 Kasper, Dennis L.
A2 Hauser, Stephen L.
A2 Longo, Dan L.
A2 Loscalzo, Joseph
SR Print(0)
ID 1178487135
T1 Hyponatremia
T2 Harrison's Principles of Internal Medicine, 20e
YR 2018
FD 2018
PB McGraw-Hill Education
PP New York, NY
SN 9781259644016
LK accessmedicine.mhmedical.com/content.aspx?aid=1178487135
RD 2024/10/08
AB Disorders  of  serum  Na+  concentration  are  caused  by  abnormalities  in  water  homeostasis,  leading  to  changes  in  the  relative  ratio  of  Na+  to  body  water.  Water  intake  and  circulating  AVP  constitute  the  two  key  effectors  in  the  defense  of  serum  osmolality;  defects  in  one  or  both  of  these  two  defense  mechanisms  cause  most  cases  of  hyponatremia  and  hypernatremia.  In  contrast,  abnormalities  in  sodium  homeostasis  per  se  lead  to  a  deficit  or  surplus  of  whole-body  Na+-Cl–  content,  a  key  determinant  of  the  ECFV  and  circulatory  integrity.  Notably,  volume  status  also  modulates  the  release  of  AVP  by  the  posterior  pituitary,  such  that  hypovolemia  is  associated  with  higher  circulating  levels  of  the  hormone  at  each  level  of  serum  osmolality.  Similarly,  in  “hypervolemic”  causes  of  arterial  underfilling,  e.g.,  heart  failure  and  cirrhosis,  the  associated  neurohumoral  activation  encompasses  an  increase  in  circulating  AVP,  leading  to  water  retention  and  hyponatremia.  Therefore,  a  key  concept  in  sodium  disorders  is  that  the  absolute  plasma  Na+  concentration  tells  one  nothing  about  the  volume  status  of  a  given  patient,  which  furthermore  must  be  taken  into  account  in  the  diagnostic  and  therapeutic  approach.