Urine sodium and FEna in AKI

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the learner

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Hi all,

A few quick questions about the interpretation urine Na and FEna AKI.

I note that the following are considered "normal" in patients with the following conditions:

Prerenal azotemia: Urine sodium <20mEq/L; FEna <1%
Acute Intrinsic Kidney Injury: Urine sodium >40eEq/L; FEna >2%

However, at first glance, these value seem contradictory.

Here is how I am explaining it to myself - can anyone tell me if this is correct?

In prerenal azotemia, the kidney attempts to conserve fluid by concentrating the urine and reabsorption free water. The loop of henle reabsorbs a greater amount of sodium (than usual) causing a higher concentration of sodium in the renal parenchyma. The now increased concentration of sodium in the interstitium drives increased free water reabsorption in the collecting tubules which results in concentrated urine. However, the urine sodium concentration is low due to the amount of sodium the was reabsorbed in the loop, and even though a great deal of free water was reabsorped in the collect duct, there is still less sodium relative to water in the excreted urine. The FEna remains <1% due to the signicant reabsorption of sodium in the loop.

In (some forms of) acute intrinsic injury, the cells lining the lumen are damaged and not able to effectively regulate sodium handling. This results in the inability of the kidney to reabsorb sodium leading to a higher concentration of sodium in the urine, but the urine is still considered dilute as a significant amount of free water is still excreted (just not enough to drop the urine sodium concentration). The FEna climbs to >2% since sodium in the tubule is not efficently reabsorbed.

If you made it this far...thanks for reading. Is this right? I highly appreciate any feedback.

the learner

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Hi all,

A few quick questions about the interpretation urine Na and FEna AKI.

I note that the following are considered "normal" in patients with the following conditions:

Prerenal azotemia: Urine sodium <20mEq/L; FEna <1%
Acute Intrinsic Kidney Injury: Urine sodium >40eEq/L; FEna >2%

However, at first glance, these value seem contradictory.

Here is how I am explaining it to myself - can anyone tell me if this is correct?

In prerenal azotemia, the kidney attempts to conserve fluid by concentrating the urine and reabsorption free water. The loop of henle reabsorbs a greater amount of sodium (than usual) causing a higher concentration of sodium in the renal parenchyma. The now increased concentration of sodium in the interstitium drives increased free water reabsorption in the collecting tubules which results in concentrated urine. However, the urine sodium concentration is low due to the amount of sodium the was reabsorbed in the loop, and even though a great deal of free water was reabsorped in the collect duct, there is still less sodium relative to water in the excreted urine. The FEna remains <1% due to the signicant reabsorption of sodium in the loop.

In (some forms of) acute intrinsic injury, the cells lining the lumen are damaged and not able to effectively regulate sodium handling. This results in the inability of the kidney to reabsorb sodium leading to a higher concentration of sodium in the urine, but the urine is still considered dilute as a significant amount of free water is still excreted (just not enough to drop the urine sodium concentration). The FEna climbs to >2% since sodium in the tubule is not efficently reabsorbed.

If you made it this far...thanks for reading. Is this right? I highly appreciate any feedback.

the learner

too many words
 
Water follows sodium, so in pre-renal azotaemia, when sodium is reabsorbed in the PCT due to the perceived hypovolaemia, water is pulled out as well, and the osmolarity of the urine actually increases (probably because of the loss of water with respect to other ions, not just sodium).
 
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