Arieff A, Gabbai R
Cerebral salt wasting syndrome: Role of volume contraction and
potassium wasting.
ASN Annual Meeting -- Philadelphia
J Am Soc Nephrol
(Nov) 16:532A 2005

Cerebral salt wasting syndrome (CSWS) has been described as a clinical
syndrome in patients with hyponatremia (plasma Na < 128 mmol/L), a
cerebral lesion and urine Na concentration > than plasma Na. The main
differential diagnosis has been SIADH.
Over 4 yrs we prospectively
studied 26 patients (12M, 14F: 56
22 yrs) who
presented with symptomatic hyponatremia and urine monovalent cation (Na+K)
concentration > 150 mmol/L. Patients had plasma Na 118
8 mmol/L, normal renal function (Cr Cl =110
31 ml/min), hypertonic urine (671
156 mOsm/kg) and became hypotensive (systolic BP
< 100 mm Hg) with fluid restriction. Presenting features included:
dementia; recurrent seizures; and recurrent falls with orthopedic injury. The
24 hr urine monovalent cation loss was 356
195
mmol (21
6 gm)/day of which 27% was K (102
101 mmol/day) and the rest Na (261
148 mmol/day).
Twelve patients, initially
believed to have SIADH, were fluid restricted, which led to hypotension. When
diagnosed, all initially required treatment with IV 3% NaCl. Eight died of
underlying illness (7 malignant brain tumors) but 18/26 recovered. Survivors
were eventually maintained with oral NaCl (6-14 gm/day). All 18 are active
and maintained on oral NaCl tablets for over 3 years.
Conclusions: a)
CSWS can be defined as a patient with symptomatic hyponatremia who is volume
contracted and has lost sufficient (Na+K) in the urine to lower plasma Na
below 128 mmol/L; b) Urinary loss of K is a major component in the
pathogenesis of hyponatremia associated with CSWS; c) CSWS can be
differentiated from SIADH by fluid restriction, which leads to hypotension;
d) most patients with CSWS require emergency therapy with IV 3% NaCl, but can
then be effectively managed with oral NaCl.

© Copyright 2005-2006,
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