It is widely believed that the cerebral salt-wasting syndrome (CSWS) exists
as an entity distinct from the syndrome of inappropriate ADH secretion, an
d that it is characterized by evidence of severe renal salt wasting that re
sults in volume depletion and hyponatremia. Proof of the existence of CSWS
as an entity requires documentation of renal salt wasting and volume deplet
ion. The present review has been undertaken to examine the evidence that th
e CSWS is a separate entity. In this effort, we have discussed various meth
ods of documentation of volume depletion, and then reviewed reported cases
of CSWS to determine whether volume depletion and renal salt wasting have b
een clearly demonstrated. Our review has led us to conclude that not one ca
se of purported CSWS has demonstrated clear evidence of volume depletion an
d renal salt wasting. If renal salt wasting had been proven in these cases,
we would conclude that the likely site of renal salt transport was the pro
ximal tubule, The proximal site of salt transport defect has been suggested
by the absence of hyperreninemia and hypokalemia, which would be a disting
uishing feature of Bartter's syndrome and Gitelman's syndrome.