Renal Physiology Step 2: Tubular Reabsorption - Online Tutor, Practice Problems & Exam Prep

Tubular reabsorption is crucial for reclaiming essential substances from filtrate, primarily occurring in the proximal tubule, nephron loop, distal tubule, and collecting duct. Key processes include primary active transport via the sodium-potassium pump, secondary active transport for nutrients like glucose, and passive transport through aquaporins. Hormones such as aldosterone and antidiuretic hormone (ADH) regulate reabsorption rates, adapting to the body's needs. Understanding transport maximum and renal threshold helps assess kidney function, indicating how effectively substances like glucose are reabsorbed or excreted in urine.

Introduction to Tubular Reabsorption

Alright. So let's get into tubular reabsorption. Now, a quick note before we begin, this topic is going to involve quite a bit of membrane transport. So things like primary transport, secondary active transport, and passive transport. If you don't remember those very well, I do recommend you go back and refresh your memory before diving in here. We are going to be talking about them, but we're not going to have time to redefine them and go over them in detail. So keep that in mind as we go forward. Now, as we've mentioned previously, tubular reabsorption is the process of moving water and other solutes out of the filtrate and putting them back into the bloodstream. The filtrate is formed at a very high rate. As I've said, about 99% of the filtrate gets reabsorbed back into the blood. And can we just geek out over our kidneys for a second? Because your kidneys filter your entire plasma volume every 24 minutes, which, like, is insane by itself. But then without reabsorption, that means that you would lose all of the plasma in your body through urine in under 30 minutes. Like, insane. Kidneys are incredible. Like, I cannot get over that fact. Like, kidneys are amazing, you guys.

So, as you can imagine, reabsorption is going to prevent the body from losing very useful substances that end up in the filtrate. So water, obviously, electrolytes like sodium, potassium, calcium, nutrients like glucose. We don't want to lose all of that in urine. We want to keep all that good stuff in our body, and that is the whole purpose of reabsorption. Now, there are 2 routes that substances can take when they are being reabsorbed. First is our transcellular route, and this is when substances pass through tubule cells. And I'll show you this in our image in one second. Then, we also have our paracellular route which is when substances pass between tubule cells. So if you look down at our image here, just to kind of orient you to what you're looking at, we're basically looking at like a cross-section of the proximal tubule, and we're kind of zooming in on the wall of that proximal tubule. So that is what you're seeing here in this, like, tannish yellow color. We have this interstitial space in between the tubule and the capillary, and then over on the right of the image is, of course, our capillary. And so, formally, this inside of the tubule is kind of empty space where filtrate would be flowing is called the tubule lumen. And then on the actual cell that makes up the walls of this tubule, we have our apical membrane which is the side closest to our lumen, and our basolateral membrane, which is the side closest to the interstitial fluid. And I always remember that because it just goes in order of like a and then b. So if we're going from the inside out, it's just alphabetical order, apical, and then basolateral. Now what we are looking at here, we can tell that it's definitely the proximal tubule because we have all these microvilli. Remember, the proximal tubule is where about 65% of reabsorption will be happening. And so it needs to have those prominent microvilli to increase surface area. So that is what we are looking at here. So as you can see in this little purple box, we have our transcellular route, and we are going to have our water and other solutes passing right through the middle or anywhere within that cell. And then here in blue, we have our paracellular route where we're going to have water and other solutes squeezing in between the tight junction between these cells. And it is quite a tight junction, but there's usually enough space that these cells are leaky enough that water and very small solutes can just kind of squeak through and get into that interstitial fluid. Alright. So that is our little introduction to tubular reabsorption, and I will see you guys in the next one. Bye bye.

Renal Physiology Step 2: Tubular Reabsorption Example 1

Okay. So what is the route taken by substances being reabsorbed via the transcellular route, which means we're going through the cell? Now our answer choices here are just like a mishmash of anatomy in all different orders. So to help us solve this, I'm just going to draw it out and then we can just label what we're seeing in the order that we're seeing them. So bear with me. It might not be pretty, but we will get there in the end. I'm just going to draw a little, you know, lumen here. So this will be the cavity of our proximal tubule. We're going to draw some tubule cells. These are the microvilli, which I'm sure you knew, but just in case you were like, what the heck is that? Those are the tubule cells. I'm going to label those as TC. We're going to label our apical and basolateral membrane, the number in alphabetical order from the inside out. So the apical membrane is closest to the lumen and then the basolateral membrane is over here closest to the interstitial fluid, which I'm just going to label as IF. And then we'll have our capillary over here, which I will label with a C. We'll just draw that in red there. And our transcellular route is going to, again, take us straight through one of those tubule cells. So in order, we are looking at the lumen, the apical membrane, the tubule cell, the basolateral membrane, the interstitial fluid, and then the capillary, which means our answer is going to be C. So there you have it.

Which of the following is NOT a purpose of tubular reabsorption?

• A. To avoid losing important nutrients in urine such as glucose & amino acids.
• B. To ensure urea is taken back up by the blood.
• C. To maintain fluid balance in the body.
• D. To avoid losing too much sodium.

Map of the Lesson on Tubular Reabsorption

Okay. So reabsorption actually looks slightly different in each part of the nephron. There are different, like, membrane transport processes; different substances are going to be absorbed in different sections. So, I just have a quick little map of how we structured the next few videos just to kind of preface what you're going to be seeing, pretty soon. So, we're going to begin by talking about reabsorption in the proximal tubule, and we're going to have a separate video talking about reabsorption of sodium and other nutrients like glucose. And then we'll have a video talking about the reabsorption of water in the proximal tubule. And then we'll move on to reabsorption in the nephron loop. So we'll be talking about how reabsorption looks in the descending limb versus the ascending limb. Then we will finish by talking about reabsorption in the distal tubule as well as the collecting duct. Those two structures have pretty similar reabsorption. And those structures are unique because reabsorption is partly regulated by hormones in those structures. So we'll talk about that when we get there. All right. So that is our little map of the lesson and I'll see you guys in the next one to start diving into this.

1a) Reabsorption of Sodium & Nutrients in the Proximal Tubule

Alrighty. Let's begin talking about the reabsorption of sodium as well as other nutrients in the proximal tubule. And if you're wondering why sodium gets its name in the title versus, like, potassium or calcium, it's just because sodium is one of the most abundant substances that gets reabsorbed from the filtrate. So that's why it gets its name in the title there. And when I say nutrients, I'm going to be focusing a lot on glucose in this video just because glucose is one of the other most abundant substances that gets reabsorbed by the kidneys. So sodium and glucose are kind of the stars of this video.

Now, reabsorption in the proximal tubule can either be active, which just means that it uses ATP, or it can be passive, which just means that it doesn't use ATP. Now, sodium reabsorption specifically is driven mainly by active transport, and that is going to be primarily through the transcellular route or going right through those tubule cells. Despite this, mainly driving sodium through active transport, sodium and other nutrients can also travel via secondary active transport as well as passive transport. So we're going to go through some specific examples of all of those.

Now, focusing on primary active transport, we are going to have our old friend, the sodium-potassium pump. And gosh, I have missed her. I'm so happy to see her. And this sodium-potassium pump is going to be fairly abundant in the basolateral membrane. So, you guys remember that the basolateral membrane is the one closest to the interstitial base. We go A, apical, B, basolateral, kind of in order there. So we're going to have a whole bunch of sodium-potassium pumps on that basolateral membrane that are going to be actively transporting sodium ions into our interstitial base. You guys remember that our sodium-potassium pumps, we think of our little pumpkin, right? We pump K⁺ in and we toss all that Na⁺ out. So we're going to get, 3 Na⁺ getting chucked out of that valve as we're bringing in 2 K⁺. And so that is kind of the main way that sodium is going to be leaving our proximal tubule cell.

And so if you look down at our image here, just to kind of orient you to what we're looking at, we have our filtrate over here. All these little purple dots that you see represent sodium ions. So these are those prominent microvilli. You can see how that's really going to be increasing the surface area of this proximal tubule. We have our tubule cell here, our interstitial space, and then, of course, our capillary. And so you can see along this basolateral membrane here, we have this little sodium-potassium pump right there, And so that is going to be a form of active transport. K. So it's pumping all of our little purple sodium ions out into our interstitial space where they can then be reabsorbed by that capillary.

Now, you may be wondering, well, how did the sodium get into that tubule cell in the first place? And what a fantastic question. You are on the ball today. And that is going to be via secondary active transport. So what's happening here is that basically because this sodium-potassium pump is working so hard to get sodium out of these tubule cells, this sodium over here in the filtrate now has a pretty steep concentration gradient pulling it toward these tubule cells. Remember, sodium ions are introverted. They want to get out of this crowded filtrate and into this nice quiet tubule cell with no other sodium. And so these pumps establish this concentration gradient, and then sodium ions from the filtrate are going to get pulled into our tubule cell via co-transporters that also carry some kind of specific nutrient. So things like glucose or amino acids. And those are usually moving against their concentration gradient, but the energy that is created by that sodium concentration gradient is enough to pull both of them in. So if you look down at our image, you can see we have this, kind of blue oval right here on the apical membrane now, and that is a sodium-glucose co-transporter. What it's going to be doing is basically pulling in one of our little green glucose and one of our sodium, and they get pulled in simultaneously using the energy from that sodium's concentration gradient. And so that co-transporter is going to pull them both in and put them into that tubule cell. So that is our secondary active transport. I'm going to label that now.

Alright. And then finally, we also have passive transport happening. So this is when solutes travel from the tubule cell into the capillary passively. So either via simple diffusion, and that will typically just be lipid-soluble substances like some vitamins will travel that way, as well as facilitated diffusion. And that will be things like glucose as well as other nutrients as well as other ions even. So if we're thinking of facilitated diffusion, we're usually just thinking of like some kind of nutrient-specific channel that's going to be along that basolateral membrane. So here, we're looking at just a little glucose channel there on that basolateral membrane that will allow the glucose to leave the cell. So that is our passive transport.

So just to summarize what's happening here really briefly, we have some glucose and some sodium hanging out in our filtrate. Those are going to simultaneously get pulled into our tubule cell via secondary active transport through this sodium-glucose co-transporter. That's going to be using the energy of the concentration gradient of the sodium. So now they are both in our tubule cell, but they're going to take different routes to get out of it. So our sodium is going to get sucked out of the cell, via primary active transport with the sodium-potassium pump, and that will dump it into our interstitial space where it can then enter our capillary. And then our glucose will just travel through this tubule cell and then exit passively via this glucose channel, enter our interstitial space, and then enter our capillary from there. Alright. So that is our little summary of reabsorption of sodium and other nutrients in our proximal tubule, and I'll see you guys in our next one. Bye-bye.

Renal Physiology Step 2: Tubular Reabsorption Example 2

Alright. So, which of the following substances primarily utilizes secondary active transport at the apical membrane and facilitated diffusion at the basolateral membrane? Based on what we just discussed, both sodium ions and glucose are entering the tubule cells using secondary active transport. These typically utilize cotransporters, like the sodium-glucose cotransporters. Just as a quick aside, both water molecules and urea tend to move through more passive transport means.

Both sodium and glucose will enter our tubule cell using secondary active transport. However, only one of them uses facilitated diffusion at that basolateral membrane. Remember, the basolateral membrane is going to have quite a few sodium-potassium pumps. This is a form of primary active transport and that will be the main form of transport that sodium will take during the process of reabsorption. On the other hand, glucose will be traveling through more passive means through the glucose channel. So, our answer here is going to be glucose; it primarily utilizes secondary active transport at the apical membrane and then facilitated diffusion at the basolateral membrane. And there you have it.

Which of the following solutes are primarily reabsorbed by primary active transport?

• A. Potassium ions.
• B. Sodium ions.
• C. Urea.
• D. Glucose.

1b) Passive Reabsorption of Water & Solutes in the Proximal Tubule

Okay. So let's get into the passive reabsorption of water in our proximal tubule. And we're also going to be talking a bit about solutes here as well, because what happens in the proximal tubule is that water and solute reabsorption follows kind of a cyclical pattern. So first, like we just talked about, we're going to see all this movement of sodium and other solutes. You can see here in our capillary, we have all of this sodium and glucose, and all of these solutes have left the tubule cell, and they're now hanging out in the interstitial distal base. They're going to hang out in that capillary. And the movement of all of those solutes is going to establish a strong osmotic gradient. Remember, water wants to move toward high concentrations of solute. So, now all of our little water molecules over here are being drawn toward those high solute concentrations in the interstitial space and the capillary. And so, this osmotic gradient causes water molecules to be reabsorbed via aquaporins. You can see we have our little aquaporins here on our apical membrane of our tubule cell as well as our basolateral membrane, and those water molecules will just travel right through those aquaporins following that osmotic gradient to get them closer to those high solute concentrations. And this is sometimes known as obligatory water reabsorption. And it's called that because the water is basically obliged to follow that osmotic gradient. So now we have a whole bunch of water hanging out in our capillary, and that is going to create a steep concentration gradient for other solutes in the filtrate because now the filtrate is becoming more and more concentrated. And those solutes want to escape the high concentrations and they want to go toward low concentrations. So these solutes essentially follow the water. And so all of these solutes over here in the filtrate are going to be drawn away from these high concentrations toward low concentrations. And so you can see how it basically, the reabsorption of solutes and water essentially creates a cyclical pattern that drives really fast and very efficient reabsorption in the proximal tubule. And that is how we get the whole much of that filtrate reabsorption happening in that very tiny section of our nephron.

Alright. So I'll see you guys in our next video. Bye bye.

Renal Physiology Step 2: Tubular Reabsorption Example 3

What is the primary driving force that causes water to follow salt out of the tubule and into the capillary? Remember, when sodium and all those other solutes are leaving the filtrate and entering the capillary, that creates a strong osmotic gradient, which draws the water toward those high concentrations of solute. So our answer here is an osmotic gradient. Let's just keep in mind that the presence of aquaporins is what allows the water to follow all of that salt, but the aquaporins themselves are not driving the water movement at all. Aquaporins do not pull water into them or anything like that. The water is following its osmotic gradient and the aquaporins are just acting as a channel through which water can move. Movement through aquaporins is considered passive. It is not considered a form of active transport. So, the primary driving force of water movement in the proximal tubule is going to be its osmotic gradient.

In the proximal tubule, _________ ions are pumped out of the tubule via ____________ transport. This creates an ____________ gradient, causing water to be reabsorbed through _______________.

• A. Potassium; active; osmotic; gaps between cells.
• B. Sodium; passive; osmotic; aquaporins.
• C. Potassium; active; ionic; gaps between cells.
• D. Sodium; active; osmotic; aquaporins.

2) Reabsorption in the Nephron Loop

Alright. Let's get into reabsorption in our nephron loop now. So for the most part, reabsorption in the nephron loop is going to be employing the same mechanisms that we saw in the proximal tubule. However, the permeability of our descending and ascending limbs actually differ. So, they are basically permeable to different substances. Now, one thing to note is that about 65% of the filtrate gets reabsorbed in our proximal tubule and that includes about 65% of water and 65% of ions, as well as over 99% of organic solute. I'm going to write that like this. So that includes things like glucose and amino acids. So for all intents and purposes, organic solutes are basically out of the filtrate by this point. And once filtrate reaches our nephron loop, it is mostly water and ions with sodium, of course, being the most abundant of those ions. Of course, there's also some waste products in here as well like urea, which don't get reabsorbed. So mostly water and ions. So, we're going to go through our descending and ascending limbs separately talking about what water and ion reabsorption looks like in each one.

Starting with our descending limb. Our descending limb contains abundant aquaporin. And so, in this limb, water is going to get reabsorbed via osmosis the exact same way that we saw in the proximal tubule. However, our descending limb is impermeable to ions. There are no cotransporters. There is no sodium-potassium pump. There is none of that. Thus, there is no ion reabsorption happening in the descending limb at all. So, if you look at our image here, we have the capillary over on the left. We have the lumen of the tubule here on the right, and our little tubule cells. And they do look quite different than what we just saw previously. The tubule cells in the descending limb are quite skinny and small, so that's why they look so different. And you can see we've got aquaporins all along that basolateral membrane and a ton of water movement happening. And about 20% of water is going to get reabsorbed in our descending limb. And, again, no ion reabsorption at all happening here.

Now, moving over to our ascending limb. Here, aquaporins are going to be very scarce. And so, basically, osmosis does not occur and we really don't have any water movement happening here. However, there is plenty of ion movement happening. So we're going to have some secondary active transport happening along our apical membrane and some primary active transport happening along our basolateral membrane. And so, if you look at our image, we have the lumen of the tubule and you can see it's all full of ions. We've got our purple sodium, our pink potassium, our little orange chloride there. I mean, we've got cotransporters all along that apical membrane, and we've got our sodium-potassium pumps along that basolateral membrane there. So we've got all kinds of active transports of ions happening and about 25% of ions are going to get reabsorbed in the ascending limb of the nephron loop.

Alright. So that is our reabsorption in the nephron loop. And I'll see you guys in the next video. Bye bye.

Renal Physiology Step 2: Tubular Reabsorption Example 4

Okay. So this is a true or false question. If it's false, we're going to be correcting the statement. The descending limb of the nephron loop is very permeable to water, but impermeable to ions. And that is true. Right? Our descending limb is abundant in aquaporins, which allows for a huge amount of water reabsorption. About 20 to 25 percent of the water in our filtrate will get reabsorbed in that descending limb. However, there is a notable absence of transporters and pumps that makes it fairly impermeable to ions. So our answer here is that this is true.

Predict what would happen if the tubule wall of the descending limb suddenly lost all its aquaporins.

• A. More reabsorption would occur in the nephron loop.
• B. Urine would be higher in volume & more dilute.
• C. Urine would be lower in volume and more concentrated.
• D. Urine would have the same volume but be more concentrated.

3) Reabsorption in the Distal Tubule and Collecting Duct

Okay. So let's dive into the reabsorption in the distal tubule and the collecting duct, which, in my opinion, is the coolest type of reabsorption. Though, one thing to note is that reabsorption in the proximal tubule and the nephron loop tends to occur at a pretty constant rate. Now, it just kind of is what it is, but the distal tubule and the collecting duct kinda shake things up a little bit. The reabsorption in these locations actually varies depending on your body's need. So, there are actually 4 main hormones that can influence the rate at which certain substances are going to be reabsorbed within our distal tubule and our collecting duct. So I always think of these as kind of like our little urine customization sections of our nephron where, like, you know, maybe your body needs a little more water to be retained. They can handle that. Maybe you have to get rid of some salt. Maybe you have to reabsorb some calcium, you know, who knows? Your distal tubule knows, which is like so cool, right? So we're gonna go over these 4 hormones and we'll talk a little bit about what they each do. So first up, we have our old friend aldosterone. Remember him from the renin-angiotensin-aldosterone system mechanism. So this is our salt-retaining hormone, remember, and it's going to increase the rate of sodium reabsorption. So it's making sure that sodium is leaving the filtrate and getting put back into the blood. And this can actually create an osmotic gradient that will also increase water reabsorption via osmosis. Remember that from the renin-angiotensin-aldosterone mechanism. So the aldosterone itself specializes in salt retention and salt reabsorption, but it can have the indirect effect of more water reabsorption as well. So if you look at our image here, number 1, I'm gonna label this as aldosterone flora. And you can see we've got sodium channels over here on the apical membrane. We've got sodium potassium pumps here on the basolateral membrane, and a whole bunch of sodium reabsorption is going on in that image there.

Alright. Next up, we have our atrial natriuretic peptide or ANP. And this is basically the opposite of Aldosterone. So it's going to actually reduce the rate of sodium reabsorption. Which just means that sodium is going to be staying in the filtrate and it will end up in the urine. So if you look down at our image, you see number 2. We have our atrial natriuretic peptide there. I mean, we've got all these little sodium ions just hanging out and they're not really doing anything. They're not getting reabsorbed. They're just kinda sitting in that filtrate and they're gonna end up in the urine. And I always remember that this one deals with salt because I look at that NA in natriuretic, and I think NA means sodium. So that's how I remember that one.

Next up, moving on from sodium, we have an antidiuretic hormone or ADH. And an antidiuretic hormone is pretty intuitive based on its name. So it's going to reduce the volume of urine by increasing the rate of water reabsorption. Of course, a diuretic would put more water into the urine and it would increase urine volume, and so our antidiuretic is doing the opposite. It's helping us reabsorb water, and then it's reducing the urine volume, through that reabsorption because it's all ending up back in our blood. So looking at our image on number 3, we have our antidiuretic hormone, and you can see we've got little aquaporin here, and they are helping water get reabsorbed and put back into the blood.

And then finally, we have our parathyroid hormone or PTH, and this will be stimulating calcium reabsorption specifically in the distal tubule. So if you look down at our last image, we have our parathyroid hormone, and you can see we have all of our little triangular calcium ions there and they are getting reabsorbed and put back into the blood. Alright. So those are kind of the 4 main hormones that work in our distal tubule and our collecting duct, and that is how they kind of customize our urine which is so neat, Alright. So I'll see you guys in our next video. Bye bye.

Renal Physiology Step 2: Tubular Reabsorption Example 5

Okay. So which hormone causes aquaporins to be inserted in the wall of the collecting duct? If we're going to be inserting aquaporins into the wall of the collecting duct, what that will do is increase water reabsorption. And out of all the hormones listed here, the one that deals with water reabsorption is our antidiuretic hormone. So that is our answer. Remember how that name is nice and intuitive. It's basically the opposite of a diuretic. A diuretic would increase the amount of water that ends up in the urine. This is doing the opposite; it's increasing the amount of water that is being reabsorbed. Remember, our aldosterone and our atrial natriuretic peptide both work with sodium, and our parathyroid hormone focuses on calcium. So this one would be our antidiuretic hormone.

Dr. Miller is a pediatric nutritionist working with a patient who has a low dietary calcium intake. Concerned about the possibility of hypocalcemia, she orders bloodwork. What hormone would you expect to be elevated in this patient’s bloodwork?

• A. Aldosterone.
• B. Atrial Natriuretic Peptide.
• C. Antidiuretic Hormone.
• D. Parathyroid Hormone.

Transport Maximum (TM) & Renal Threshold

In this video, we're going to be talking about transport maximum and renal threshold, and these are both constructs that give us information about our kidney's ability to reabsorb certain substances and they can also be useful indicators of health. So transport maximum is the maximum amount of a substance that can be reabsorbed within a certain unit of time and it's measured in milligrams per minute. Now, transport maximum is generally reflective of the number of transport proteins that are in the renal tubule that can actually carry or ferry that substance, across that tubule cell and into that interstitial space to get reabsorbed. And, generally speaking, what we see is that for substances that we really want to reabsorb like water, glucose, sodium, we have plenty of transport proteins because we don't want to hit transport maximum for those. We want to be able to reabsorb as much of that as we can. Whereas for substances that, you know, we don't really care about reabsorbing, like urea, for example, we're going to have very few if any transport proteins. Now what can happen is that when all transport proteins are saturated, any excess of that substance is going to get excreted into the urine. So if you look at our little cartoon here, we have this lovely little riverbank going on and this, little tan sandy area is our filtrate and we have our little green glucose. And you can see that the glucose are trying to leave the filtrate and cross through this channel protein, this little bridge here. They're trying to get into that interstitial space to get reabsorbed. Now what has happened here is that this little bridge, this, channel protein is at capacity. It is fully saturated. And now these glucose are basically stuck in the filtrate. They have no way to get reabsorbed and they are going to end up in urine. And that's why a really common example of transport maximum is going to involve, glucose levels and diabetes because what's going to happen is in some diabetics, they're going to have a lot of glucose in their blood which means they have a lot of glucose in their filtrate. And what happens is that, you know, they basically hit transport maximum for glucose. All of those channel proteins get totally saturated and maxed out and there have an abundance of glucose in the filtrate that cannot get reabsorbed. And so they'll have high glucose levels in their urine. So that can be indicative of hyperglycemia. So that is transport maximum. Now, renal threshold is the blood concentration or the plasma concentration at which a given substance will begin to appear in the urine. And, this is measured in milligrams per deciliter. So to continue with our glucose example, in a typical healthy adult, the renal threshold for glucose is about 180 milligrams per deciliter. Now imagine, for example, in my body right now, my glucose my blood glucose level was about 160 milligrams per deciliter. So at that point, I have not hit renal threshold yet, which means that all of this glucose can get reabsorbed. And that that's all going to go right back into my bloodstream. I can use it for energy. That's great. Now let's imagine my current glucose level was 220 milligrams per deciliter. At that point, I have hit renal threshold, which means we are going to start to see glucose in my urine. So my blood glucose level has hit renal threshold, and we're going to start to see the excess, glucose entering my urine. Now, I know at first glance, these can seem like very similar constructs, but they are measuring very different things. So keep in mind that transport maximum is looking at the maximum amount of a given substance that can be reabsorbed within a certain unit of time at a certain rate basically. Whereas renal threshold is examining the blood concentration at which that given substance is going to start appearing in urine. So they are related concepts, but they are measuring, and looking at very distinct things. Alright. So I will see you guys in our next video. Bye bye.

Renal Physiology Step 2: Tubular Reabsorption Example 6

Alright. So, in which of the following conditions would you expect to see high levels of glucose in the urine? If we are seeing glucose in the urine, that means we have reached our renal threshold for glucose, which, as a reminder, is the blood concentration or the plasma concentration at which that substance would appear in the urine. So, if we're seeing glucose in the urine, that means we have an excess of glucose in our blood, which is what is making us hit that renal threshold. Based on these answer choices, that would be hyperglycemia or an excess of glucose. Obviously, hypoglycemia would have our glucose levels below the renal threshold, so we would not be seeing it in the blood at all. Hypercalcemia involves too much calcium, so we'd be seeing more calcium in the urine. Lupus is an autoimmune disease, which is unrelated to seeing glucose in the urine. So, our answer here is hyperglycemia.

Ryan just ate a very protein-rich meal. Because of this, the amino acid levels in his blood currently exceed the transport maximum and the renal threshold for amino acids (65 mg/dL). What will happen to the excess amino acids?

• A. They will be reabsorbed.
• B. They will bond to sodium ions.
• C. They will end up in the urine.
• D. They will build up in the nephron.

Review of Tubular Reabsorption

Okay. So we have learned a lot in this section. There's a lot of information in here. We're just going to do a quick review to help us kind of step back and process the most important takeaways. We're going to go over each section of the renal tubule and talk about what type of reabsorption that section specializes in. So as a quick summary, reabsorption helps our body reclaim important substances from the filtration. So starting with our proximal tubule, we're going to be reabsorbing a little over 99% of glucose and other organic volumes. So things like amino acids and vitamins. So that gets reabsorbed almost in its entirety right off the bat. This area will also be reabsorbing about 65% of the water from the filtrate and about 65% of the ions. So things like sodium, potassium, chloride, and calcium. There's a lot going on in that proximal tubule very quickly. Keep in mind that this tubule has those microvilli to really help increase surface area to make all that reabsorption possible. So then, moving on to the descending limb of our nephron loop. We're going to be reabsorbing about 20% of the remaining water. Remember the descending limb is impermeable to ions but is highly permeable to water. And then in our ascending limb, we see kind of the opposite pattern where here we're reabsorbing about 25% of the remaining sodium and chloride. And then, finally, in our distal tubule and our collecting duct. Honestly, by this point, we are reabsorbing most of the remaining water and solute. Keep in mind that 1% or even less than 1% of the filtrate. So that is kind of our quick little review there. I hope that that was helpful, and I will see you guys in our next video. Bye-bye.

Renal Physiology Step 2: Tubular Reabsorption Example 7

Okay. So how much of the water filtered through the glomerulus is normally reabsorbed in the proximal tubule? Remember that the proximal tubule is doing the bulk of reabsorption in general and reabsorption of all materials, ions, water, and solutes is quite high. So we're looking more at the right side of the screen over here at this at C and D. Now it's not going to be as high as D. The only thing that gets reabsorbed at a rate of about 99% in the proximal tubule is going to be glucose and other organic solutes. So our answer here is C, about 65% of the water from the filtrate will get reabsorbed in the proximal tubule.

In which section of the nephron is the process of reabsorption influenced by hormones?

• A. Proximal Tubule.
• B. Descending limb of nephron loop.
• C. Ascending limb of nephron loop.
• D. Distal tubule & collecting duct.

Here’s what students ask on this topic:

What is tubular reabsorption and why is it important?

Tubular reabsorption is the process by which the kidneys reclaim water and essential solutes from the filtrate back into the bloodstream. This process is crucial because it prevents the loss of vital substances such as water, electrolytes (e.g., sodium, potassium, calcium), and nutrients (e.g., glucose) in the urine. Without reabsorption, the body would lose all its plasma volume in under 30 minutes, leading to severe dehydration and nutrient deficiencies. Reabsorption ensures that the body maintains homeostasis by retaining necessary substances while excreting waste products.

How does the sodium-potassium pump function in tubular reabsorption?

The sodium-potassium pump (Na⁺/K⁺ ATPase) is a primary active transport mechanism located in the basolateral membrane of tubule cells. It actively transports 3 Na⁺ ions out of the cell and 2 K⁺ ions into the cell, using ATP for energy. This creates a concentration gradient that facilitates the reabsorption of sodium from the filtrate into the tubule cells. The gradient also drives secondary active transport, allowing other nutrients like glucose to be co-transported with sodium into the cells. This process is essential for maintaining electrolyte balance and fluid homeostasis in the body.

What are the differences between transcellular and paracellular routes in tubular reabsorption?

In tubular reabsorption, substances can take two routes: transcellular and paracellular. The transcellular route involves substances passing through the tubule cells, crossing both the apical and basolateral membranes. This route often involves active and passive transport mechanisms, such as the sodium-potassium pump and aquaporins. The paracellular route, on the other hand, involves substances passing between tubule cells through tight junctions. This route is typically used for the reabsorption of water and small solutes, which can move through the leaky junctions between cells. Both routes are essential for efficient reabsorption in the kidneys.

How do hormones like aldosterone and ADH regulate tubular reabsorption?

Hormones such as aldosterone and antidiuretic hormone (ADH) play crucial roles in regulating tubular reabsorption. Aldosterone increases sodium reabsorption in the distal tubule and collecting duct, which indirectly promotes water reabsorption due to the osmotic gradient created. ADH, on the other hand, directly increases water reabsorption by inserting aquaporins into the membranes of the distal tubule and collecting duct cells. This reduces urine volume and helps maintain body fluid balance. These hormones allow the kidneys to adapt reabsorption rates based on the body's needs, ensuring homeostasis.

What is the transport maximum (Tm) and renal threshold in the context of tubular reabsorption?

Transport maximum (Tm) is the maximum rate at which a substance can be reabsorbed by the kidneys, measured in mg/min. It reflects the number of transport proteins available in the renal tubules. When these proteins are saturated, any excess substance is excreted in the urine. Renal threshold is the plasma concentration at which a substance begins to appear in the urine, measured in mg/dL. For example, the renal threshold for glucose is about 180 mg/dL. If blood glucose levels exceed this threshold, glucose will appear in the urine, indicating that the transport maximum has been reached.