Table 3.

Proposed utilization of urinary furosemide and urinary sodium with decreased urine response to FST.

	Urinary furosemide (FEM2)
	FEM high	FEM low
Urine Sodium
High Sodium	Physiology: Consistent preserved proximal tubular function and distal injury preventing sodium reabsorption Syndrome: This profile would be consistent with kidney injury that has a TAL or distal injury profile	Physiology: Consistent with tubular injury resulting inability to reabsorb sodium or to secrete furosemide Syndrome: This profile would be consistent with acute tubular injury and acute tubular necrosis
Low Sodium	Physiology: Demonstrates sufficient oxygen transport to the kidney to enable effective bi-directional proximal tubular function as evidenced by sodium reabsorption and furosemide secretion Syndromes that would show this pathophysiology: decreased effective circulating volume, congestive heart failure, cardiorenal syndrome, central venous congestion	Physiology: Demonstrates sufficient oxygen transport to the kidney to maintain sodium reabsorption but inability to secrete furosemide. Syndrome: This physiology would be consistent with a profound hypo-albuminemia state and may be indicative of the threshold wherein albumin replacement therapy is indicated