Differentiating SIADH from Cerebral/Renal Salt Wasting: Failure of the Volume Approach and Need for a New Approach to Hyponatremia

Abstract

Hyponatremia is the most common electrolyte abnormality. Its diagnostic and therapeutic approaches are in a state of flux. It is evident that hyponatremic patients are symptomatic with a potential for serious consequences at sodium levels that were once considered trivial. The recommendation to treat virtually all hyponatremics exposes the need to resolve the diagnostic and therapeutic dilemma of deciding whether to water restrict a patient with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or administer salt and water to a renal salt waster. In this review, we briefly discuss the pathophysiology of SIADH and renal salt wasting (RSW), and the difficulty in differentiating SIADH from RSW, and review the origin of the perceived rarity of RSW, as well as the value of determining fractional excretion of urate (FEurate) in differentiating both syndromes, the high prevalence of RSW which highlights the inadequacy of the volume approach to hyponatremia, the importance of changing cerebral salt wasting to RSW, and the proposal to eliminate reset osmostat as a subtype of SIADH, and finally propose a new algorithm to replace the outmoded volume approach by highlighting FEurate. This algorithm eliminates the need to assess the volume status with less reliance on determining urine sodium concentration, plasma renin, aldosterone and atrial/brain natriuretic peptide or the BUN to creatinine ratio.

Cisplatin-induced syndrome of inappropriate antidiuretic hormone secretion (SIADH) with life-threatening hyponatraemia

“…However, clinical volume assessment is notoriously difficult and unreliable 27. Fractional excretion of sodium and urate have been suggested as additional investigations to aid in the diagnostic approach 28. Although these values were not calculated in our patient, the low aldosterone level would argue against a hypovolaemic state and support the diagnosis of SIADH.…”

The clinical management of hyponatraemia

“…The mechanism of the syndrome is thought to be initiated by the release of a natriuretic factor which results in the increased renal excretion of sodium and subsequent volume depletion. As a result of the subsequent intravascular volume depletion, there is release of ADH and increased renin–angiotensin–aldosterone activity to reduce the rate of diuresis 18. Crucially, it must be recognised that the release of ADH in this setting is an appropriate response to the volume depletion, and this often makes it clinically difficult to differentiate cerebral/renal salt-wasting syndrome from SIAD.…”

Aneurysmal subarachnoid hemorrhage

“…This algorithm is useful only with normal glomerular iltration rate GFR, because FEurate can exceed normal values in patients with reduced glomerular iltration rate (GFR) [20].…”

“…The only clinical diference is the state of their extracellular volume (ECV): being hypervolemic or euvolemic in SIADH and hypovolemic in CSW ( Table 7) [20].…”

“…Rapid correction of hyponatremia can cause central myelinolysis and should be avoided, but insuicient correction of hyponatremia can result in brain edema, convulsion, and death [17,[20][21][22].…”