b. Renal tubular disease as in post obstructive diuresis,
recovering ATN, PCKD, chronic tubulointerstitial nephritis,
medullary cystic disease and congenital NDI.- Pituitary ADH deficiency (CDI) which is due to either trauma,
neoplasm, vincristine or idiopathic (50%).
B- Non-renal causes of water loss: gastrointestinal loss.
C- Sodium intake in excess of water.
Clinical features:
1- Manifestations of the etiologic cause.
2- Polyuria, polydipsia, nocturia and functional dilatation of the bladder
and ureters, this is seen in patients with D.I.
3- Hypernatraemia occurs only if there is lesion in osmostat
(hypothalamic lesion) or patients unable to drink, it manifests as
muscle twitches, lethargy, weakness, seizures or even coma and
death.
With hypernatraemia, there is a shrinkage of brain cells and a
decrease in brain size which if severe it may lead to rupture of blood
vessels with focal intracerebral or subarachnoid hemorrhage. If the patient
survived, brain cells will adapt and regain size.
Treatment:
1- Acute hypernatraemia could be corrected quickly but chronic
hypernatraemia must be corrected slowly to prevent cerebral oedema
(decrease plasma sodium by about 2 mmol/litre/hour).