Cr. Cooke et al., INAPPROPRIATE ANTIDIURESIS AND HYPONATREMIA WITH SUPPRESSIBLE VASOPRESSIN IN GUILLAIN-BARRE-SYNDROME, American journal of nephrology, 18(1), 1998, pp. 71-76
Studies in which plasma osmolality was altered acutely by oral water l
oading and hypertonic sodium chloride infusion were performed to furth
er identify the mechanisms involved in the pathogenesis of the syndrom
e of inappropriate secretion of antidiuretic hormone (SIADH) in a pati
ent with Guillain-Barre syndrome. Although resetting of the osmotic th
reshold for vasopressin release was demonstrated in these studies, thi
s does not seem to have been a primary factor in the development of SI
ADH in this patient. Downward resetting of the osmotic threshold by su
stained hypoosmolality has been previously demonstrated, and it is pos
sible that this may account for the initially low osmotic threshold id
entified by our studies. These studies suggest that inappropriate anti
diuresis, as shown by the absence of a diuretic response to low thresh
old suppression of the plasma arginine vasopressin concentration was d
ue either to a vasopressin-independent mechanism or to markedly increa
sed renal tubular sensitivity to vasopressin.