Pre and post-renal azotemia

[tiedyeddog]

It's been awhile since I have had renal.

I am trying to understand the solute changes in the azotemias. can someone tell me if my logic is good here?

Pre-renal: hypovolemic state. kidneys want to conserve as much solute as possible to keep as much water as possible. Na and urea is reabsorbed, making urine Na slow, FEna under 1, and BUN/creatine ratio high.

intrinsic: damaged tubules, kidney loses all of it's solutes. this one is easy.

post-renal: I am very confused about this on. Urine Na is high because of high pressure??? Why is the serum BUN/Cr so high???

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[bangarang]

It's been awhile since I have had renal.

I am trying to understand the solute changes in the azotemias. can someone tell me if my logic is good here?

Pre-renal: hypovolemic state. kidneys want to conserve as much solute as possible to keep as much water as possible. Na and urea is reabsorbed, making urine Na slow, FEna under 1, and BUN/creatine ratio high.

intrinsic: damaged tubules, kidney loses all of it's solutes. this one is easy.

post-renal: I am very confused about this on. Urine Na is high because of high pressure??? Why is the serum BUN/Cr so high???

Post-renal: think about the Starling equation with the capillary and glomerular oncotic and hydrostatic pressures. Bilateral ureter block > increased glomerular hydrostatic pressure > decreased GFR > less excretion/more resorption of urea. Not sure why the urine Na+ is high, but maybe since there's no hypovolemia/CHF, the kidneys might not be trying to reabsorb more sodium than it needs > build-up of urine sodium.

 

[Charles_Carmichael]

It depends on time-frame. If it's early on after obstruction, you decrease the urine flow rate and increase reabsorption of Na, BUN, etc. However, if it's long-standing obstruction, you'll eventually damage the tubular epithelium -- this causes an ATN-like picture with a FeNa > 2%, low urine Osm, decreased BUN:Cr, etc.

Does that make sense? It's all dependent on how long the obstruction's been around for.

 

[Zzmed]

It depends on time-frame. If it's early on after obstruction, you decrease the urine flow rate and increase reabsorption of Na, BUN, etc. However, if it's long-standing obstruction, you'll eventually damage the tubular epithelium -- this causes an ATN-like picture with a FeNa > 2%, low urine Osm, decreased BUN:Cr, etc.

Does that make sense? It's all dependent on how long the obstruction's been around for.

Exactly. Initially, there is backup of urea and creatinine in blood (urinary tract obstruction etc etc) and proportionate increase. So BUN:Cr>15
But later on, if obstruction persists, it's like we have renal azotemia because the tubular epithelium is damaged. That's why ratio<15

As far as the urine Na is concerned, I am not 100% sure either, but I believe that the renal tubules are unable to concentrate or dilute the glomerular filtrate effectively so that's why it's elevated. (but obviously after postrenal becomes renal).

tiedyeddog why would high tubular pressure cause increased urinary Na? (except for the reason I said, destroying renal tubules)

 

[sab3156]

Bump.

Anyone know why the urine concentration of short term (mild) post-renal AKI is > 40? Shouldn't the urine concentration of Na actually be < 20, since tubular reabsorption is not affected yet?

 

[68PGunner]

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[sab3156]

It's affected, not not as severe, as evident by mild post renal azotemia FENa being over 1%.

The point of the distinction between mild/short-term post renal azotemia and severe/long-term post renal azotemia is that one has tubular injury (long-term) and one doesn't (short-term). This is why the BUN/Cr levels differ between them. The FENa is said to be < 1% in mild, until the tubules are affected. Then it starts to rise as the tubular reabsorption is affected. This is something mentioned in literature. However, Firecracker does not mention anything about the urine concentration of Na in the short-term postrenal azotemia... but First Aid gives this graph:

It says > 40 urine Na... and does not make a distinction between mild and severe, YET... it makes a distinction between FENa between mild and severe. Which makes no sense... if you change FENa aren't you going to change the urine Na?

So is urine concentration of Na actually pretty normal (< 20) in the MILD case? Can someone point to a paper or a textbook that mentions this?

 

[68PGunner]

The point of the distinction between mild/short-term post renal azotemia and severe/long-term post renal azotemia is that one has tubular injury (long-term) and one doesn't (short-term). This is why the BUN/Cr levels differ between them. The FENa is said to be < 1% in mild, until the tubules are affected. Then it starts to rise as the tubular reabsorption is affected. This is something mentioned in literature. However, Firecracker does not mention anything about the urine concentration of Na in the short-term postrenal azotemia... but First Aid gives this graph:

View attachment 226454

It says > 40 urine Na... and does not make a distinction between mild and severe, YET... it makes a distinction between FENa between mild and severe. Which makes no sense... if you change FENa aren't you going to change the urine Na?

So is urine concentration of Na actually pretty normal (< 20) in the MILD case? Can someone point to a paper or a textbook that mentions this?

It's a Zanki error based on an older version of FA. Thanks for the new chart.

 

[68PGunner]

...

 

[sab3156]

Thanks man but we shouldn't assume. It can lead us down a dark road.