Acute Renal Failure Explained Clearly by | 2 of 3

By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , /

welcome to part two of acute renal
failure let’s little let’s review a little bit
here about what we were talking about we were talking about chem seven we have
the BUN and we’ve got the creatinine bu n stands for the blood urea nitrogen
remember it’s made in the liver it is both filtered and reabsorbed
whereas the creatinine is the end product of muscle metabolism and it is
filtered and secreted so let’s look at our nephron once again that’s the loop
of Henle that’s distal convoluted tubule
collecting duct and you’ve got the toilet down here okay and you’ve got the the a Ferentz and the efferent arteriole
and remember what we said about the U n bu n is the blood urea nitrogen it goes
through and also gets reabsorbed okay so that’s B u N and you’ve got the
creatinine cratan n’ goes does not get reabsorbed but instead goes out actually
a little bit gets secreted here okay so if you’ve got acute renal failure remember that the GFR the glomerular
filtration rate is going to go down so if that’s the case then your B UN the UN
is going to go up just because of the fact that the glomerular eighth is lower
therefore not as much as being filtered the B UN is going to go up but because
it’s going by slower because the GFR is down then
more of it is going to be reabsorbed and so it’s going to go up by even more
that’s opposed to the creatinine creatinine is going to go up why because
the GFR is low and the GFR is low because there’s a cute renal failure
going on and that means that Crichton is going to go up but it’s not going to go
up any more than that because it’s not being reabsorbed and so
what you see here is that the BU n goes up more than the Kratt name does when
you have a decrease in your GFR just based on the fact that there’s lower
flow so lower flow means higher Buick writing ratio okay so what would be a
number here that we could associate with it so normal would be for instance 15
over 1 so if the B went over cratan een if the b1 went up by more than that of
the crannium we could say for instance that this would go to a2 and a 30 okay
so the B would go up to 30 in the grant would go up to 2 so you could go up by
instead of having a 15 to 1 ratio you would have more like instead of even
30 would even go up high or go to 40 so 40 to 2 ratio which is the same as a 20
to 1 ratio so here we would see the normal ratio is 15 to 1 and it would go
up to 20 to 1 or in this case 40 over 2 and that would be from a low flow State
now what would happen here if for some reason there was a shutdown a different
type of acute renal failure at acute renal failure not because there’s less
flow coming to the glomerulus but instead because the actual tubules which
line the nephron something we call renal renal failure if they weren’t working
well what would happen is that you would still get a slow down here
because these cells are not working and the b1 would go up but it would only go
up for one reason and that’s because the GFR is low you would not get
reabsorption of this the UN and so what you would have is this would be more of
a pre renal what I mean by that is is that there is a reduction in the flow
coming here and because of that you’re getting the BU when increasing because
of the low flow and also the vun is being reabsorbed because these cells are
working so that would be a pre renal situation or in a renal situation in a
real situation these cells are not working and so if these cells are not
working the flow is going to be low as a result of that but you’re not going to
get bu and reabsorption and so it’s going to go up instead of being 50 into
one okay it’s going to go to 30 over two which is still the same 15 to one ratio
but they’re both going up but this is not going up more than that it so it
still holds the same ratio so in a renal situation where there’s a problem with
the kidney itself you hold and maintain that 15 to one ratio but when there is a
pre renal State in other words there’s not enough flow coming to the glomerulus
you’re going to get a reabsorption of the BU n preferentially and that’s going
to increase your bu and ratio to 20 to 1 okay so the bottom line here is that the
bu and the correcting ratio can kind of tell you what kind of renal failure have
is it pre renal sot mia or is it renal a zootie mia pre renal azo to me is where
there’s not enough blood coming to the kidney renal azo t Mia is where there’s
something wrong with the kidney itself if it’s 20 to 1 ratio like this you’re
thinking of pre renal sot mia if it’s still 15 to 1 ratio its renal sot mia
okay another way of looking at that is just looking at sodium and
concentration so let’s go ahead and draw our glomerulus again a little bigger
this time here’s the glomerulus the proximal convoluted tubule loop of Henle
and then out okay so pretend you’re a nephron and you’ve got two different
situations you’ve got a situation where you have a pre renal situation where
there is not enough blood coming in to the kidney and you’ve got a renal
situation where there’s a problem with the actual tubules that are supposed to
be transporting fluids and reabsorbing in a pre renal situation there’s not
enough blood coming in and you have a reduction in your GFR well the kidney
thinks that there’s not enough volume and the way the kidney regulates volume
is by reabsorbing sodium so if there’s not enough volume all the kidney is
going to do is just try to reabsorb more sodium and so what’s going to happen to
your urine that’s coming out you think it’s going to be high in sodium or low
in sodium well it’s going to be very low in sodium in a pre renal situation and
of course as sodium goes up guess what else comes with it water and so are you
going to have a lot of water in the filtrate in the urine that’s coming out
the answer is no so you’re going to be very low in sodium and very low in water
so that leaves a high concentration or a high osmolarity to the urine that’s
coming out okay let’s look at the flip side of that again here’s our Clare Ulis Oh Mary Alice proximal convoluted be a
loop of Henle and collecting tube you’ll going out to the toilet down below okay
so in this situation we’ve got a renal problem the renal problem is is that
these cells are not reabsorbing in fact none of them are reabsorbing there’s a
problem all over and so what’s the situation here here we’ve got plenty of
fluid coming to the kidneys but because these cells are not working all of that
sodium water is just going right through and out so we would expect to see a high
sodium concentration a high water concentration and therefore a low
osmolarity to the fluid and that’s in renal when there’s a problem with renal okay so let’s summarize once again make
sure everyone’s on the same page here so we’ve got the B UN okay what are some of
the points that we learned about the B UN it’s synthesized in the liver okay
it’s filtered and absorbed okay what are things that can increase it that have
nothing to do with the kidney we’ve talked about that we’ve talked about
fever we’ve talked about GI bleeding okay
there’s antibiotics that tip like tetracycline there is catabolic effects steroids all that what are some things
that can decrease it well liver failure okay and then what about proximal
convoluted tubule we see there we see that it parallels the reabsorption of
sodium and water and so we know that it’s reabsorbed okay
and so at because of that in a low flow state and a low flow state it’s going to
be really absorbed it’s going to go up okay now what about granting all right
we know that it’s the end product of muscle and that it is filtered and
secreted okay so what are some things that can increase it they have nothing
to do with the kidney function we know that it can be increased by drugs that
prevent its secretion in the kidney and that would be cimetidine and
trimethoprim what are some things that they can decrease it muscle wasting okay
and we know that it goes up in renal failure okay well let’s talk about the B
UN to creatinine ratio we know that because the B UN goes up even higher in
a low flow state that it’s usually 20 to 1 ratio if it’s pre renal pre renal
again is any reason that causes a decrease in blood flow to the kidneys
and that it’s 15 to 1 in renal okay and in renal remember is where there’s a
problem with the kidney itself and pre renal is where there’s a problem with
the amount of blood flow that’s going to the kidney okay now join me for part three for the final
wrap-up of acute renal failure thanks for joining me

64 thoughts on “Acute Renal Failure Explained Clearly by | 2 of 3

  1. Thanks for the question. Most of the Na reabsorption is via the Na+/K+ ATPase in the basolateral membrane.

  2. At the luminal membrane, sodium is reabsorbed via cotransporters (ex – sodium-glucose cotransporter), the energy for which is provided via secondary active transport (Na+/K+ ATPase) on the basolateral membrane. Hope this helps.

  3. I know I'm not a Med student… but you explain this way better than my nursing instructor did! Better educated nurses make for better patient which make happy, less stressed Doctors (maybe). Thanks for the videos!

  4. i have a question though , why does the renal blood flow decrease if the cells in the PCT aren't working for some reason? is that because Na and H2O aren't absorbed so the blood volume will decrease which will cause a decrease in the blood flow to the kidneys ? will that cause a constriction of the afferent arteriole ? please explain , thank you .

  5. It's really the glomerular filtration rate that decreases (GFR). Creatinine clearence is an estimate of this. renal blood flow is only one determinant of the GFR. For instance, low RBF can cause prerenal azotemia.

  6. hello thank you for the vidoe ;=) .. i have a question though.. what biology results do you get in an obstructive acute renal failure?

  7. its amazing, i've relied on my memory of the associated lab values for pre-renal vs renal, (BUN/CR 20:1 pre-renal and 15:1 for renal) and have used them to distinguish for awhile, but this video explains it so easily; no more memorization required. thanks!

  8. if you're talking about serum creatinine at 11:47 muscle wasting and damage should increase it not decrease it because you said it comes from muscles

  9. Can muscle wasting occur rapidly/acutely enough to diagnostically affect serum creatinine levels? I don't know. But it does make sense that less muscle tissue = less muscle breakdown products (creatinine) in the blood.

  10. wasting can be a very slow process and it doesn't present the same as damage like crushing etc. I think as you slowly lost muscle mass from wasting it would decrease proportionally to the mass you lost. If there was actually damage then you'd expect an increase bc like his burn example there is a lot of protein that is broken down. That's my thoughts on it, you might be right of course, I'm not expert.

  11. The more you educate the greater impact you are having in the medical community, and the better we can take care of our patients! Thank you for doing this, I am a nurse and because of your lectures I am able to understand and help treat my patients that I have better.

  12. The reason this is such a remarkable explanation and brilliantly explained is because the doctor obviously understands the subject in depth.  Thank you for taking the time to share with us

  13. Love this videos, pretty helpful. I was wondering what kind of software do you use to make them? I mean, all the drawings and stuff. Thanks.

  14. My lab measured Urea in mmol/l not BUN and creat in umol/l.., how do I appreciate this ratio without need to convert it to BUN??what is the ratio using this units, to say its pre renal or renal????

  15. i love your videos. very informative. i am working now but i still have a lot to learn so thanks for this clear explanations. simplified!!!!

  16. I don't understand acute tubular necrosis. I get that since the tubules aren't functioning, they can't reabsorb sodium so it goes to waste. But In First Aid 2015, there is a mnemonic device (MAD HUNGER) and the "N" stands for "Na+ and water retention". So how is there both wasting and retention of sodium? Is it that the kidneys start out by wasting sodium because the tubules are not reabsorbing it, which increases FENa, and then after prolonged periods of necrosis, the condition worsens to the point where GFR decreases and leads to sodium retention?

  17. Thanks For Another video , But One of causes of Renal ARF is Acute rubular necrosis in that case we shouldnt have High sodium or H2O in Urine , we will be having oligria right?

  18. what is the difference between (acute and chronic) Renal failure and Nephrotic or Nephritic Syndrome?

  19. This lecture is better than anything I got in PA school. Perfect review for internal medicine rotations!

  20. See the whole series at along with other top quality videos including reviews in pulmonary, cardiology, infectious disease, and hematology!

  21. sir, in acute renal failure, oliguria is important manifstation . then why in renal acute kidney failure increased sodium occur(that mean polyuria)….

  22. Such a helpful video! (Sidenote: 'osmolarity' or 'osmolality'? Does it change from latter to former when outside the body?)

  23. in the example of BUN: creatinine ratio for intra-renal (intrinsic) AKI, it is shown as changing from 15:1 to 30:2, however i don't understand why serum creatinine goes UP. in the previous example of pre-renal AKI, it is clear that low GFR leads to higher serum creatinine. i understand the logic here that both BUN and creatinine are filtered less, but that BUN is reabsorbed in the PCT and thus serum levels are elevated proportionally more than creatinine. however, in the second example, GFR is not necessarily lower, just reabsorption is prevented. as creatinine is not reabsorbed anyway, i dont see why serum levels would go up.

  24. I can't find a better doctor who can draw a toilet quickly and it still look like a toilet than this man right here. If that doesn't deserve a subscribe, I don't know what does.

  25. Why wouldn't tubular cells be working if we only have Glomerulonephritis? WOuldnt then Renal ABI have the same Lab as Pre-renal ABI ?

  26. This video seriously changed my life… I completely understand the kidneys SO MUCH better! Thank you!

  27. Omg thx so much, I will watch all your videos, I feel like all my unanswered questions being answered in your video, and I hope you make more and more videos for students like us!!!

  28. I am currently writing my master’s thesis which aims to better understand the needs and values of nurses and physicians who perform continuous renal replacement therapies (CRRT) in cases of acute kidney failure.
    Please support me by taking part in my online survey:

  29. verrry helpful thanks

    I have Q in pre renal cases if urine has low sodium and water as well why high osmolarity ? as solutes are even low ?

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