Friday, February 27, 2009

Renal (Cerebral) Salt Wasting versus SIADH

The term "cerebral salt wasting" has always been a confusing one to me, and in the most recent issue of C-JASN, the authors of an article "More on Renal Salt Wasting Without Cerebral Disease : Response to Saline Infusion", the authors advocate abandoning the term altogether in favor of the term "renal salt wasting." They make this suggestion based on the identification of a subset of patients with salt wasting in the absence of cerebral disease.

Whether renal salt wasting (RSW) even exists has been the matter of controversy. In this paper, the authors compare and contrast a patient with SIADH with another with RSW. The distinction is a tricky one to make, but important as the treatment for SIADH is water restriction whereas the treatment for RSW is saline infusion.

SIADH, as we all know, is due to the inappropriate secretion of ADH which results in unregulated water absorption; patients are generally euvolemic on clinical examination. Usually (but not always) the urine Na is >20 mmol/L and there is an elevated fractional excretion of urate (FE-urate) on initial presentation. Once the sodium corrects, however, the FE-urate normalizes as well.

RSW, on the other hand, is due to a defect in tubular sodium transport that results in sodium wasting and resultant hypovolemia. The serum renin and aldosterone levels at presentation are elevated. Urine Na is >20 mmol/L because the tubular loss of Na is the primary cause of extracellular volume depletion. The entity is differentiated from garden-variety pre-renal azotemia based on the presence of other abnormalities indicative of other defects in renal tubular function: for instance, RSW patients commonly have an elevated FE-phosphate (>20%) and elevated FE-urate whereas patients with pre-renal azotemia tend to have reduced FE-phosphate & urate.

The authors claim that it is possible to differentiate between SIADH and RSW based on the response to correction of the serum sodium: in SIADH, the FE-urate should normalize, whereas in RSW, the FE-urate remains elevated. I understand the logic, but what would be more helpful would be to differentiate between the two entities during the initial patient encounter. Perhaps FE-phosphate is one way to do this--though I'm not sure if the test has a quick enough turnaround time to be useful in this way. Assessment of volume status is another possibility, though difficult even for seasoned clinicians in many instances.

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