Step I who can answer this strange Q about kideny?!

Moslem Doctor · Sep 2, 2006

we all knows that in prerenal azotemia the bun : creatinine >15:1
becuz the GFR decreased and reabsorbtion or urea increase
and when we see glomerulonephritis we find that main patholgy is also decrease GFR , but we find its bun:creatinine< 15:1 . So What make glomerulonephritis differ than pre renal azotemia in pathology and make it difffer also in bun :creatinine ratio ?!

chintu · Sep 3, 2006

That's a question I wondered about too. This is what Goljan has to say about this: In Prerenal Azotemia decreased GFR results in increased creatinine as you properly put but not the same case with BUN because the proximal tubule is intact and BUN gets reabsorbed from the proximal tubule. Also, I found from tulane's website that reabsorption of BUN is related to rate of blood flow; decreased blood flow in prerenal azotemia (hypotension, hypovolemia, etc) results in increased reabsorption of BUN and hence BUN/Cr >20.
In ATN, there is decreased GFR also so the Cr is high again but there's also an actual damage to the tubules so BUN wouldn't be able to get reabsorbed from the Proximal tubule as in the case of prerenal and so it is also high and hence the BUN/Cr is <15.

chintu · Sep 3, 2006

I just realized I said some things in my explanation that might have been a little confusing. Basically, the moral is that in both prerenal azotemia and ATN both BUN and Cr increase due to decreased GFR but in prerenal azotemia BUN increases disproportionately due to intact prox. tubule but in ATN damaged tubule doesn't allow reabsorption of BUN so it is not increased disproportionately and hence the ratio of BUN/Cr is not as high.

Moslem Doctor · Sep 3, 2006

Thank u dr chintu
but it seem u answerd another issue
we talk about glomerulonephritis , why its effect on bun/cr ratio differ than pre renal pathology although both only affect GF rate!
?

Idiopathic · Sep 3, 2006

I think you need to view glomerulonephritis as an intrinsic kidney problem (since it is) regardless of whether the pathological process is decreased GFR. Intrinsic kidney disease typically has a BUN:Cr ratio of ~10:1, whereas prerenal kidney disease is usually >15:1

dynx · Sep 3, 2006

Idiopathic said:
I think you need to view glomerulonephritis as an intrinsic kidney problem (since it is) regardless of whether the pathological process is decreased GFR. Intrinsic kidney disease typically has a BUN:Cr ratio of ~10:1, whereas prerenal kidney disease is usually >15:1

Ah yes, it is because it is. Thats a good reason.

Glomerular dysfunction is characterized by a couple of things, one of those things is protein wasting (leak through the damaged glomeruli which does not occur in dehydration). BUN is a marker for metabolism of protien, less protein => less breakdown products of protien, still increases but the ratio is less. This is the gist, if you have allready studied glomerular dysfunction this should probably have ocurred to you, if not, then you are asking the right kind of THINKING questions to get a 250+ on the test. So this question is either an indication that you need to study in more detail....or....you're on your way to doing really well.

Idiopathic · Sep 3, 2006

This reasoning is precisely why I would consider glomerulonephritis to be a subset of ATN, for the purposes of answering this question (I dont think its too simplistic of an explanation).

If you have damage to the nephron and leakage of protein, and poor concentration capability, it doesnt matter if its GN, ATN or whatever, it is because it is.

The 'concentration' principle definitely applies to prerenal syndromes, where teh kidney thinks its volume depleted and concentrates BUN, which it cant do in this case.

Moslem Doctor · Sep 3, 2006

iam so thankful for both of you doctor Idiopathic and doctor Dynx
Doctor Dynx i love your explanation really , it seem logic for me .

doctor Idiopathic says (The 'concentration' principle definitely applies to prerenal syndromes, where teh kidney thinks its volume depleted and concentrates BUN, which it cant do in this case.)

i say : why in this case cant do ??? there is no pathology at tubules in glomerulonephritis ,so its function preserved ,and ATN differ than glomerulonephritis in this point , so we cant say simply that all intrinsic kidney disease do same effect by same mechanism ,surely they must differ

Idiopathic · Sep 3, 2006

Moslem Doctor said:
there is no pathology at tubules in glomerulonephritis ,so its function preserved

in fact, this is not true. you lose protein in the urine due to the fact that either a) you cant keep it from leaving or b) you cant reclaim it

it really doesnt matter which in this case

also, several types of GN exist and tubular injury/malfunction is certainly possible. In theory, tubular function is preserved because no direct injury exists (i.e. ischemic sloughing of tubular epithelial cells) and intrinsic function should still be intact, but to say that you can lay down immune complexes all over the place and not damage effective tubular function is incorrect.

jmelan · Mar 23, 2007

i ran across this while studying for a clin path test. i have added a comment here so that this may be further discussed. i feel that the previous conclusion was misleading.

please see this publication:

http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1442-200X.2007.02295.x

with PSAGN, tubular function should be pretty much preserved, as a rapid recovery is common.

as a result the BUN:Cr ratio should be >15:1.

In the case presented in this publication, even when protein levels in the urine become high (nephrotic syndrome), the BUN:Cr ratio is close to 50:1.

can anyone explain the apparent discrepancy here?

thanks

Step I who can answer this strange Q about kideny?!

Moslem Doctor

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chintu

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chintu

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Moslem Doctor

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Idiopathic

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dynx

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Idiopathic

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Moslem Doctor

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Idiopathic

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jmelan

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