What is the pathophysiology of cerebral salt-wasting syndrome (CSWS) (renal salt wasting)?

Updated: May 13, 2020
  • Author: Sudha Garimella, MBBS; Chief Editor: Sasigarn A Bowden, MD  more...
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Cerebral salt-wasting syndrome, or renal salt wasting, may be more common than SIADH and may even occur in the absence of cerebral disease. [4, 5, 7] Although the exact mechanism that underlies the development of cerebral salt-wasting syndrome is unclear, it is known that the initiating defect in renal sodium transport leads to extracellular volume depletion and that a cascade of compensatory changes occurs.

Abnormalities in the proximal tubule result in excessive sodium losses, which lead to decreased effective circulating volume. This activates baroreceptors, which increase antidiuretic hormone (ADH) secretion. This results in water conservation and a return to an equilibrated state. In contrast, SIADH primarily occurs due to an inappropriate euvolemic rise in ADH secretion.

The relationship among serum urate, fractional excretion of urate, and hyponatremia in cerebral salt-wasting syndrome is unclear. Fractional excretion of urate may remain elevated even after correction of hyponatremia in patients with cerebral salt-wasting syndrome. This is distinct from SIADH, in which the fractional excretion of urate returns to the reference range once the hyponatremia is corrected. [6] The physiologic basis for this in cerebral salt-wasting syndrome may be related to the receptor-mediated processing of sodium and urate in the proximal tubule, which may be defective in this syndrome. The physiologic basis for hypouricemia in SIADH remains unclear.

The abnormalities in proximal tubular transport may be secondary to a plasma natriuretic factor that reduces proximal and, possibly, distal sodium transport in cerebral salt-wasting syndrome. It may also inhibit the tubular transport of urate, phosphate, and urea in addition to sodium. [8]

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