1/ #UncleBob presents a #5goodminutes tweetorial on the FeNa. The idea is simple, with normal kidneys and volume contraction, the kidney should avidly reabsorb sodium. With acute tubular injury, the problem is that the tubules cannot reabsorb Na.
2/ Here are the cautions - with a non-oliguric patient the stimulus to reabsorb Na is either not there (patient not volume contracted) or the patient has underlying CKD. When you understand the concept of fractional excretion, this will make sense.
3/ Here (from Wikipedia) is a good definition of FeNa: The fractional excretion of sodium is the percentage of the sodium filtered by the kidney which is excreted in the urine. You can substitute any measurable for sodium.
4/ As renal function worsens in CKD, each nephron has to excrete more sodium to maintain sodium balance. Therefore, patients with GFR < 50 will generally have an elevated FeNa - so we should not use this as a test in such patients.
5/ W/ acute tubular injury, there are (I believe) 2 theories. Either GFR drops precipitously & the tubules respond by excreting a higher % of Na, or more likely, the injury is tubular. These patients waste Na & water, & thus GFR decreases to prevent severe volume contraction
6/ What makes this complicated is the volume contraction is a major risk factor for ATN! The FeNa concept works best in oliguric patients. In non-oliguric ATN the FeNa is not as helpful.
7/ Two more interesting findings - acute glomerulonephritis gives a very low FeNa - pure glomerular disease without tubular injury. Obstruction gives a very high FeNa - reminding us to always exclude obstruction with acute creatinine rise.
8/ I hope this helps. FeNa is not a perfect test - but it does provide some important information. For those who like a fluid bolus first - please grab a urine sodium and creatinine in advance - in case the bolus does not work. Same for trying a diuretic.
