Kidney

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Temperature101

Membership Revoked
Removed
10+ Year Member
Joined
May 27, 2011
Messages
3,486
Reaction score
82
This question is from a passage, but one does not need the passage to answer it...

Amino acids are reabsorbed in the proximal tubule by a secondary active transport mechanism down the concentration gradient of sodium. A high protein diet would most like ly lead to:

A. a decrease in glomerular filtration rate and renal blood flow
B. an increase in glomerular filtration rate and renal blood flow
C. a decrease in glomerular filtration rate and an increase in renal blood flow
D. an increase in glomerular filtration rate and a decrease in renal blood flow

See if you can answer it and provide a good explanation to your answer. I will come back to give the answer. I got it wrong by the way. I HATE KIDNEY PHYSIOLOGY.

Members don't see this ad.
 
Increase in amino acids=increase in creatinine (both synthesized by the body, and ingested directly from meats). Increased creatinine present in the blood=increased creatinine secreted. Since we know that creatinine clearance is analogous to GFR then we know that GFR increases.

Most of the time when GFR increases, there is an associated increase in renal blood flow. So I'm going to go with choice B.
 
If I remember correctly (almost) no amino acids should be excreted from the urine? I know glucose should be entirely reabsorbed in the PCT and I also thought in a healthy kidney reasborbs all amino acids too, or at least most. In any case because you have a higher protein diet, more amino acids will be traveling through the bloodstream so the GFR would INCREASE, eliminating A and C.

In terms of renal blood flow logically you would think that an increase in filtration rate would result in an increase in renal blood flow to deal with the increase solute absorption. But other than an osmotic solute reasoning I can't really think of a reason why renal blood flow would increase.

But yeah B sounds good
 
Members don't see this ad :)
You all are right...B is the answer. but I am still having trouble to see why it's B. I think if someone's diet is high in protein, that means the plasma oncotic pressure should be high, which I think will decrease the GFR. Can someone explain in lame terms why in that case GFR is high?

Edit...I think I got it.
 
Last edited:
This question is from a passage, but one does not need the passage to answer it...

Amino acids are reabsorbed in the proximal tubule by a secondary active transport mechanism down the concentration gradient of sodium. A high protein diet would most like ly lead to:

A. a decrease in glomerular filtration rate and renal blood flow
B. an increase in glomerular filtration rate and renal blood flow
C. a decrease in glomerular filtration rate and an increase in renal blood flow
D. an increase in glomerular filtration rate and a decrease in renal blood flow

See if you can answer it and provide a good explanation to your answer. I will come back to give the answer. I got it wrong by the way. I HATE KIDNEY PHYSIOLOGY.

B. Without knowing any specific physio that is beyond the level of the mcat (like the relationship of creatinine), you know from the question that high protein will have an effect on sodium. You don't urinate out proteins, even if you have a high protein diet, so increased AA absorption results in increased absorption of sodium. You know that water follows sodium around like a little a puppy on a leash so you know that blood pressure is going to go up. GFR is dependent on BP (you should know this for MCAT) so GFR up = renal flow up.
 
You all are right...B is the answer. but I am still having trouble to see why it's B. I think if someone's diet is high in protein, that means the plasma oncotic pressure should be high, which I think will decrease the GFR. Can someone explain in lame terms why in that case GFR is high?

Edit...I think I got it.

Problem with this line of thinking is that when you eat a high protein diet, it doesn't increase the amount of protein floating around in your blood stream. When you digest dietary proteins, you break them down into free amino acids that your body can then use to build it's own proteins that have human function. So instead of having proteins floating around in the blood stream, you have free amino acids floating around. With an excess of amino acids, your muscle cells can generate more creatine which is like a little energy shuttle that your muscles use. But creatine naturally re-configures to creatinine after a certain amount of time. Creatinine has absolutely no physiologic function in the body so it's simply filtered out at the kidneys for excretion.

Cool thing about creatinine is that it's freely filtered, not secreted, and not re-absorbed anywhere in the nephron. So you can measure the creatinine excretion in a patient and have a pretty good idea of what their GFR is. That's why you'll hear physicians constantly fussing over creatinine clearances etc, it's a measure of how healthy the kidneys are and has a ton of implications for pharmacology, and for the patient's overall health.

I have to say, I think this question is way outside the scope of the MCAT though.
 
Problem with this line of thinking is that when you eat a high protein diet, it doesn't increase the amount of protein floating around in your blood stream. When you digest dietary proteins, you break them down into free amino acids that your body can then use to build it's own proteins that have human function. So instead of having proteins floating around in the blood stream, you have free amino acids floating around. With an excess of amino acids, your muscle cells can generate more creatine which is like a little energy shuttle that your muscles use. But creatine naturally re-configures to creatinine after a certain amount of time. Creatinine has absolutely no physiologic function in the body so it's simply filtered out at the kidneys for excretion.

Cool thing about creatinine is that it's freely filtered, not secreted, and not re-absorbed anywhere in the nephron. So you can measure the creatinine excretion in a patient and have a pretty good idea of what their GFR is. That's why you'll hear physicians constantly fussing over creatinine clearances etc, it's a measure of how healthy the kidneys are and has a ton of implications for pharmacology, and for the patient's overall health.

I have to say, I think this question is way outside the scope of the MCAT though.
It's from an MCAT prep book; therefore, it might be fair game.
 
I just think your understanding and explanation (that of a med student) is beyond the scope of the MCAT. I think Med's explanation is apt. In any case increased protein intake will result in increased free A.A, resulting in higher GFR to reabsorb them, and higher renal blood.


In fact, would there ever be a situation when an increase in GFR would result in a decrease in renal blood flow, or vice versa?
 
I just think your understanding and explanation (that of a med student) is beyond the scope of the MCAT.

Perhaps, though I don't see how you could expect an increase in GFR any other way.

I think Med's explanation is apt. In any case increased protein intake will result in increased free A.A, resulting in higher GFR to reabsorb them, and higher renal blood.

The only problem I have with this statement is that there's nothing about an increased GFR on it's own that leads to a higher reabsorption rate. Increased GFR usually means increased excretion of a filtered solute as the transporter channels in the PCT that are responsible for reabsorption would be saturated at a certain concentration or flow rate. Therefore you would arrive at your maximal reabsorption level fairly quickly (which I admit I have no idea what that value would be) and after that you'd be peeing out amino acids at a higher than normal rate. This is the basic mechanism by which the body eliminates excess substances, even those which are re-absorbed.


In fact, would there ever be a situation when an increase in GFR would result in a decrease in renal blood flow, or vice versa?

Angiotensin II can cause an increased GFR and a decreased Renal Blood Flow. Certain drugs can do it also. It's accomplished by causing selective constriction around the efferent arteriole of the glomeruli which increases filtration pressure in the glomerulus, and with it then GFR. But this simultaneously reduces the total blood throughput of the kidney. think of it like kinking a hose with nail holes in it. The kinked area is the efferent arteriole, and the holes are the glomerular capillaries.

Conversely, certain nephrotoxic drugs such as COX-2 inhibitors (ibuprofen, aspirin, etc) cause preferential constriction of the afferent arteriole, decreasing GFR and decreasing renal blood flow. This is why high amounts of these drugs are bad for the kidneys; they cause renal ischemia and eventually necrosis.

Enough of the Nephrology lecturing though, I think we've covered this topic sufficiently.
 
Last edited:
Problem with this line of thinking is that when you eat a high protein diet, it doesn't increase the amount of protein floating around in your blood stream. When you digest dietary proteins, you break them down into free amino acids that your body can then use to build it's own proteins that have human function. So instead of having proteins floating around in the blood stream, you have free amino acids floating around. With an excess of amino acids, your muscle cells can generate more creatine which is like a little energy shuttle that your muscles use. But creatine naturally re-configures to creatinine after a certain amount of time. Creatinine has absolutely no physiologic function in the body so it's simply filtered out at the kidneys for excretion.

Cool thing about creatinine is that it's freely filtered, not secreted, and not re-absorbed anywhere in the nephron. So you can measure the creatinine excretion in a patient and have a pretty good idea of what their GFR is. That's why you'll hear physicians constantly fussing over creatinine clearances etc, it's a measure of how healthy the kidneys are and has a ton of implications for pharmacology, and for the patient's overall health.

I have to say, I think this question is way outside the scope of the MCAT though.

The AA in the blood get to the proximal tubule and get reabsorbed. They are reabsorbed with sodium. Sodium brings in water, water increases BP, BP increases GFR, GFR increases renal flow. That's the only way to solve this with MCAT-only knowledge.
 
I just think your understanding and explanation (that of a med student) is beyond the scope of the MCAT. I think Med's explanation is apt. In any case increased protein intake will result in increased free A.A, resulting in higher GFR to reabsorb them, and higher renal blood.


In fact, would there ever be a situation when an increase in GFR would result in a decrease in renal blood flow, or vice versa?

The GFR doesn't increase to reabsorb them. The GFR increases as a result on the increase in blood pressure resulting from the increased water absorption resulting from the increased sodium absorption necessary to absorb the increased plasma amino acid content resulting from increased protein ingestion.
 
The AA in the blood get to the proximal tubule and get reabsorbed. They are reabsorbed with sodium. Sodium brings in water, water increases BP, BP increases GFR, GFR increases renal flow. That's the only way to solve this with MCAT-only knowledge.

It's not a bad way to look at it. But it's just not correct. If it helps you understand it then by all means have at it. Just know that you'll have to unlearn it in medical school. The proximal tubule's reabsorption of Na+ and H20 has very little to do with blood pressure.

It might be simpler to strip everything away and just think about the fact that if you increase the plasma AA concentration, then the natural response in the kidney is to secrete more AA in the urine. The only way to do that is to increase the GFR.
 
The only problem I have with this statement is that there's nothing about an increased GFR on it's own that leads to a higher reabsorption rate.

I thought that an increase reabsorption rate would lead to higher GFR, I just finished our section on amino acid synthesis and degradation in biochem so my thought process was ultimately related to that. So I ended up at the right answer but with the wrong reasoning. This could be a reasonable explanation:

"Normal conscious dogs were given 100 mmol glycine, L-serine, L-alanine, L-threonine, L-proline, L-glutamic acid (50 mmol), L-aspartic acid and L-valine by stomach tube. All these amino acids increased glomerular filtration rate (G.F.R.). There was no increase in G.F.R. following L-cystine or D-serine. The intravenous infusion of L-proline, but not glycine, caused increase in G.F.R. The results suggest that the increase in G.F.R. was not due to a high plasma concentration of the individual amino acids but was related to the metabolism of amino acids with production of urea. It is postulated that after meat and during the metabolism of amino acids a factor is released which reaches and acts on the kidney to cause the increase in G.F.R."

from http://www.ncbi.nlm.nih.gov/pubmed/7111666
 
I thought that an increase reabsorption rate would lead to higher GFR, I just finished our section on amino acid synthesis and degradation in biochem so my thought process was ultimately related to that. So I ended up at the right answer but with the wrong reasoning. This could be a reasonable explanation:

"Normal conscious dogs were given 100 mmol glycine, L-serine, L-alanine, L-threonine, L-proline, L-glutamic acid (50 mmol), L-aspartic acid and L-valine by stomach tube. All these amino acids increased glomerular filtration rate (G.F.R.). There was no increase in G.F.R. following L-cystine or D-serine. The intravenous infusion of L-proline, but not glycine, caused increase in G.F.R. The results suggest that the increase in G.F.R. was not due to a high plasma concentration of the individual amino acids but was related to the metabolism of amino acids with production of urea. It is postulated that after meat and during the metabolism of amino acids a factor is released which reaches and acts on the kidney to cause the increase in G.F.R."

from http://www.ncbi.nlm.nih.gov/pubmed/7111666

Postulation (fancy for assumption), rather than observed phenomena. Also published 30 years ago. A lot can change in that amount of time.

My sources are the fact that I'm in the middle of my renal block right now so I'm reading a ton of stuff on ways to manipulate GFR; and the fact that this GFR crap has been done to death by my professors (you'll see someday). And also influenced by what I could dig up on UpToDate.
 
My PR book doesn't even really mention GFR other than that it "depends directly on pressure". Nor does it get into A.A.

My Kaplan book says "glucose, amino acids, and small proteins are freely filtered but should be fully reabsorbed". Now from what I've tried to find on-line and my biochem textbook it would seem that no amino acids should be excreted in the urine. Rather the excess amino acids will simply be broken down into glucogenic and ketogenic intermediates and stored/used as energy and the excess N will be metabolized and excreted as urea.

So my thinking was that because all amino acids should be reabsorbed, a higher GFR due to increased intake of AA will necessarily result in an increased absorption rate. But this is getting further and further away from the question.

I can understand that a high protein diet will lead to a higher GFR, but why will the renal blood flow also necessarily increase in this case?

And I am not trying to drag this conversation on for no reason, first of all I want to understand this more fully and second I think reasoning through things like this is excellent practice for the MCAT.
 
My PR book doesn't even really mention GFR other than that it "depends directly on pressure". Nor does it get into A.A.

Same here. I was thrown off by this question, and I probably would have gotten it wrong. Jesus Christ I'm so underprepared for this.
 
My Kaplan book says "glucose, amino acids, and small proteins are freely filtered but should be fully reabsorbed". Now from what I've tried to find on-line and my biochem textbook it would seem that no amino acids should be excreted in the urine. Rather the excess amino acids will simply be broken down into glucogenic and ketogenic intermediates and stored/used as energy and the excess N will be metabolized and excreted as urea.

There will be trace amounts of amino acid in the urine, large excess indicates some serious problems (inborn errors of metabolism) which we won't get into.

http://www.nlm.nih.gov/medlineplus/ency/article/003366.htm

As I described earlier in this thread, mainly you'd get an increase in creatinine (which is a byproduct of one of the muscle's uses for amino acids), and this is how you'd track and identify an increased GFR. But you are also correct in saying that your urea would increase as well, as proteins were being metabolized. Still, I'd also expect to see an increase (even if it was a modest one) in the free amino acids in the urine.

But now we're splitting hairs and getting way outside what the original question was getting at.
 
Top