Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Abstract

Hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a frequent cause of hypotonicity. Although the differential diagnosis with other causes of hypotonicity such as salt depletion is sometimes challenging, some simple and readily available biologic parameters can be helpful in the diagnosis of SIADH. In SIADH, urea is typically low; this is less specific for elderly patients, for whom lower clearance of urea accounts for higher values. Low levels of uric acid are more often seen in SIADH (70%) compared with salt-depleted patients (40%). Typically, patients with SIADH will show a lower anion gap with nearly normal total CO 2 and serum potassium, this despite dilution. In patients with hyponatremia secondary to hypocorticism, total CO 2 is usually lower than in nonendocrine SIADH despite low urea and uric acid levels. Urine biology can also be helpful in diagnosis of SIADH because patients with SIADH have high urine sodium (Na; >30 mEq/L), and most of them will have a high fractional excretion of Na (>0.5% in 70% of cases), reflecting salt intake. Conversely, low urine Na in patients with SIADH and poor alimentation is not rare. Finally, measurement of urine osmolality is useful for the diagnosis of polydipsia and reset osmostat and could further help in the choice of therapeutic strategy because patients with low urine osmolality will benefit from water restriction or urea, whereas those with high urine osmolality (>600 mOsm/kg) would be good candidates for V 2 antagonist.

Impact of hyponatremia and the syndrome of inappropriate antidiuresis on mortality in elderly patients with aspiration pneumonia

“…Several studies have used test infusions of isotonic saline to discriminate between these alternatives, but because our study was retrospective, we were unable to use this test. 11,20 Some studies have reported that, in patients in a state of volume depletion, volume repletion removes the stimulus for antidiuretic hormone release, allowing excess water to be excreted in a dilute urine and the serum sodium concentration to return toward normal. 21,22 According to this theory, instead of using an isotonic test infusion, we added in our study a criterion of volume depletion in which patients with a sustained increase in serum sodium concentration of !5 mEq/L and a sustained decrease in blood urea nitrogen, even with administration of hypotonic solution, were classified as volume depleted.…”

“…Those variables with P < 0.2 in the univariate analyses were included in the multivariate 9 Hannon and Thompson, 12 and Decaux and Musch. 20 analyses. The Hosmer-Lemeshow test was used to assess the goodness-of-fit for multivariate logistic regression models.…”

More on Renal Salt Wasting Without Cerebral Disease

“…Graph demonstrating serum sodium concentrations in mmol/L and urine osmolalities in mosm/kg during infusion of 0.9% saline at 50 ml/h over 36 h. Note dilution of urine at 24 h of the study and prompt correction of hyponatremia 36 h after initiation of saline therapy. mmol/L if sodium intake is low (23). Uosm is always increased above plasma osmolality, although 2 L of isotonic saline infused at 16 ml/min has been shown to dilute the urine to 151 mosm/kg by unknown mechanisms (24).…”

Syndrome of inappropriate antidiuresis and cerebral salt wasting syndrome: are they different and does it matter?

“…A key means of distinguishing SIAD from other causes of hyponatremia has been the use of serum and urine biochemistries. SIAD is usually associated with an elevated spot urine sodium (> 20 mEq/L), elevated fractional excretion of sodium (> 0.55%), low blood urea nitrogen (BUN) and plasma uric acid, and low plasma renin activity and aldosterone, whereas the converse of these biochemistries is noted in hypo-and hypervolemic causes of hyponatremia [5].…”