Supersimplified Pathology | Renal pathology Glomerulonephritis E01| Dr. Priyanka Sachdev

Hello everyone, a very, very good morning to all of you. I hope I'm clearly visible and audible to you guys. Am I? If I'm clearly visible and audible to you, please give me a thumbs up in the chat box. Okay, I guess it's working, and I am clearly visible and audible to all of you.

So, a very, very good morning to all of you. I welcome you all for today's session. I am Dr. Priyanka Sajdev here, and today I am here to teach you renal system pathology. Now, renal system is one of the complicated systems in which students find difficulty in understanding the various diseases, various pathologies. So, I will be teaching you, first of all, the most important pathology in the renal system, the various types of glomerulonephritis, in a super simplified manner, in a comparative manner. So, I will teach you everything about glomerular nephritis.

But before jumping on the pathology, that is glomerulonephritis, it's important to understand the anatomy of the kidney, the anatomy of the nephron, what is the structure of the glomerulus, without which you cannot understand glomerulonephritis, and the physiology of urine formation. So, in the first five to ten minutes, a little bit about the anatomy, physiology, and histology, normal histology. Then it will be easy for you to understand the diseases. Can I start now? Can I start? Give me a thumbs up.

So, here you can see in this diagram, humans have a pair of kidneys. So, in this diagram, you can see kidneys are the bean-shaped organs, and all humans, I guess, have a pair of kidneys. On the medial surface of the kidney, there is a point, uh, at the midpoint of the medial surface of the kidney. This point is known as the hilum of the kidney. At the hilum of the kidney, the renal artery enters into the kidney, the renal vein comes out of the kidney, and the ureter comes out of the kidney, and lymphatics are present. So, you can see this is the renal artery entering the kidney, renal vein coming out of the kidney, ureter coming out of the kidney, and lymphatics are present. So, this point is very important in the kidney, and it is the, uh, known as the hilum of the kidney.

So, after that, you can see this is a kidney. Inside the kidney, uh, the structural and the functional unit of the kidney is a nephron. So, can you appreciate a nephron? Yes. So, inside each kidney, nearly one million nephrons are present. So, humans have a pair of kidneys. So, nearly, humans have, normal healthy human beings have two million nephrons, and nephrons are the structural and functional unit of the kidney.

So, let me show you the diagram of a nephron before coming on the various pathologies. So, you can see in this diagram, we can see a nephron. Can you see a nephron? Yes. So, we can see the five portions of the nephron. What are the five portions of the nephron? The first portion of the nephron is Bowman's capsule. Can you appreciate this capsulated structure? This is known as Bowman's capsule. Along with the Bowman's capsule, uh, the tuft of capillaries present inside the Bowman's capsule is known as glomerulus. So, the first structure of the nephron is glomerulus.

So, today I am going to teach you the various types of glomerulonephritis. I will be teaching you all types of glomerulonephritis, the primary one, the secondary one, the hereditary one. So, before that, you must understand the structure of the glomerulus, so that the inflammation of the glomerulus will be glomerulonephritis. Itis, it is the inflammation of the glomerulus, right?

The second portion of the nephron is a tubule. It is known as the proximal convoluted tubule, that is PCT. You can see the third portion of the nephron is the loop of Henle. You can appreciate this is the loop of Henle, having two limbs. The first limb is the descending limb, and the second limb is the ascending limb. Can you see the fourth portion of the nephron? You can appreciate here is DCT, that is distal convoluted tubule. And the last portion of the nephron, you can appreciate here, it is the collecting duct.

Now, these four portions, that is PCT, loop of Henle, DCT, and collecting duct, that is this all portion apart from glomerulus, these are known as tubules. These are known as tubules. So, we have glomerulus in the nephron, we have various types of tubules in the nephron, and the background. Can you appreciate the background? The background around the tubules. This is all background around the tubules. This background is known as interstitium.

So, in the kidney, various types of diseases, basically four types of diseases are present inside the kidney. So, when the diseases involve the blood vessels of the kidney, can you appreciate here are the blood vessels? So, it is known as vascular diseases of the kidney. The diseases which involve the glomerulus of the kidney are known as glomerular diseases, that is glomerulonephritis. The diseases which involve tubules of the kidney are tubular diseases, and the diseases which involve interstitium of the kidney are interstitial diseases. Now, usually tubules and interstitium are always involved together. That's why we have a combination, tubular interstitial diseases, in the kidney, right?

So, after that, let me move ahead. So, we have already seen the five portions of the nephron. You can see the first portion of the nephron is glomerulus, the second is PCT, then loop of Henle, then DCT, then collecting duct. And nephrons are the structural and functional unit of the kidney. Now, you have seen the diagram of the nephron. Let me have an overview on the anatomy of the kidney and move ahead on the topic that is glomerulonephritis.

Now, in the kidney, we can divide the kidney into three portions: cortex, medulla, and pelvis. So, here you can see in this diagram of the kidney, you can appreciate the three structures of the kidney. The outermost is the cortex. Can you appreciate the outermost thin rim? This outermost thin rim, one centimeter thin rim, this is cortex. This is cortex. This portion is medulla, the middle one. And the innermost, this yellow portion, is the pelvis. So, we can divide the kidney from outer to inner into three portions. The outermost thin rim is cortex, the middle one in which these pyramids are present. So, pyramids are present in the medulla. This is an entire medulla, having multiple pyramids. And the innermost yellow portion, you can see here, that is the pelvis.

Now, nephrons are present where? The nephrons are present in these. The nephrons are basically present in the cortex. The nephrons, all the one million nephrons are present in the outermost one rim, outermost one centimeter thin rim of the kidney. All the neurons are present. All the nephrons, I'm sorry, all the nephrons are present. So, cortex is about one centimeter thick. It is the outermost rim of the kidney. You can appreciate the outermost rim. It is the cortex, right? So, that is the cortex. We have seen.

Now, let me cut a section of the kidney from here. If I cut the section of the kidney from here, I can see this is the outermost cortex. This one, this portion is the outermost cortex. You can see, and the inner portion is the medulla. You can appreciate this inner portion is the medulla. So, in this diagram, you can see this is the outermost cortex, I am talking about, and this is the inner medulla, I am talking about. So, outer, this one is cortex, from here to here, it's cortex, and this portion is medulla. You can appreciate this portion is medulla. This portion is cortex. So, I hope you got it. What is cortex?

Now, based on the location of the nephron, nephrons in the kidney are of two types. I have told you, inside the kidney, one million nephrons are present. So, where they are present? Where no, there are no. See this diagram, you can appreciate the cortex and medulla with change in color, yes? Now, there are some nephrons, the complete nephron is inside the cortex only. All the five portions of the nephron is inside the cortex only. Can you appreciate this nephron? So, you can see this is the glomerulus, this is, this is PCT, this is loop of Henle, this is DCT, this is collecting duct. All the five portions of the nephron is inside the cortex only. Such nephrons are known as cortical nephrons, because the complete nephron is present inside the cortex, right? So, such a nephron is known as cortical nephron.

Now, see this nephron. I'm marking another nephron for you. Can you appreciate this one? This nephron, in which glomerulus, PCT, DCT, and collecting duct, these are present in cortex, but the loop of Henle is going in medulla only. Loop of Henle is going in medulla, not in cortex, in contrast to the loop of Henle of the other nephron, in which everything was in cortex. Here, loop of Henle is going in medulla. Such a nephron is known as juxtamedullary nephron. So, juxtamedullary nephrons are the nephrons in which glomerulus are still in cortex, but the tubule, the loop of Henle is going in the medulla. So, basically, summary is that all the nephrons, 100% of the nephrons, glomerulus lie in the cortex only, whether the nephron is cortical or whether nephron is juxtamedullary. The glomerulus is always, always, always in the cortex of the kidney.

Now, depending on the type of the nephron, tubules may be in cortex, may be in medulla. But 85% of the nephrons are cortical, out of total 100%, in which the complete nephron is in the cortex. And 15% nephrons are juxtamedullary nephrons, in which loop of Henle is going in the medulla. Give me a thumbs up in the chat box if you got the meaning of the two types of nephrons. These are the basics, I guess you know. So, you can appreciate the two types of nephrons here. Can you appreciate the first type of nephron is cortical nephron, which are 85% of the total nephrons, in which glomeruli as well as complete tubules lie in the cortex only. The complete nephron is in the cortex only. On the contrary, the other type of the nephrons are juxtamedullary nephrons, which are nearly 15% of the nephrons, in which nephrons send their loop of Henle. The loop of Henle are going in the medulla. Give me a thumbs up if you got the two types of nephrons.

Now, coming on the second portion of the kidney is medulla. You can see just below the cortex. This is medulla. Let me draw the boundary. Let me draw the boundary of the medulla. So, medulla is starting from here and ending here. Can you appreciate? So, inside the medulla, you can appreciate multiple pyramidal structures are present. These pyramidal structures are known as renal pyramids. These pyramidal structures are known as renal pyramids, and renal pyramids are present inside the medulla.

Now, the tip of the pyramid, can you see the apex of the pyramid? The apex of the pyramid is known as papillae. So, whatever urine or filtrate or urine formed here, it will be sent into the pelvis of the kidney via these papillae. So, can you see? So, inside the medulla, there are multiple pyramids. These pyramids are known as renal pyramids. The apex of the pyramid is known as renal papilla, the opening for the urine into the pelvis. So, we have seen medulla also. We have seen cortex also. Medulla also, right?

Now, you can see between the adjacent pyramids, the portion of the kidney between two adjacent pyramids. This portion of the kidney, this portion of the kidney, this portion between two adjacent pyramids, the portion of the kidney, it is known as renal column of Bertin. It is known as renal column of Bertin. Can you see the renal column of Bertin? So, what is? Does the empty queue, you know, what is renal column of Bertin? So, you can appreciate renal column of Bertin. It is the column of renal tissue between adjacent pyramids. So, that is renal column of Bertin.

After that, coming on the third portion, that is pelvis. Can you see the yellow color portion in this diagram? Let me go to the diagram. The yellow color portion is the pelvis. Now, in the pelvis, there are calyces. Can you see one, two, three? This one is the fourth, fifth, sixth, seventh, in this diagram, I can see seven minor calyces. All these are minor calyces. So, pyramids are opening in minor, in minor calyces. So, these are known as minor calyces. So, how many minor calyces are there in this diagram? And how many normally are present in a kidney? So, let me show you, there are eight to eighteen minor calyces. So, in this diagram, we can see seven to eight in number. And minor calyces open in major calyces. So, you can appreciate these three are opening in this, this structure. These three are opening in the structure. And these, so these are the few major calyces. So, minor calyces open in major calyces, and major calyx opens into the ureter. So, ultimately, this is how ureter of the kidney is formed.

So, whatever urine formed here in the nephron, I told you one million nephrons are present here in the cortex. So, in the cortex, the glomerular filtration is formed. After that, urine is formed. So, urine goes in the pyramid, that is in medulla. From the pyramid, it is coming into the minor calyces. From minor calyces, that is coming to major calyces. And from major calyces, it comes to the ureter. So, and from ureter, of course, it will go to the bladder and it will be voided out of the body through urethra. So, this is the complete pathway how urine formation takes place.

Now, I will teach you the complicated topic, glomerulonephritis. Itis, it is the inflammation of the glomerulus. You cannot understand glomerulonephritis if you don't understand the structure of the glomerulus in a nephron. Now, you know what is kidney, you know what is the structural and functional unit of the kidney, that is a nephron. Inside the nephron, we are having five portions. You already know that. The first portion of the nephron is the glomerulus.

Now, let me teach you the structure which is very complicated, the structure of the glomerulus. Once you've got the structure of the glomerulus, it will be easy for you to understand the inflammation of the glomerulus. So, that the disease, glomerulonephritis, will become very easy, or it will become fun for you. So, let me teach you glomerulus. So, what is glomerulus? I guess everyone knows that this is glomerulus.

So, in this glomerulus, can you see? Can you see that this is the artery entering inside the glomerulus? This is known as afferent arteriole. Afferent arteriole. This is Bowman's capsule. This yellow color structure, it is a capsulated structure. It is the Bowman's capsule. Now, inside the Bowman's capsule, afferent arteriole comes, forms multiple, multiple capillaries, a tuft of capillaries. Can you appreciate these multiple tufts of capillaries? A bundle of capillaries are there, and then exit out, drain out in the form of efferent arteriole. So, first, afferent arteriole is coming, forming a tuft of capillary, and exit out as efferent arteriole. Have you got it? Give me a thumbs up if you got it. So, okay. So, this is the thing.

And after exiting out, what happens to this efferent arteriole? Can you see this efferent arteriole? Once it exits out, after that, it will form a bunch of capillaries over the tubules. The bunch of capillaries over the tubules, that is the continuation of the efferent arteriole. This is known as peritubular capillaries or vasa recta. So, this is the normal structure. Vasa recta or peritubular capillaries that is formed by the efferent arteriole once it comes out of the Bowman's capsule. So, okay.

In this diagram, you can see the vasa recta. Can you see in this diagram? Please everyone appreciate this afferent arteriole. This one is afferent arteriole. It is entering inside the Bowman's capsule. Appreciate the Bowman's capsule first. After entering in the Bowman's capsule, it is forming multiple tufts of capillaries. And then it exits out in the form of efferent arteriole. After exiting out in the form of the efferent arteriole, this efferent arteriole forms a bunch of capillaries over the tubules. By tubules, I mean the fourth thing, that is proximal convoluted tubule, PCT, loop of Henle, DCT, and collecting duct. So, the efferent arteriole forming a bunch of capillaries over all the tubules, it is known as vasa recta or peritubular capillaries.

So, you hear also, you can appreciate this is renal artery. Can you appreciate this is renal artery? From the renal artery, this is afferent arteriole coming out. It is entering inside the Bowman's capsule. Appreciate the Bowman's capsule. After entering inside the Bowman's capsule, it is forming a tuft of capillaries. And then it exits out in the form of the efferent arteriole. Once efferent arteriole exits out of the Bowman's capsule, it will form a tuft of capillary over the tubules, that is vasa recta. I guess everyone got it, right?

Now, before understanding glomerulonephritis, what is glomerulonephritis? It is the inflammation of the filtration barrier inside the glomerulus. So, you must ask me, ma'am, what is this filtration barrier inside the glomerulus? Okay. So, look at this diagram. I will zoom this portion for you. You can understand this diagram. You can see this is Bowman's capsule, right? You can see this is afferent arteriole entering inside the Bowman's capsule. It is forming multiple tufts of capillaries. I will draw only one to explain you, and then it exits out in the form of efferent arteriole. Let me zoom this structure for you.

So, can you see in this diagram? What I have drawn? You tell me. In this diagram, you can appreciate this is the Bowman's capsule, the blue one. This one is the Bowman's capsule, which is continued as PCT. So, Bowman's capsule is continued as PCT. We can see. So, this is the Bowman's capsule. Now, please give me a thumbs up. Have you got it? Have you got it, gaming? Have you got it? Others are new. Have you got it? This is the Bowman's capsule continued as PCT, right?

Now, this is the afferent arteriole. Can you appreciate it? It is the afferent arteriole entering inside. I have drawn only one tuft of capillary. It is forming one tuft of capillary. Can you see it is forming one? There are multiple, but for the sake of understanding, we have drawn only one capillary loop. And it exits out in the form of efferent arteriole. So, this is afferent arteriole entering, forming the capillary, and exit out as efferent arteriole. Is there any problem in understanding that? I guess no. It is there is no problem in understanding that.

Now, uh, whatever blood is entering in the afferent arteriole, the blood is entering here in the afferent arteriole. Whatever substances present in the blood, which are here, are the substances present in the blood which are supposed to get excreted, which are supposed to get excreted in the urine, in the urine. They will get filtered here, glomerular filtration. They will get filtered here, and they will accumulate in Bowman's space. This space is known as Bowman's space. Do you have a problem in understanding that? I guess no. So, whenever the impure blood is entering in the afferent arteriole, you can see the impure blood. Now, in the blood, these are the vestigial products. It can be uric acid, it can be urea, it can be BUN, it can be creatinine, it can be other vestigial products, the metabolic waste is present in the blood. The body wants to excrete the metabolic waste. So, all the substances which are supposed to get excreted, they will get excreted in urine, right? They will get filtered here, right? And get collected here.

Now, the liquid, the filtrate which is collected here, it is known as glomerular filtrate. We will not call it urine right now. We will call it as a glomerular filtrate. Do you have any problem understanding that? I guess everyone got it. Now, my point, what is my point here? My point, these substances which are filtered here, they have to cross a membrane here, before coming from the blood into the Bowman's space. The substances which are, which are leaving the blood and coming in the Bowman's space, they have to cross a barrier in between. They have to get filtered from this barrier. And this barrier is known as filtration barrier.

Now, tell me, the layers of the filtration barrier, what they have to cross? You got my point? You got my point? So, what they have to cross? So, these substances have to cross three layers here. Three layers are present, right? So, there is a basement membrane of the capillary. This is the capillary. Now, so, this is the afferent arteriole coming, forming multiple capillaries. It is one of the capillaries. All capillaries have basement membranes. So, this is a basement membrane. So, the first thing is the basement membrane, right? So, the first thing is basement membrane.

On the inner side of the basement membrane, this is the endothelial lining, because all capillaries are lined by endothelium. All blood vessels are lined by endothelium. So, capillary is also lined by endothelium. So, this is the endothelium lining. So, there is a basement membrane. On the inner side, there is endothelium. There is endothelium, endothelial lining, the capillary, right?

Now, what is the lining of the Bowman's capsule? Do you know the lining of the Bowman's capsule? The Bowman's capsule is lined by two types of epithelia. This epithelia, I'm drawing with green color, can you see this one? The Bowman's lining. This is the first epithelia, I'm drawing with green color. And let me use another color, red color, and drawing the another epithelia by this color. This is another epithelia. So, the Bowman's capsule is lined by two different types of epithelium. In this diagram, the green one, can you see the green one? The green one is known as visceral, visceral epithelium. Visceral epithelium, absolutely right. Also known as podocytes. I will tell you the reason why it is known as podocyte. It is visceral epithelium. And the outer one, the red one, can you appreciate the red one? The outer one, this is known as parietal epithelium. Parietal epithelium.

Now, you tell me, you tell me that while a substance, this is the metabolic waste, while it is crossing the blood vessel and entering in the Bowman's space, what three spaces it has? What three layers it has to cross? The three layers which it has to cross is forming the barrier, that is known as filtration barrier. So, you will say, ma'am, in the center, there is a basement membrane. On the inner side, there is endothelium of the capillary. Endothelium. And the outer surface of the basement membrane, there is epithelium. Which epithelium? It is visceral. So, parietal is the parietal one is here, parietal covering it, that is not crossed by the metabolic waste. So, metabolic waste is crossing three layers. What is the sequence? First, endothelium, then basement membrane, then visceral epithelium. The visceral epithelium is known as podocyte. First, everyone give me a thumbs up. You got my point.

So, the same thing. So, here in this diagram, this is the capillary again. See, this is the afferent arteriole entering. This is afferent arteriole entering, and it is forming multiple capillaries. Let me draw one of the capillary. So, can you see in this diagram? This is one of the capillary. All capillaries have two things: number one, the basement membrane, and number two, the inner lining of the capillary is endothelial cells. The red cells are the endothelial cells. Can you see the basement membrane and the endothelial cells are present? So, this is the capillary which is present inside this Bowman's capsule. I have drawn this capillary separately to explain you the lining of the capillary. Now, appreciate the same lining. The two things: basement membrane and endothelium, here. Can you appreciate? I guess everyone can understand. So, the black color is the basement membrane of the capillary. Give me a thumbs up. And the inner red color cells are the endothelial cells. So, basement membrane and endothelial cells are there.

Now, let me come on the lining of the Bowman's space. As I have told you, in Bowman's space, two types of cells are present. The green one is the visceral, visceral epithelial cell. And this purple one, the outer one, this one, the outer one, this one, the outer one, can you see the outer one? This one, the outer one, is known as parietal. Have you got it? This green one is the visceral. Green one. Now, you tell me that when a substance, this is a substance, let me show you one of the substance. So, imagine one of the metabolic waste is present here. I don't know why the pen is not working. Okay. This is one of the metabolic waste. Can you see? It has to cross. It has to cross. It has to get excreted in urine. So, it has to cross the filtration barrier. So, can you see the three layers it is crossing? Tell me the three layers in sequence. What are the three layers in sequence? This metabolic waste has to cross while coming out of the blood into the urine. So, this is the yellow color dot is the metabolic waste. It can be urea, BUN, creatinine, anything. It has to get excreted in urine. So, it has to leave the blood and go in the urine. So, it has to cross a barrier. So, in the barrier, three things are there. So, can you see in the center, basement membrane is there, right? In the center, there is basement membrane. On one side, inner side of the basement membrane, there are endothelial cells. And on the outer side of the basement membrane, there is epithelial cell. To be specific, this epithelium is visceral epithelium, not parietal epithelium. Everyone, give me a thumbs up. Have you got it?

So, these three things, the triad, the three things, the triplet, is known as filtration barrier. In the filtration barrier, triplet, there is the basement membrane in the center. On the inner side, endothelium. On the outer side, epithelium. Epithelium is visceral epithelium, that is podocyte. I guess it is crystal clear to all of you, right? So, this is the same labeling done in front of you. You can see the labeling. You can appreciate the three things which are present in the filtration barrier. So, in the center, there is basement membrane. On the inner side, endothelium. On the outer side, it's epithelium. It's visceral epithelium, which is known as podocyte. Parietal epithelium is not a part of the filtration barrier. You can appreciate this is parietal epithelium, the outer covering of the Bowman's capsule, the purple one here, shown. I'm marking here. So, this is not a part of filtration barrier. But yeah, it is present. So, I guess everyone got it. What is filtration barrier? Give me a thumbs up if you got it. What is filtration barrier? Okay. Just a second.

Okay. So, let me draw a filtration barrier for you. Just a second. Okay. So, in the filtration barrier, you can see in the center, there is a basement membrane. In the center, there is the basement membrane. On the inner side of the basement membrane, these are endothelial cells of the capillary. These are endothelial cells of the capillary. And on the outer surface of the basement membrane, these are epithelial cells. These are epithelial cells of the Bowman's capsule. The green color cells. These are visceral epithelial cells. Now, why they are known as podocytes? What do you mean by podo? Podo means human foot. See your foot. What is the shape of your foot? Can you see your foot? The shape of human foot is somewhat like this. So, there is a toe and the four fingers. So, see the shape of these cells. The shape of these cells is more or less like the human foot. Since it is same as that of human foot, these are known as podo. So, the cell is resembling the foot, that is podocyte. So, that is because of their shape, they are known as podocyte. But actually, they are epithelial cells, the visceral epithelial cells. Everyone, give me a thumbs up. Everyone.

So, this is filtration barrier. In the center, there is basement membrane. On the inner side, there is endothelium. On the outer side, there is epithelium. Epithelium is visceral, not parietal. And due to their shape resembling the human foot, it is known as podocyte. I guess the concepts are, if the concept is clear now, in all glomerulonephritis. Now, today I'm going to teach you nearly 20 or 25 different types of glomerulonephritis. I will teach you all primary, all secondary, all hereditary, all congenital, all types of glomerulonephritis and the differences between them. Now, in all the glomerulonephritis, one thing is common: the inflammation of the glomerulus. Glomerulonephritis. Itis, itis, and pathology is the inflammation of that particular tissue. So, glomerulonephritis is the inflammation of the glomerulus. Inside the glomerulus, the filtration barrier gets inflamed. This triplet gets inflamed. So, actually, it's the inflammation of the filtration barrier. So, actually, it's the inflammation of the fill.

Now, in this diagram, the same filtration barrier is shown. Now, let me show you this diagram. This is the basement membrane in the center. Please appreciate the basement membrane is in the center. Can you appreciate? On one side, these pink color cells are the endothelial cells. On one side, you have to draw endothelium. And on the other side, you have to draw visceral epithelium. So, please appreciate on the other side, these are the epithelial cells. These are the epithelial. Now, see the shape of the cell. It is looking like a foot. It is looking like a foot. That's why it is known as podocyte. So, now, one more thing. In the basement membrane, there are three portions. Can you appreciate the three things in the basement membrane? If you see the zoomed version of the basement membrane, that is electron microscopy of the basement membrane of the glomerulus, you will find it is divided into three portions. The central portion is dark, and the peripheral two portions are light. That's why the central portion of the basement is known as lamina densa, and the peripheral two portions, which are lighter in color, they are known as lamina rara. They are known as lamina externa and interna. Everyone, give me a thumbs up.

So, this is actually filtration barrier. This is actually. Now, see the electron microscopy diagram. In the electron microscopy diagram also, you can, just a second, you can appreciate the same filtration barrier. I have to go back. You have to wait for a while. Unable to go back. Yeah. Here, in this diagram, can you see? This is the filtration barrier. If you can appreciate that in this filtration barrier, please appreciate the central portion, which is darker. The central is darker, and the peripheral two are lighter. So, the central darker portion is lamina densa, and the peripheral two lighter portions are lamina rara. Lamina externa, lamina rara interna. Have you got it?

Now, in this, you can appreciate on one side of this basement membrane, I guess this one is the endothelium. This one is the endothelium, which is flattened, relatively flattened. And on the other side of the basement membrane, you can appreciate, you can appreciate the epithelial cells, the visceral epithelial cells, the podocytes. See the shape. The shape is like the fingers of the foot. So, these are the foot processes of the podocyte. The fingers are known as. Now, appreciate the triplet. Appreciate the filtration barrier. Now, when I will teach you various types of glomerulonephritis, ah, so in each type of glomerulonephritis, I will tell you there is inflammation of the barrier. But which portion of the barrier? Is there inflammation of the basement membrane? Is there inflammation of the podocytes? Or is there the inflammation of the endothelial cells? So, various types of immune complexes, I will teach you. The location will be different in each of them. So, let me move ahead. You got it. What is the filtration barrier? I guess the triplet, we all understand what is this triplet about.

Now, let me move ahead. Now, this is the diagram. This is the master diagram. Today, in this diagram, I am going to teach you all glomerulonephritis. Today only. Today, we have a marathon for renal system. I will complete all glomerulonephritis today only. Right? So, we will take various episodes, one, two, three, four, and finish entire glomerulonephritis, renal system, today only, right?

Now, this is the master diagram. In this, this is from Robbins, a beautiful diagram. You can see, if I'm cutting the glomerulus from here, give me a while, uh, if I'm cutting the glomerulus from here, imagine if I'm giving a cut here and looking it from above, how does it look like? If I'm giving a cut here and looking from above, the cross-section from the above, it will look like this. It will look like this. So, what is it? So, there are multiple capillaries, not one. So, can you appreciate these are? So, how many capillaries are shown? Capillary number one, capillary number two, capillary number three, capillary number four. I guess in this diagram, four capillaries are shown. Can you see? I'm cutting the glomerulus from here. I'm giving a cut from here and looking from above. So, it is looking like this. So, this is the diagram which I can see if I'm giving a cut and looking from above. So, there are multiple capillaries, not one. For the sake of understanding, we have drawn one in that diagram. But these are the multiple capillaries, right?

In these multiple capillaries, in each capillary, appreciate the triad. Appreciate the filtration barrier. So, please appreciate this orange color, penetrated lining on the inner surface of each capillary. On the inner surface of each capillary, this orange color penetrated lining, this is endothelium. This is the endothelium. The the lining which I have marked with this black color, this is, um, this is basement membrane. And the outer surface, these are podocytes. These are actually the food processes of the podocyte. These all are podocytes. These blue color cells are producing. So, you can appreciate the triplet everywhere. The triplet is the filtration barrier. So, basically, we are having multiple capillaries. The inner surfaces lined by endothelium. The outer surface is lined by podocytes or epithelium. In the center, there is a basement membrane. This is the summary. We all got till now. And these multiple capillaries are there. And can you tell me, what are these yellow color cells? Anyone? You can write in the chat box if you know the answer. The yellow color outer cells, which are bounding everything, which are forming the boundary of the complete thing. The yellow color thing, this, this outer, this outer thing here, which are giving the boundary to everything. Can you tell me, Sachin, Arvind, Lakshmi, Aishwarya, anyone who is watching me, gaming, who's watching me live? Can you tell me what is this thing? It is, yes, it is parietal, uh, Bowman's capsule. But I tell, epithelium of the Bowman's capsule. I'm talking about this, this one. So, it is the complete covering. That one, the parietal. That is not coming in the filtration barrier. But yeah, it is present. So, can you see this one, the yellow cells? Yes, very good, gaming. It is the parietal epithelium of the Bowman's capsule. Okay, we got it. What is this?

Now, the last thing. The green color cells in the center. There are few green color cells. Can you tell me what are these green color? Those are. Gaming, what are these green color cells? Sachin, what is it? Yes. What are these green color cells? These green color cells are the fillers. As I have told you, multiple capillaries are there. The space between multiple capillaries, capillary one, two, three, four, whatever capillaries are there, the space between them is filled by supporting cells, the filler cells. These are known as mesangial cells. So, these green color cells here are the mesangial cells. Have you got it? These are mesangial cells. The green color cells are the mesangial cells.

So, this is the complete diagram of a glomerulus. Actually, on microscopy, this is the diagram of the glomerulus. Can you see? This is the diagram of the glomerulus on microscopy. In this, one of the glomerulus is shown to you on light microscopy. You can see this lining, this complete boundary. Can you see this complete boundary? So, this is parietal epithelium, which I have marked. Right? So, this is complete boundary. Now, inside, which see the multiple capillaries. Capillary one, capillary two, so multiple capillaries are there, right? This is the basement membrane. Now, see the inner lining is the red color cells, the endothelial cells. See the outer lining. It is the pink cells, that is foot processes, uh, that is podocytes or visceral epithelium. See this pillar cells, the filler cells are the mesangial cells. I hope everyone got this diagram. Now, if you got this diagram, I'm going to teach you multiple glomerulonephritis in this diagram. You can understand this diagram.

This is a diagram of a normal kidney. Now, if you don't understand what is normal, how you can understand how it is abnormal? If you have now understood, man, this is normal kidney. This is the normal glomerulus of a kidney. Not if I show you any abnormality in that, so you can appreciate the abnormality if you know the normal. So, before understanding pathology, it's important to understand the physiology, anatomy, and histology. That's why these are first proof subjects before coming to the pathology. You must know all these, so that you will have a better understanding.

Now, let me start my disease, glomerulonephritis. That was an overview. If you got how we reach on this diagram, you can understand the entire diagram ahead, right? I would like to launch only one question here from the previous year question papers based on the normal structure of the glomerulus, right? Can you answer this question? Can anyone answer this question? I guess the question is very easy. Podocytes. What are podocytes? Podocytes are the cells which are visceral epithelial cells. Where they are present? Are they present in Bowman's capsule? Are they present in PCT? Are they present in DCT? Are they present in collecting duct? So, in which portion of the nephron they are present? Here, I guess that it's a very easy question. In which portion of nephron? So, podocytes are the lining of the Bowman's capsule. The inner lining of the Bowman's capsule is podocyte, that is visceral epithelium. And outer lining will be parietal epithelium. So, yes, the correct answer here is A. And yes, gaming, absolutely right. Arvind, absolutely right. The correct answer here is A. And most of you are absolutely right. Okay. So, this is a question from based on the normal structure.

Now, coming on the diseases of the kidney. As I have told you, that we can divide the diseases of the kidney into four portions. So, in the nephron, which portion is involved? In the nephron, if afferent and efferent arteriole along with the capillaries in between. So, first, afferent arteriole is coming, forming multiple capillaries, and exit out as efferent arteriole. If the arterioles and capillaries are involved, it is known as vasculature disease. But currently, I'm not teaching you vasculature disease. If glomerulus is involved, they are known as glomerulonephritis. So, I am teaching you glomerulonephritis. If PCT, loop of Henle, DCT, and collecting duct are involved, these all are tubules. So, these are known as tubular diseases. And if the background is involved, it is known as interstitial diseases. Tubules and interstitial are always involved together. That's what is known as tubular interstitial diseases.

So, let me start the disease, glomerulonephritis. Currently, I am teaching you glomerulonephritis. Again and again, I am telling you, itis means inflammation. So, basically, it is the inflammation of the glomerulus. So, it is the inflammation of the glomeruli. The disease of the glomeruli. It is also known as Bright's disease, right?

So, before again coming on the glomerulonephritis, let me teach you the clinical features of all glomerulonephritis in one shot. Then I will teach you individual various types of glomerulonephritis. Once, let me teach you clinical features before starting the topic of overall all glomerulonephritis in one, one, one, um, single shot only. So, when I will teach you individual one, it's, it's not necessary that in each of them I will teach you the clinical features, because I'm teaching you here only. So, all glomerulonephritis, uh, present, just a second. Okay. No, I'm not coming on the clinical features. I will come on the clinical features after a while. Let me teach you the pathogenesis of glomerular disease or glomerulonephritis, which is the most difficult topic, I guess, in the entire Romans, as per my knowledge, according to me, I found this topic very difficult. But I will explain you like with such a simplicity now that it will become fun for you.

Now, as I told you, glomerulonephritis is the inflammation of the glomerulus. Inside the glomerulus, the filtration barrier, the triplet, is present. Now, you should ask me the question, ma'am, who is causing the inflammation? How the inflammation of the glomerulus is occurring? So, that is the pathogenesis of the glomerular injury. So, there should be some injury to the glomerulus, right? So, what is the injury? Now, you can understand this diagram. I guess everyone can understand this diagram. Those students who can understand this diagram, everyone give me a thumbs up. In this diagram, you can see we are cutting the glomerulus at this level and looking from above. If we are looking from above, we are finding this diagram. In this diagram, we can appreciate multiple capillary loops. We can appreciate in each capillary, the triplet, that is filtration barrier, the filler cells are the mesangial cells, and outermost is the parietal Bowman's capsule. We all can appreciate this diagram. If we can appreciate this diagram, now let me tell you the various ways of injury in which this triplet is injured. I will, I will always talk about this triplet. This triplet I'm talking, this triplet I'm talking, this triplet, this triplet, everywhere you can see the triplet. But triplet, I mean three things: in the center, there is basement membrane. On the inner side, this is the endothelial cell. On the outer side, these are the, can you see these all are visceral epithelial cells? So, this triplet will get injured.

Now, the question is, who is causing the injury? Who is causing the injury? So, injury can be caused by three things. One of the three things: either injury is caused by antibody. You know, humoral immunity. And humans have two types of immunity: cell-mediated and humoral. In humoral immunity, antibodies are there. So, either the injury to the glomerulus is caused by humoral immunity, that is antibody. So, here, antigen-antibody complexes are formed, and those antigen-antibody complexes will injure the triplet. Which portion of the triplet? I will tell you. I will tell you. Don't worry. I will tell you everything, right?

Or else, the injury is caused by T lymphocytes. T lymphocytes, killer T cells, T lymphocytes will cause the injury. CD4 T cells, CD4 T cells, that is killer T cells, that is cell-mediated injury. So, this is humoral immunity. This is cell-mediated immunity. So, injury concurrent injury, antibody correct injury, cell care, cell conscious, cell killer T cell, that is CD4 T cell. So, either the injury is caused by antibody, or the injury is caused by CD4 lymphocytes, or the third way, injury is caused by complement. You know, human blood has complement system. In the complement system, there are C1 to C9, nine complements are present in blood, but they are inactive. But sometimes they become active, and they cause injury to the glomerulus. Such an injury is known as alternate pathway. Alternate means complement. So, there are three ways to injure the triplet, the filtration barrier inside the glomerulus. Either the injury is caused by antibody, humoral immunity, or the injury is caused by the cell, by cell, I mean T lymphocyte, killer T cell, CD4 T cell, that is known as cell-mediated injury. And the third one is the alternate pathway, in which I mean the injury is caused by the complement. You know, C1 to C9, nine complements are present in the human blood. You may be knowing that. So, who is causing the injury? So, most complicated to understand is the antibody. How antibody? In antibody, antigen-antibody complexes are formed, right? Now, these complexes are formed where? Where? Right? These complexes are formed either inside the kidney, in situ, I mean, inside the kidney only, inside the kidney, in the nephron, in the triplet, filtration barrier, or they are first formed in the circulation and then coming into the kidney. What I mean? I will explain you. Don't worry. What do you mean by in situ complex formation or circulating complex formation? So, antibody-mediated antigen-antibody complexes are formed. Antigen-antibody complexes, where they are forming? In the kidney directly, or first they are forming in the blood and then going to the kidney? So, in situ complex formation, circulating complex. Okay, I will explain you. Don't worry. The things are simple if you understand.

Let me draw a human body, a rough diagram of a human body, a rough sketch diagram to help you with the understanding of what is actually happening, right? A rough diagram I'm just drawing to explain you the mechanism. Let me draw the two kidneys. These are the kidneys. Inside each kidney, one million nephrons are present. Inside each nephron, one nephron has one filtration barrier. So, in each kidney, one million filtration barriers are present. I am interested in the filtration barrier, the triplet, the whole chapter, the triplet, inside the glomerulus of the nephron. To imagine, this kidney, under nephron is present. I am interested in the nephron inside the kidney. So, this is the nephron. This is glomerulus, PCT, loop of Henle, DCT, collecting duct. So, in the nephron, I am interested in the glomerulus. I am interested in only in the glomerulus. In the glomerulus, I am interested in the triplet. So, now imagine inside this kidney, the filtration barrier is present. Multiple filtration barriers are present inside each kidney. That is multiple glomeruli. Each glomerulus has one filtration barrier. Give me a thumbs up. Yes. So, that we can imagine.

Now, let me draw a blood vessel here. Okay. This is the blood vessel of a person, right? This is the blood vessel. Just for the

Of understanding, I'm drawing this diagram now. There can be any antigen. Let me draw any antigen. The antigen can be bacteria, can be virus, can be fungus, any foreign thing is the antigen. Imagine the antigen is present in the blood. This is antigen present in the blood. It can be bacteria, virus, fungus, parasites, some foreign substance. It can be anything, some toxins, some poison, any foreign material is known as antigen. We know the definition of antigen, right? Now, this is the antigen. Right now, there are two possibilities. Let me draw two antigen. Let me draw two antigen. Right.

Whenever antigen is formed, the body gives immune response by humoral immunity by forming antibodies against the antigen. So, this is the antigen. Now, there are two possibilities. Kidney bedo henna? So, let me draw one more. Um, in both the kidney, I will show you one mechanism. Right. In both the kidney, you can see the nephron. One nephron here, one nephron here.

Now, the first possibility is that this antigen, this antigen is going to the kidney directly and antigen gets deposited on the filtration barrier. Antigen gets deposited on the filtration barrier. Now, this antigen was not initially present in the kidney. It is, it is at this time it got deposited. So, such an antigen is known as planted antigen. It is known as planted antigen. Give me a thumbs up. This antigen is known as planted antigen. This antigen is known as planted antigen. You got my point? This is the thing. This is planted antigen.

And sometimes, uh, the, so this is the antigen. So, first antigen is coming. It is going to the kidney, getting planted on the filtration barrier. Uh, on what portion of filtration barrier? That depends on the type of glomerulonephritis. As I've told you, there are 10, 20, 30 types of glomerulonephritis. In various rheumatoid arthritis, the location of this antigen can be different in the triplet, whether in the basement membrane, whether in the endothelium, whether in the epithelium. So, I will teach you individually when I will teach you the individual glomerulonephritis. So, whatever is the location, it is in filtration barrier. That is triplet. Right.

Now, body is forming antibodies against the antigen. Angle, the word to be picked here is pjpg. Antigen-antibody complexes are not formed in the blood. First, antigen is coming. It is going to the kidney, getting deposited in the barrier. Then, antibody is also coming. Pj ph, behind, behind that is also going to the kidney. Antigen and it will form antigen-antibody complexes in the kidney. Antigen deposited, antibody deposited, complex vinegar. When the complexes form, the glomerulus will have inflammation. That is glomerulonephritis.

So, you tell me, antigen-antibody complex kahana? Is it formed in the blood? No. Blood has individual antigen, individual antibody, but the complexes are formed in situ. This is known as in situ complex formation. Give me a thumbs up. This is known as in situ formation.

So, first antigen is coming. Imagine a bacteria is coming. The first antigen is coming. That is one of the bacteria is coming. That bacteria is going to the kidney, getting deposited in the nephron, in the glomerulus of the nephron, in the filtration barrier, triplet of the nephron. One of the location of the three cells, either the center basement membrane, or endothelium, or epithelium. Now, body is showing the immune response by forming antibodies. The antibodies are also going behind, behind. Pj p g antigen guys. So, antibody will also get deposited on the same point where antigen is there. So, antigen-antibody complexes are formed. That lead to inflammation and that lead to the disease known as glomerulonephritis. That is my chapter today. Give me a thumbs up.

So, my question is, where is the antigen-antibody complexes are formed? I know individual antigen is present in blood. Individual antibodies present in blood, but the complexes are formed in situ. That's why this is known as in situ antigen-antibody complex formation. You got my point? This is in situ. This is in situ. In which the antigen was planted first. It was not initially present there. It is planted there.

Now, sometimes what happens? The antigen is not planted. The antigen is the integral part of the glomerulus. It is already present inside the glomerulus. It is present in me, you, every healthy human being. Ah, what is the filtration barrier? Can you tell me? What is the filtration barrier? Let me draw one of the filtration barrier on side here. I am drawing it. It is basement membrane in the center, endothelium on one side. This is endothelium and epithelium on other side. This is the epithelium. That is visceral epithelium on other side. I guess everyone knows this till now.

Now, I'm talking about this filtration barrier inside the kidney. Right. I'm saying this time, antigen is not planted. It is a part of basement membrane. You know, basement membrane is made up of collagen type 4. Collagen. So, antigen is type 4 collagen. Antigen is type 4 collagen. And body is forming antibodies against that. You may ask me, man, why body will form antibody against its own antigen? It is not a foreign. So, in my kidney, I am having one million nephron. Inside each my kidney, inside each my nephron, I'm having this structure present inside me. Right. So, inside, I'm having millions of basement membrane. Inside my each kidney. Right. Now, my body is not forming antibodies against the collagen of the basement membrane. But some individuals in which autoimmune diseases are there. But what do you mean by autoimmune diseases? In autoimmune diseases, body form antibody against the self-antigen. Normally, body form antibodies against the foreign antigen. But sometime in autoimmune diseases, immunity become deranged. Immunity become mad. And immunity, that is antibodies, are started forming against the self-antigen. Here, collagen is one of the self-antigen. Collagen to sub mahena. It is present in everyone. But some of the individuals will form antibodies against them.

Now, this antigen, this collagen is known as fixed antigen. It is already fixed in everyone's kidney. It is not planted like here. Yeah, bacteria. Bacteria. Collagen is always present. So, this one antigen is fixed antigen. And body started forming antibodies against that. So, antibody will go. Antibody will come. Antibody will go and uh, deposit on the collagen. So, antibody will come. Antibody will get deposited here. So, again, antigen-antibody complexes are formed in situ. Again, they are formed in situ. But against a fixed antigen. You got my point? Against a fixed antigen.

And the third, these are the two in the in situ. Planted, in situ, fixed. And the third is that, what is the third scenario? The third and the last scenario in which antigen-antibody formation complexes formed in the blood only. And after forming complexes, they will go and deposit in the kidney. You got my point? So, I'm summarizing. Those who are confused, for them, especially for them, those who are confused, still confused. I am drawing the super three diagrams for you. No one will explain you pathogenesis of glomerular injury with such a simplicity today. After my lecture, I request all of you to read Robbins today only. So, Robbins will become a cakewalk for you if you are watching my lecture with attentivity and after that you are reading Robbins today only. Okay.

So, let me, uh, draw three human bodies. I'm drawing a rough diagram. So, don't laugh. I'm drawing just to show you the pathogenesis. Here, I want to show you the pathogenesis. The three type of pathogenesis of antigen-antibody complexes. I want to explain you what is in situ, in situ maybe though option planted or fixed antigen or what is circulating. So, what is circulating? What is in situ? So, in each of them, I'm drawing kidney. Let me draw only one, one kidney. You know, there are two kidneys, but for the sake of understanding, I'm drawing only one, one kidney. Right. Inside one, one kidney, uh, okay. Let me draw the filtration barrier. So, this is the basement membrane, endothelium, epithelium. I'm not drawing nephron. Nephron key and filtration barrier is important for me currently. I know inside the kidney, nephrons are present. And inside the nephron, inside the glomerulus, this filtration barrier is present. But currently, I'm drawing just filtration barrier to explain you. So, this is basement membrane, this is endothelium, this is epithelium. This is basement membrane, this is endothelium, this is epithelium. I want to you understand that inside, parallel humans have two kidneys, not one. For the sake of understanding, I'm drawing only one. Inside each human number one. After that, inside each kidney, one million nephron are present. But I'm not drawing the entire nephron. Inside the nephron, there is glomerulus. And inside the glomerulus, there is filtration barrier. So, I am interested in the filtration barrier of the glomerulus of the nephron. That's why I have drawn only filtration barrier. Everyone give me a thumbs up. Everyone can you see the three diagrams? Yes, you all can. You all can see the three filtration barriers? Yes, you all. Let me draw the blood vessel in each of them. One, one blood vessel will be required to explain you the meaning of the in situ and circulating. Right.

Let me take the first example. The first example is a bacteria. This is the antigen. The antigen here is the bacteria. The antigen may be any antigen can be there. Bacteria, virus, parasite, fungus. It is the antigen, basically foreign antigen is there, right? This foreign antigen is there. So, body will form antibodies. So, let me draw this foreign antigen here also. The same foreign antigen here also. So, this is the foreign antigen. This is a foreign antigen, right? So, body will form antibodies against it. Now, there are two possibilities. Um, the anti, so these are the antibodies. So, antigen-antibody complexes are formed in circulation only. So, let me draw this antigen and let me draw this antibody. These complexes are formed in the blood only. See, it is blood, blood means circulation. And after forming, they are going to the kidney and getting deposited here. So, what is this mechanism known as? You will say, ma'am, complexes are formed in circulation. The complexes are formed in circulation. After forming antigen-antibody complex, as the complex, they are going to the kidney and getting deposited. So, this is the first mechanism. A antigen is coming. Antigen can be any. It can be bacteria, virus, fungus, parasite, any foreign material. So, as soon as the antigen is coming in the blood, the body is forming antibodies against it. So, antibody will bind with the antigen in the blood only, in the blood only, in the circulation only. And antigen-antibody complexes are formed in the circulation. And after forming in the circulation, as blood goes everywhere in the body, this blood is going in the kidney also. So, this blood is going via afferent arteriole. It is entering the filtration barrier. It is entering the capillary. You understand the capillary. And after that, it is getting deposited here. So, it is destroying it. It is causing inflammation of this portion. And it will lead to glomerulonephritis. So, this mechanism is circulating antigen-antibody complex formation. The antigen-antibody complex are formed in the circulation. Circulation means blood.

See the second possibility. The second possibility is that here antigen is there. Here also antigen is there. You can see like this. Here also antigen is there. But this antigen will go to the kidney, get deposited on the filtration barrier. Now, you will ask me, where it will deposit? It will deposit in the basement membrane, or on the endothelium, or on the epithelium. So, my answer is, it varies from glomerulonephritis to glomerulonephritis. In different type of glomerulonephritis, this deposition will be different. The site of the filtration barrier may be triplet enough to replace exact location without have different type of uh, deposition. The location. So, that I will discuss my individual glomerulonephritis. Here, antigen is coming and getting deposited anywhere in the barrier. Triplet, anywhere. It can be anywhere. Now, body will form antibody. Now, body will form antibody. And antibody will come behind, behind. Antigen-antibody complexes are not formed in circulation. The antigen-antibody complexes are formed inside the kidney, directly inside the filtration barrier, directly. Give me a thumbs up. So, this is known as in situ antigen-antibody complexes are formed here. Complexes are formed in situ. Here, complexes were formed in the circulation. After forming, as the assembly, as the assembly, antigen-antibody assembly complex, they are coming in the filtration barrier and getting deposited there. Here, first antigen is coming. Then pjpg antibody is coming. And the result is same. And result here also, filtration barrier is destroyed, inflamed. Here also, filtration barrier is destroyed and trimmed. Both of them are destroyed or inflamed by antigen-antibody complexes. But here, complexes were formed in the blood and then get deposited here. First antigen is coming, then pjpg antibodies coming. So, complexes are formed in situ. By in situ, I mean the kidney itself. Give me a thumbs up. Everyone, give me a thumbs up. So, here in situ complexes are formed, right? Hence, e2.

Now, what is the antigen here? Again, come on. The antigen. You will say, my antigen was not initially present. First, it is coming in the blood and from the blood, first it is coming to the kidney and getting deposited in the filtration barrier. So, such an antigen is known as planted antigen. We have planted the antigen first. What is the nathan? We have first planted it. Antibody cola. You got my point? Here, antigen is not planted. It is present in blood only. In the blood only, antibody is coming and forming the anti. So, see the complex. See the complex. Here, here the antigen-antibody complex, the word complex is formed in the blood. And as the assembly, it is going to the filtration barrier in the kidney and getting destroyed. Um, the glomerulus filtration barrier. Here, first antigen is going, or skip phpg is going. Ultimately, antigen-antibody complexes, they are formed in situ. See the circle. This circle is in the circulation. The circle is inside the kidney. So, that is the meaning of circulatory or increase. Give me a thumbs up. Shall I come on the third possibility? Shall I come on the third possibility? This one is circulating complex formation. This one is in the two complex formation against a planted antigen. First, we have plant antigen there. Mumbo palace antigen. So, first, I, I brought a bacteria in the body. That bacteria is my antigen. The bacteria is going and getting planted in the kidney, getting fixed in the kidney. So, planted there. Give me a thumbs up. Give me a thumbs up. Coming on the third possibility. Who is the antigen here? Who is the antigen here? Here, the antigen was bacteria, virus, fungus. Here also, bacteria, virus, fungus, parasite, any foreign and foreign material. In the third possibility, the antigen is not a foreign. The antigen is self. The antigen is the collagen of the basement membrane. Collagen of basement membrane. Can you see? This is the basement membrane. The collagen of the basement is acting as the antigen. You will ask me, ma'am, why the collagen will act as a basement membrane? The collagen of the basement membrane will act as antigen. Why it is not a foreign? It is self. But person is having autoimmune disease. There are few persons in which there is a disease that is autoimmune disease. In autoimmune disease, what is the problem? The body form antibodies against the self-antigen, not the foreign cells. Immunity become deranged. Immunity become mad. The plasma cells of the lymphocyte become mad. They start forming antibodies against the self-antigen. Who is the antigen here? Antigen is type 4 collagen of the glomerular basement membrane. So, this antigen, this is an antigen. But this antigen is not planted. It is not planted like this. Initially, it is coming in the body in the blood and then going to the kidney. No, it is already present here. So, this antigen is known as fixed antigen. What this antigen is known as? Now, see the difference. This antigen is planted antigen. And this antigen is fixed antigen. You give me a thumbs up. So, it is never present in blood. With blood, these two antigens were first present in the blood and then going to the kidney. But this is not present in blood at all. It is already present in the kidney. So, you tell me, khabib complexes in this scenario? So, body is forming antibodies in the blood. And these antibodies are coming and forming antigen-antibody complexes in the kidney. So, here also in situ. In situ complexes are formed. Is not present in blood. Antigen directly present inside the kidney, right? So, here also in situ complexes that form. Now, see, this is also in situ. This is also in situ. But this is against a planted antigen. And this one is against a fixed antigen.

Now, everyone appreciate my efforts. How many audience are watching me live? Give me thumbs up right now. Give me thumbs up if you got the three mechanisms. So, ultimately, what are the three mechanisms? You tell me. You will say, man, antigen-antibody complexes, where they are forming? Based on that, we divide. So, whether they are forming in blood, or they are forming in kidney, or they are forming in kidney. They are forming in blood, that is circulating antigen-antibody complex formation. If they are forming in situ, there are two possibilities. Whether the antigen is fixed, that is collagen of the basement membrane, type 4 collagen, or whether the antigen is planted, like a bacteria. Everyone gave me a thumbs up. Right. You got it. I guess you got it. So, same thing. This is the diagram from Robbins. Now, I will show you which I have simplified for you, forming three human beings. Right. So, this is the diagram Robbins have not given three human beings. Robbins directly have given the filtration barrier. Now, you can understand the three mechanisms in the three filtration barrier, one by one. I will be explaining you the same in this diagram. Now, let me zoom the first one. One by one, we will be taking zoom. Right. There are three possibilities in front of you. Let me zoom the first diagram only. First diagram, we will be discussing. Can you see this diagram? What you can see in this diagram? In this diagram, we can see this is the lumen of a capillary. This is the basement membrane. First, appreciate this. This, this light pink color is the basement membrane, right? On the inner side of the membrane, this is endothelial cells. And on the outer side, these are the podocytes. Can you appreciate this? This is visceral pore. So, this is a filtration barrier. Now, appreciate the lumen. Appreciate the lumen. Lumen of the capillary. Can you appreciate the lumen of the capillary? In the lumen of the capillary, can you appreciate? Can you appreciate this thing? They are present already in blood in the lumen of the capillary. Can you appreciate? So, the red is the antigen. Black is the antibody. So, you can appreciate multiple antigen-antibody complexes. They are already formed in the blood in the lumen of the capillary. They are already formed. So, this is the first scenario. Antigen is coming. Antibody formed. Antigen-antibody complexes. The assembly formed in the blood only. And after forming in the blood, they are coming and see, they are depositing. They are depositing in the filtration barrier. So, this is circulating formation. Circulating antigen-antibody complexes formation. Give me a thumbs up. Can you appreciate the antigen-antibody complex formation takes place in the lumen of the blood?

Now, see the three diagrams together. You will have a better overview. See the three diagrams together. What I want to show you in the three? They come as specific. But only both. Everyone look here. Can you see here? The lumen. Appreciate the lumen of the capillary. Lumen under hollow lumen. And avodeco. In the lumen of the capillary, what is present here? In the first diagram, what all these structures are there in the lumen of the capillary? What is present here? In this diagram. And in the lumen of the capillary, what is present here? You see the three diagrams and you yourself tell the answer. In the first diagram, I can see the complexes. I can see the complexes. So, in the first diagram, antigen-antibody complexes already formed in the blood in the lumen of the capillary. Means blood. So, this is antigen-antibody complexes formed in the circulation. Antigen-antibody complexes formed in the circulation. After forming in the blood, they are coming and depositing there. Here, here, I can see multiple deposition. Can you see? Filtration barrier. They are depositing on the basement membrane also, on the epithelium also, endothelium also, everywhere they are depositing. But they are formed already formed in the blood. Blood. But in the second and the third diagram, in the lumen of the blood, I can find only antibody. So, the complexes are not formed in the blood. Only antibodies present here. Can you see? This is the antibody. This is the antibody. Blank, empty antibody. So, where is the antigen? So, can you see in this diagram? The antigen is the collagen of the basement membrane. Can you see these red dots? These red dots are present on the basement membrane. So, the antigen here is the fixed. And can you see from the lumen, the antibodies are coming here and getting deposited? So, antigen-antibody complexes are formed. But the complexes are formed in situ. They are formed in situ. Inside the kidney only. And against a fixed antigen. See the third diagram. In the third diagram also, we have only antibodies there. Like the second. In the third also, we have lumen have only antibodies. So, here also, antigen-antibody. This is the antigen. Now, this antigen is a bacteria, which is planted here. It was initially not present. But from the blood, first bacteria is coming, getting planted. Or pjpg antibodies coming and getting deposited. So, please appreciate antigen-antibody complexes are formed. Everyone gave me a thumbs up. Yes or no? Have you got it? So, these are the three diagrams. You can see. I guess everyone got the three diagrams. Looking at the lumen of the capillary, you can decide whether the antigen-antibody complexes are formed in the circulation or in situ. If the lumen of the capillary directly contain complexes, so they are formed in circulation. If the lumen of the capillary contain only antibody and the deposits are formed in situ, it is the in situ one. I guess everyone got it. Yes or no? Yes or no. So, we are done. We are done with this thing. Uh, that is antibody mediated. Now, I'm not giving the explanation of each of them. Uh, so, let me skip this portion. Right. Uh, okay. Just a second. Let me skip this portion. So, we have exp, I have already explained you. You can read the theory later on from the notes. You can ask me for the notes. I will send you the notes. And you can read the theory directly from the notes. Now, coming on the second mechanism, that is cell mediated. Coming on the second mechanism, that is cell mediated. Just a second. We are done with the antigen-antibody complex deposition. Coming on the second mechanism, that is cell mediated. In cell mediated, whatever is the antigen, the T lymphocytes, CD4 and CD8 T lymphocyte will come and they release cytokines. They release various type of cytokines that will cause destruction of the filtration barrier. That will cause inflammation in the self-iteration. Here, antibodies are not formed. It is cell-mediated immunity, not humoral immunity. Since antibodies are not formed, that's why cell-mediated immunity is also known as posse immune. Posse means less. Posting pathology is less. Less immune means less antibodies. Here, antibodies are not there. Since antibodies are not there, it is cell-mediated immunity. The another name of segmented immunity is posse immune. So, this immunity is cell-mediated. Here, antibodies are not formed. Here, CD4 and CD8 lymphocytes causes the destruction of the filtration barrier. CD4 and CD8 lymphocytes will cause the destruction of the barrier. And this immunity is known as posse immune. Give me a thumbs up. The third pathway is the alternate pathway. In the alternate pathway, complement will come in the rule. Complement will come in the road. Right. Complement, especially C3. You know, in the blood, C1 to C9 complement are present. That complement and propelled in. These are the components of the complement system that will cause the inflammation of the barrier, that is filtration barrier, filtration membrane. So, that is the three.

Now, coming on the location of the deposit. The next thing. Can you tell me the diagram, uh, of a glomerulus? Can you tell me the diagram? So, in the diagram of the glomerulus, what I am drawing? This, this one is the outer boundary that is parietal. This one is parietal Bowman's capsule layer. But I tell layer of the Bowman's capsule. Now, let me draw multiple capillaries. Capillary number one, capillary number two, capillary number three. I can draw multiple capillaries inside one glomerulus. Right. All of them are like this. This is the red color is the basement membrane. Can you see? On the inner side, I will draw endothelial cells on each of them. On each of them, I will draw endothelial cells on the inner side. So, this is the inner side appearance of red color in the basement membrane. See the color. Blue is the endothelium cell. And on the outer side, these are the visceral podocytes. These are the food processes of the visceral podocytes. So, see the shape is like the food of a human. These are the visceral. So, I can draw the same and all. So, that is the, you can appreciate the filtration barrier. The triplet. You can appreciate the triplet here. Everyone, give me a thumbs up. If you can appreciate this. Now, the space between multiple capillaries is filled by mesangial cells. So, these are the filler cells. They are present everywhere. Supporting cells are there. So, these cells are mesangial supporting cells. Everyone, give me a thumbs up. Have you got it? So, this is the diagram of a normal glomerulus. Now, as I have told you, antigen-antibody complexes are formed. So, where the complexes are formed? What is the location? Currently, I'm telling you the four locations. Four possible locations where the complexes. As I told you, various glomerulonephritis have various location. So, sometime the deposits are present in the basement membrane. Can you see a red colored basement membrane? So, these deposits are known as intra-membranous. Such deposits are known as intra-membranous. That is deposits in the basement membrane. Sometimes, the deposits are on the endothelium. Can you see? I'm drawing the deposits on the inner cell. This deposit. And I'm not drawing both. It can be antigen and antibody both are there. So, I cannot draw every time antigen and antibodies. So, these are the deposits. Imagine antigen as well as antibody. So, such deposits are known as, they are on the endothelium. Now, that's why these are known as sub-endothelial. Sub-endothelial. So, on the basement membrane, on the inner side of the basement membrane. Now, coming on the outer side of the basement membrane. They can be present on the epithelium. That is visceral epithelium. So, such deposits are known as sub-epithelial deposits. So, what are the three main locations? Basement membrane is intra-membranous. Sub-endothelium and sub-epithelium. And the large deposits can be present in the mesangium. Mesangial cells. So, the fourth location is the mesangium. So, these are the four locations of the deposits. But the term deposit, the antigen-antibody complex itself is known as deposit. Give me a thumbs up. That deposit is where? What is the location? So, four parts. Let me simplify this diagram. It's the diagram for simplifying. Draw the basement membrane again. I will draw the basement membrane again with a simplicity like this. This is the basement membrane. Right. We all know on one side of the basement membrane, we all have endothelium of the capillary. This is the endothelium of the capillary. On other side of the basement membrane, we have visceral podocytes or epithelium. So, this one, the visceral podocyte and epithelium. And surrounding cells are the mesangial cells. So, let me draw a few surrounding cells, that is mesangial cells, around this triplet. So, let me simplify it. Everyone, give me a thumbs up. Have you got it? Have you got it? Now, draw the location of the deposits. There can be four possibilities. What are the four possibilities? Who will tell me the four possibilities? The first possibility, the deposits are here, inside the basement membrane. When the antigen is collagen itself, the fixed antigen, autoimmune disease, that is Goodpasture syndrome. I will tell you. So, this deposit is known as intra-membranous. This location is known as intra-membranous. Sometimes, the deposits are on the endothelium. The deposits, multiple deposits are there on the endothelium. On the endothelium. So, these deposits are known as, they are on the endothelium. Now, that's why these are known as sub-endothelial. Sub-endothelial. So, on the basement membrane, on the inner side of the basement membrane. Now, coming on the outer side of the basement membrane. They can be present on the epithelium. You got my point? I guess you all got it, right? So, this deposit is known as sub-epithelial deposit. And lastly, the deposits can be in the mesangial cells. These are known as mesangial deposit. I cannot simplify more than this. So, these are the four locations of the deposit. What are the four locations of the deposit? Can you tell me? Inside the basement membrane, intra-membranous. On the endothelium, sub-endothelial. On the visceral epithelium, podocytes, that is sub-epithelial. And on the mesangium. So, these are the four locations of the deposit. Not any. There can be the location. Ultimately, barrier is disturbed. This is the barrier. Now, in the barrier, there is a triplet along with the supporting cell. So, anywhere is the deposit, the filtration barrier is disturbed. It is inflamed. And the disease is glomerulonephritis. Have you got it? So, these are the four different locations in front of you. It can be ep-membranous or intra-membranous, one and the same thing, where deposits are in the basement membrane. It can be sub-endothelial. It can be sub-epithelial. And it can be mesangial. Now, whenever I will teach you individual type of glomerulonephritis, you will come to know. Now, see the three diagrams. You tell me, in diagram number one, where are the deposits? Tell me the location of the deposit. Can anyone? Arvind, can you tell me? Gaming, can you tell me? Ashman, Siddiqah, Link, anyone who is watching me live? I can see only these names currently. So, can you tell me the location of deposit in the first diagram, second diagram, third diagram? This diagram is from Robbins. We all know that. Can you tell me in the first one? Can you see this is the deposit. Antigen-antibody complexes are deposited here. They are deposited here. So, they are on the inner side of the basement membrane. So, in this, I can see the deposits are sub-endothelial. Sub-endothelial. The deposits are sub-endothelial here. Give me a thumbs up. Because they are inner side of the basement membrane. You all can appreciate. In the second diagram, I can see the deposits on the membrane itself. On the basement membrane itself, I can see antigen-antibody complexes are there. So, in this diagram, the deposits are ep-membranous or intra-membranous. On the contrary, in the third diagram, see the deposits are on the podocyte. Can you see? These are the podocytes. Can you see the deposits are on the podocyte? Antigen-antibody complexes. So, these deposits are sub-epithelial. Sub-epithelial. I guess you all got it. I guess you all got it. Mesangial is not shown here, unfortunately. Mesangial, the green color cells, the mesangial cells here, can be the deposits. Antigen-antibody deposits. Everyone, give me a thumbs up. Right. So, you can see now. These are the, the same diagram from Robbins, showing all four deposits. Here, in this diagram, the black color is the deposit. By deposit, I mean antigen as well as antibody complex. Now, in the diagram, the complex is not shown. The black color deposits are containing both antigen also, antibody also. Right. So, here, okay. In the first diagram, you can see the first one, the labeling. There are four labeling. One, two, three, four. Can you see the four? Now, tell me the four. What is one? What is two? What is three? What is four? See the location of all four of them. The four type of deposits. The diagram from Robbins. Today only, you will read Robbins. And I appreciate all these things in the Robbins only. Can you tell me what is one? In the one, I can see the deposit in the basement membrane only. This one. The pink one is the basement membrane. And can you see the black deposits? They are present on the basement membrane. That's why this is ep-membranous or intra-membranous. One and the same thing. Ep or intra, akibata. Right. In the second one, this one. See the location of the deposit. The location of the deposit is on the podocyte. On the outer surface of the basement membrane, I guess. So, this one is sub-epithelial. See, this is on the inner side. The third one. So, this is sub-endothelial. And see the fourth one. They are present in the matrix. The supporting matrix. The green color supporting matrix. So, these one are the mesangial. I guess everyone got it. Shall I move ahead? The same diagram from Harshman. The four type of deposits are there. In this diagram, the deposits are shown by pink color. In this diagram, the deposits were by black color. So, whatever color coding you are using, your concept should be clear. So, I guess we all got it. What are deposits? And, uh, what is the location of the deposit? Right. You got my point. Now, let me start glomerulonephritis. Let me classify glomerulonephritis. How many type of glomerulonephritis I'm going to teach you today? Till now, I have not even taught you a single glomerulonephritis. And the lecture is already one hour, one and a half hour. Right. So, in this, we have seen the overview of the glomerulonephritis. We have seen the anatomy, histology of the normal kidney, normal nephron, normal, uh, filtration barrier. And we have seen the pathogenesis of the nephritis. Now, let me come, the classification of glomerulonephritis. We can classify glomerulonephritis into two categories. The primary glomerulonephritis and the secondary glomerulonephritis. So, primary glomerulonephritis is predominantly involving the glomerulus only. The diseases in which mainly glomerulus is involved, primarily glomerulus is involved, that is known as primary glomerulonephritis. And in the secondary, the person has some other disease, what's called disease, and the glomerulus is involved secondarily. That's why known as secondary. So, there are nearly nine primary glomerulonephritis, which we have to study one by one. Sorry, in detail. I will tell you all nine in a comparative manner. And secondly, there are many. But usually, I teach three to four from this list, which are important. The diabetic one, the SLE one, the HSP purpura, and some other. So, yampathinya charity pathongames. I will not teach you all secondary. The important one I will teach you. But primary, we will, uh, we will complete all nine. And the third category, you can see, hereditary one. The hereditary glomerulonephritis. They are four in number. So, I request all the student to make a comparative table between all. First, make a comparative table between all nine. Then, make a comparative table between these three to four. Then, make a comparative table between these four. So, this is the complete glomerulonephritis in number, I'm going to teach you. So, let me come on the primary one. Can you see the primary? The nine I'm talking about. I'm sorry, these all are primary. Glomerulonephritis. So, let me tell you the nine names first. Austria, we will make a comparative table between them and start studying them. The first is known as post-acute proliferative glomerulonephritis. Acute proliferative glomerulonephritis, also known as post-streptococcal glomerulonephritis. One and the same thing. So, many students even don't know these two terminologies are same. Now, you have to learn the short forms because in exam, it is like PSGN and only. So, many students even don't know the full form of PSGN. APGN. You got my point. So, what is APGN? What is PSGN? It is acute proliferative glomerulonephritis, post-streptococcal glomerulonephritis. You got my point. The second one is rapidly progressive glomerulonephritis. Rapidly progressive glomerulonephritis, right? The third one is minimal change disease, which occurs in children. The most common cause of nephrotic syndrome in children. I will teach you. So, that is MCD. The fourth one is membranous. And the fifth one is membrane or proliferative. The fourth is membranous glomerulonephritis. And fifth is membrano-proliferative glomerulonephritis. So, see the change. It is MGN. It is MPGN. It is only membranous. It is along with membranous, proliferative also. So, membranous glomerulonephritis, membrano-proliferative glomerulonephritis. The next two, focal segmental. Focal segmental. Now, see both are focal segmental. One is glomerulonephritis. One is glomerulosclerosis. Then this one is not alone nephritis. This one is glomerulosclerosis. This one is known as focal segmental. This one is also known as focal segmental. But one is glomerulonephritis. One is glomerulosclerosis. What is the difference between all these? I will make a fun for you. The glomerular nephritis understanding will be super easy for you if you are attending the lecture from the beginning. If you attended the pathogenesis, it will be easy for you to understand all these. The microscopy, the gross appearance, the pathogenesis, everything I will teach you. Don't worry. So, after these two, focal segmental glomerulonephritis and glomerulosclerosis, the next one is IgA nephropathy. The next one is IgA nephropathy. The Berger's disease. And the last one is chronic. The last one is chronic. You got my point. So, count. They are nine in number. I am going to teach you all nine one by one. These all are primary glomerulonephritis. Right. Coming on primary. Keyboard. Secondary glomerulonephritis. In secondary glomerulonephritis, patients have some other disease. The patient has some other disease. But the glomerulus is involved secondarily. Not mainly, primarily. That's why these are known as secondary glomerulonephritis. Secondary glomerulonephritis. So, here, what are the diseases? SLE. Diabetes. Amyloidosis. Polyarteritis nodosa. Ragnus granulomatosis. Goodpasture. HSP. They are many. But I will teach you SLE. I will teach you diabetes. Maybe I will teach you amyloid kidney. Maybe I will teach you HSP purpura. So, these three, four, I'm going to teach you in detail. I will teach you Goodpasture also. So, these I will teach you in detail. Not all. Not all. Because others are not really very important at your level. So, that is secondary one. And the third one are the hereditary. Hereditary. The glomerulonephritis is congenital. It is present since childhood. So, Alport disease is the most important here. The first is the Alport. Second is Fabry disease. The third is Nail-Patella. And fourth, you add here. It is thin membrane. There are four in number. Thin membrane disease or thin membrane glomerulonephritis. Give me a thumbs up. Everyone, give me a thumbs up. So, let me revise the classification of glomerulonephritis. Let me divide glomerulonephritis into three categories. The primary one, the secondary one, and the hereditary one. Can any one of you help me in enumerating the various names of glomerulonephritis? First, before going to the details of all of them, we will study the detail, each and every minute detail of all type of glomerulonephritis today only. Right. So, we will finish the topic end-to-end, cover to cover, we will cover. So, first, enumerate them. The first step is to know their names. So, in primary, there are nine in number. In hereditary, there are four in number. In secondary, there are many. But I will teach you only important one. Right. Not all. So, can you enumerate the nine primary? The first one is APGN, acute proliferative glomerulonephritis, also known as post-streptococcal glomerulonephritis. The most important one. We will start from this one only. I will teach you all these in a comparative manner. In a super, super, super easy comparative manner. So, it will be fun for you to study all nine together. Right. The second is rapidly progressive glomerulonephritis, RPGN. That also known as crescentric. Here, crescents will be formed. Crescentric glomerulonephritis is this one only, right? The third one is MCD, minimal change disease. The fourth one and the fifth one, I always teach together. So, membranous glomerulonephritis and membrano-proliferative glomerulonephritis. So, in this, only membrane is involved. Here, along with membrane, proliferation is also there. So, membranous and membrano-proliferative. So, one, two, three, fourth, fifth, I always teach together. Then, sixth, seventh, also I teach together. So, the next two are focal segmental. Focal segmental. But one is glomerulonephritis. One is glomerular sclerosis. Don't worry. I will tell you the meaning of all these. Just I'm helping you to learn the names. Falling names. So, they glow. After that, I will teach you the detail of all these. Why does glomerulus clear ourselves? Where does glomerulus? I will teach you everything. Don't worry. Right. So, after that, there is IgA nephropathy. The Berger's disease. And the last one is chronic glomerulonephritis. Count. They are nine in number. One, two, three, four, five, six, seven, eight, nine. So, they are nine in number. Every one, give me a thumbs up. Shall I move ahead? In the secondary, there are many. Important ones are SLE, that is lupus. Lupus glomerulonephritis. Lupus kidney. The second is diabetes mellitus. I am teaching you. HSP purpura. Goodpasture syndrome. I will teach you all these. The important one. After that, coming on the hereditary. There are four in number. So, very, very important. The most important is Alport disease. The first I will teach you Alport disease. The most important in hereditary. After that, it is, I guess, Fabry disease. Fabry disease. Then Nail-Patella. Nail-Patella syndrome. Nail-Patella syndrome. And the last one is thin membrane disease. So, these four, all four, I will teach you in detail. So, these much we have to study today. All these glomerulonephritis we have to complete today only. Are you with me? Shall I start? Shall I start? So, I will be teaching you all the glomerulonephritis after classification is over. Let me continue. Let me continue with glomerular disease. That is glomerulonephritis. Okay. I will teach you all these. The hereditary one, the secondary one, the primary one. But all the glomerulonephritis have same clinical features. So, I cannot teach you clinical features individually. When I will teach you individual glomerulonephritis. So, before starting the individual glomerulonephritis, let me teach you the manifestations of glomerulonephritis in one shot only. Clinical manifestation. So, before starting the individual, let me teach you the presentation. The clinical feature. The manifestation of glomerulonephritis. In one shot only. Clinical manifestation. So, before starting the individual, let me teach you the presentation. The clinical features. The manifestation of glomerulonephritis. Or glomerulonephritis. Either and in nephritic syndrome or nephrotic syndrome. Either they result in nephritic or nephrotic. Now, most of the students even don't understand what is the meaning of nephritic, nephrotic. What is the difference in nephritic, nephrotic? Nephritic and nephrotic syndrome is not a disease. It is a syndrome. You know, it is a word which include multiple glomerulonephritis. Which all have same clinical features. It is also a word which have multiple glomerulonephritis. Which all have same features. So, first understand the clinical features. Make your difference. Then, so, there can be two type of patients in front of you. Right. There is a patient which is having a group of symptoms. You can label it. These are nephritic. Nephritic symptoms. There are symptoms. Again, nephritic symptoms of blood in the urine. Blood and hemoglobin. Never you will find. So, patient will come to you. My urine is red. Means the patient is having nephritic. And I'm not nephrotic. So, are they covered? So, you are having only few in the options. Now, um, come on the confirmation. You got my point. So, it narrows your diagnosis. Once you study the clinical features which come under nephritic and nephrotic syndrome. Have you got it? What is nephritic? Nephrotic? I will teach you both one by one. After that, I will start individual glomerulonephritis. Yes. So, let me start with nephritic syndrome. In nephritic syndrome, there are five clinical features. In nephrotic, there are six. So, in the nephritic, these are the five clinical features. Patient will come to you. Now, after getting your certificates, you will practice as a practicing doctor. You will be a licensed doctor. So, whenever any patient come to you with these five clinical features, the patient is having nephritic syndrome. And you should know all the causes of nephritic syndrome. So, patient is having one of them. Patient is having any one of them, right? So, the first important feature is hematuria. Hema means blood. Urea means urine. Blood and urine. So, patient complains of blood in urine. Either gross or microscopic. Sometimes, it is gross. Of the urine is gross red in color. But it is rare. Mostly it is microscopic. So, patient cannot find the urine is red. But if you do the lab, lab analysis, the urine analysis in the lab, in the microscope, RBCs are seen in the urine. But they are not that much that they give red color to the urine. Sometimes, they give. Sometimes, they don't.

Give, depending on the concentration of RBCs in the urine. So, hematuria is the first feature which differentiates nephritic from nephrotic. The most contrasting feature between nephritic and nephrotic is the hematuria, which differentiates the two. Hematuria is present in nephritic syndrome; it is absent in nephrotic. Please be crystal clear in your concept.

Right, the second thing. Patients also have protein in the urine, proteinuria, but it is very mild. Now, this proteinuria is present in both nephritic and nephrotic. But if it is mild, it is nephrotic. If it is severe, it is nephrotic. So, proteinuria is present in both. So, protein in urine is the second thing.

If you measure the blood pressure of the patient, the patient is hypertensive. The patient is having blood pressure more than 120/80. You know the normal systolic and diastolic blood pressure is 120 and 80. It is here more than 120/80, right?

The patient will complain of edema, especially below the eyes, especially in the morning. The patient has edema. In layman's language, edema is swelling. So, the patient will say, "Doctor, I'm having swelling in the body," especially on the soft tissue, in the ankles, um, in the just below the eye, that is periorbital edema. They are very typical, and in the morning, once the patient gets up, the face is puffy, the face is having edema, the eye is below the eyes, there is edema. So, that is swelling.

And last is oliguria, and that's the end stage, not at the initial stage. Only urea. What is the definition of polyuria and anuria? Oliguria: urine output in 24 hours less than 400 ml. In complete 24 hours, in complete 24 hours, the urine output of the patient is less than 400 ml, the patient is having oliguria. And if it is less than 50 ml per 24 hours, it is known as anuria. So, the patient is going in renal failure, the patient is going in acute chronic renal failure.

So, these are the five features. What are the five features? It is blood in urine, protein in urine, cast. The two: blood in urine, hematuria. Protein in urine, proteinuria. Hematuria is there, but proteinuria is mild. It is not severe, it is mild. After that, hypertension, edema, and oliguria. These are the five features of nephritic syndrome. Okay.

Hematuria, because of the blood in urine, it is blood and urine. The urine is smoky in color. This urine is red in color. Sometimes you will find RBC casts on microscope in the urine. Proteinuria is mild. Can you define mild and severe kidney protein urine? You will say, "Mam, proteinuria is mild." And kidney, there should be some cut-off, right? The cut-off is 3 grams per 24-hour urine. So, there is a patient in front of you, right? The patient is having edema, oliguria. You are suspecting some glomerulonephritis in the patient. Ask the patient to do a 24-hour urine analysis. What is 24-hour urinalysis? Start the test 8 a.m. in the morning, right, from today until tomorrow 8 a.m. in the morning. So, for 24 hours, ask the patient, "Don't void the urine in the commode, in the toilet. Collect all urine in a jar, in a bucket, in a sterile bucket." So, collect all the urine in a jar and submit it to the laboratory after 24 hours. So, in the lab, they will see how much is the volume, how much is the protein. If 24-hour urine contains protein less than 3 grams, this is less than 3 grams protein in 24-hour urine, so it is mild. Mild proteinuria. And if it is more than 3 grams of protein per 24-hour urine collection, it is severe. So, mild is seen in nephritic syndrome, and severe proteinuria is seen in nephrotic syndrome.

Proteinuria, that is protein in urine, it is seen in nephritic as well as nephrotic. Normal person's urine has protein in the urine, a very mild amount. How much? I'm saying it is 3 grams. Mother, 3000 milligrams. Normal urine, normal healthy urine, has less than 150 milligrams of protein in the urine. It is nearly nil. It is nearly negligible. 150, 100 to 150 mg may be present in urine in a normal healthy individual. But if it is 150 to 3000, it is nephrotic syndrome. If it is more than 3000 milligrams, it is nephrotic syndrome. So, that is the thing. That is the thing. So, that is proteinuria.

And proteinuria here is non-selective. Non-selective means all the protein will come in the urine. It can be albumin, globulin, transferrin, multiple proteins will come in the urine. In contrast to nephrotic syndrome, where proteinuria is selective, and only albumin comes in the urine, not other proteins. So, proteinuria occurs in both nephritic and nephrotic. But there are two differences. In nephritic, proteinuria is mild, that is less than 3 grams per 24 hours. In nephrotic syndrome, proteinuria is severe, that is more than 3 grams per 24 hours. In nephritic syndrome, the proteinuria is non-selective, that is all protein excreted in urine. In nephrotic syndrome, the proteinuria is selective, that is only albumin excreted in urine. Give me a thumbs up.

So, these are the two differences. Coming on hypertension. Hypertension is there, but it is only a feature of nephritic, not nephrotic. Edema again occurs in both. Again, here edema is mild, and in nephrotic, edema will be severe. Right? And oliguria is a feature. You know the definition of oliguria: less than 400 ml of urine per 24 hours. Again, ask the person to collect the urine for 24 hours in a jar, in a bucket, and see the volume. How much urine is excreted in 24 hours? Normal human being, normal urine excretion is um 1 to 1.5 liter, normal excretion, or more than that. Right? But less than 400 ml is defined as oliguria.

So, now tell me the examples of nephritic syndrome. So, what we have learned? What are the five features of the nephritic syndrome? First, tell me the five features of the nephritic syndrome. I'm asking nephritic, nephritic, nephritic, not nephrotic. See here, nephritic. Tell me the five features. Who will tell me the five features? It's hematuria, that is blood in urine, right? Hematuria. It's proteinuria, proteinuria, that is protein in urine. Hematuria, proteinuria. The third is hypertension, rise in blood pressure. The fourth is edema, that is swelling. And the last is oliguria. Oliguria, that is urine output less than 400 ml per 24 hours. If these five features are present in any patient, the patient is having nephritic syndrome.

Now, give me the examples of nephritic syndrome. Which glomerulonephritis presents as nephritic syndrome? Which of them? So, uh, which glomerulonephritis presents as nephritic syndrome from the primary? I have told you nine primary. Now, from the primary, it is the first one, PSGN. It is nephritic syndrome, right? The second one, RPGN. RPGN, it is also nephritic syndrome. But the third, MCD, it is not nephritic. The fourth, membranous, it is not nephritic either. Nephrotic. Membranous. The fifth, membranoproliferative, again, it is nephritic. It is nephritic. Focal segmental glomerulonephritis, FSGN, is nephritic. Like an FSGS will be nephrotic. Right? So, you have to learn the name. And IgA nephropathy is nephritic. So, out of nine, five are nephritic. Learn the name of five. Learn these five out of nine. These five are nephritic. The remaining will be nephrotic. So, you have to learn the concept. Glomerulonephritis will present with what clinical features? Now, when I will teach you all nine one by one, as I've told you, I'm going to teach you all nine one by one. So, when I will teach you PSGN, RPGN, one by one, I will not tell you clinical features. I will take it. PSGN, my nephritic syndrome, hotel. Do you understand? Nephritic. At the patient will present with five clinical features. You already know what are the clinical pictures. When I will teach you RPGN, massive fake line patient for nephritic syndrome, you will understand. Each time I will not give you the explanation of nephritic syndrome. So, in common, many shirokhan is nephritic. You got my point? So, these five glomerulonephritis present with nephritic syndrome. If you want to learn all, it's good. If you can't learn all five, learn RPGN. It is the most common cause of nephritic syndrome. It is the MCQ. The most common cause of nephritic syndrome is RPGN. Rapidly progressive glomerulonephritis. Also known as crescentic glomerulonephritis.

Coming on nephrotic syndrome. I am done with nephritic. Coming on nephrotic syndrome. In nephrotic syndrome, six features are present in the patient, not five. The first thing: hematuria is absent here. Directly start with proteinuria. Directly start with proteinuria. But this time, proteinuria is massive. It is severe. Yes, yes, Osmond. It is severe. It is massive. So, what is the definition of severe or massive, Osmond Malik? What is it? It is more than 3 grams per 24 hours. Yes or no? Yes or no? Because all maximum protein is excreted in urine. Maximum of the protein is excreted in urine. And which protein? It is selective. It is not non-selective like nephritic. It is selective. Albumin is excreted in urine. So, maximum your protein for albumin. So, blood may albumin will be low because it is excreted in urine. Now, the blood meal will be low. So, it is hypoalbuminemia. So, both things are related. If the patient has massive proteinuria, then only the person can have hypoalbuminemia. You may ask me a question, why you have not told hypoalbuminemia in nephritic syndrome? Proteinuria, you should ask me a question. There are two answers for this. Number one, the proteinuria was mild. Thought as a protein excreted in urine, not much. But yet, proteinuria is massive here. Maximum protein is excreted in urine. That's why blood meal. That's why mild was excreted in urine. The blood could cause that is the first reason. The second reason: proteinuria in nephritic syndrome, it was non-selective. All the proteins. It was mild and all the proteins were excreted in urine, not only albumin. Here, it is selective. Here, only albumin is excreted. And even severe, it is massive. That's why blood albumin concentration falls drastically. Right? That is hypoalbuminemia. Give me a thumbs up.

And that leads to edema. Mohammed, right? Edema. There was mild, and edema here is severe. Here, edema is severe. The cause of the edema in the two is different. Although edema, right? Now, it can be nephritic, it can be nephrotic. The reason is different. If the edema is mild, it is due to nephritic reason. I forgot to tell you, it is sodium and water retention in the body. Since the kidneys are not functioning, kidneys, patient was having oliguria. There, if you remember, what do you mean by oliguria? Oliguria is a feature of nephritic syndrome, which I have already told you, right? Oliguria means less urine. Less urine. What is urine contained? Urine contains sodium and water. Patient is not excreting sodium and water now. Because patient is in oliguria, so sodium and water is retained by the body. Oliguria means sodium and water is retained by the body. And this sodium water retention leads to edema. So, that is the cause of edema, nephritic syndrome. But in nephrotic syndrome, the cause of edema is decreased oncotic pressure. You know what is osmotic or oncotic pressure? The pressure due to the protein. Here, protein in the blood becomes less. Albumin in the blood becomes less. So, oncotic pressure will reduce. And that can lead to edema. You got my point?

The next patient has hyperlipidemia. The lipid in the blood will increase. You should ask me a reason. Pathology is all about why and how. What, why, how? In nephrotic syndrome, so you should ask me the reason for all these. Why the patient has increased lipid concentration in the blood? Why, why at all the patient must have increased lipid in the blood? I will tell you the reason. Increased lipid, not only blood, in urine also. So, patients have hyperlipidemia, hyperlipiduria. So, increased lipid in the blood, increased lipid in the urine. And the blood becomes hypercoagulable. I will be describing all these one by one. Let me start with the first one: massive proteinuria. As I have told you, the proteinuria is massive here. The proteinuria is severe. The definition of severe or massive is more than 3 grams per 24 hours. The protein excretion is more than 3 grams per 24 hours. And protein loss is selective, that is, only albumin is excreted in urine, not others. Right? So, that is the thing. That's why most of the albumin is lost in urine. Loss of most of the albumin in urine. That's why it leads to hypoalbuminemia. Less albumin in the blood. Blood, urine. So, blood, may albumin less. Less albumin. That reverses AG ratio. You know AG ratio, albumin globulin ratio. Albumin is the numerator, globulin is the denominator. So, you are saying numerator is reduced. So, the ratio will reduce. AG ratio reversal. You got my point? You got my point?

Now, along with albumin, some other proteins are lost. But in minor concentration. Mainly albumin is lost in urine. But what other proteins apart from albumin are lost? Can you list it? Can you tell me the name of other proteins which are lost in urine? Can you can you list it? The most important is immunoglobulin. Immunoglobulins are antibodies. There are five types of immunoglobulins in blood: gamma, Ig G, Ig A, Ig M, Ig D, Ig E. There are five types of immunoglobulins present. They will reduce. They will reduce. What is the function of immunoglobulin? They give immunity, humoral immunity. If immunoglobulin is reduced because they are lost in urine, right? The person is susceptible to infection. So, that's why a person with nephrotic syndrome is more susceptible to infection. This is the reason. Now, you can correlate. Maybe in nephrotic syndrome, patient, the patient with nephrotic syndrome or patient with glomerulonephritis can have more infection, more vulnerable to infection. Why? What is the connection? The connection is this because in nephrotic syndrome, the patient has severe proteinuria. So, most of the protein is lost in urine. One of the protein is immunoglobulin. So, patient may immunoglobulin are lost in the urine. So, less immunoglobulin in the blood. So, less immunity in the blood. So, increase chances of infection. So, name the infection which is most common in such patients. That these patients have spontaneous bacterial peritonitis very commonly. This this infection occurs very common because they are vulnerable to the infection. So, bacterial infections are common or constant bacterial infection. So, the patient with nephrotic syndrome has high chances of developing bacterial peritonitis. They have high chances of developing bacterial peritonitis. Name the most common bacteria. The answer is: infections are very common in nephrotic syndrome. So, these all things you will get in your clinical scenario question. A 45-year-old male patient having one of the glomerulonephritis, having severe proteinuria, having this, that, he is vulnerable to some infection. He is having spontaneous bacterial peritonitis. So, the clinical scenario is about the nephrotic syndrome and which is leading to the infection in the patient. Most common bacteria is pneumococcus, followed by E. coli.

Other proteins which are lost is antithrombin. You know, blood, may antithrombin is present. It is lost. It is lost in urine. But the function of antithrombin? Antithrombin prevents coagulation in the blood. In the in my blood, I am having antithrombin in me. I don't have nephrotic syndrome. I'm having antithrombin in me. So, my blood is not coagulable. So, without injury, there is no clot formation inside me. Thrombus is not formed. You know thrombus formation, three reasons I taught you in general pathology. The Virchow's triad, if you have remembered, if you have understood the Virchow's triad, the general pathology. The reason for thrombus formation. So, there are three reasons. The third reason is hypercoagulability. That is loss of antithrombin three. Now, this is the reason why a person with nephrotic syndrome has multiple thrombus formation. Renal vein thrombosis formation. So, they are it is very common to find thrombus in a person with nephrotic syndrome. What is the connection? Nephrotic syndrome, kidney may you are saying thrombus are formed in the blood. Connection. This is the connection. Because in nephrotic syndrome, patient has severe massive proteinuria. So, most of the protein are lost in urine. So, antithrombin is also a protein which is lost in urine. So, blood concentration of antithrombin will fall. That can make the blood hypercoagulable. That will give the blood hypercoagulability. You got my point? You got my point?

The next protein which is lost in urine is transferrin. That's why the patient will be anemic. Transferrin is required. Transferrin is the transporter of iron. If you know, transferrin is the transporter of iron. If transferrin is less, iron absorption will be less. Iron is less. Patients have iron deficiency anemia, which is a microcytic hypochromic anemia. So, this is the reason why a patient with nephrotic syndrome presents with anemia. You can ask me a question. Patient problem, and a patient has some problem in the kidney. Patient is having one of the glomerular nephritis which leads to nephrotic syndrome. Why the patient can have iron deficiency anemia? What is the connection? The connection is this because patient is losing losing most of the proteins in urine. And transferrin is one of the protein. So, transferrin is lost in urine. So, less transferrin in blood. Transferrin is required for iron absorption. So, less iron in the blood. Iron less, it will lead to iron deficiency anemia, which is a microcytic hypochromic anemia. So, make a flow chart for all these. Right? You got my point?

Next protein which is lost is in urine called cholecalciferol binding protein. That will lead to hypocalcemia. If you see the calcium concentration in blood, it is less in such persons. And this is the reason this patient has also thyroxine binding globulin lost in urine. That's why these patients usually have hypothyroidism. So, nephrotic syndrome patient can come to you as a complication. And the patient can have hypothyroidism. So, this is the connection. This is the connection. Right? Ceruloplasmin is also low. That is copper level will be low. All the proteins are reduced in blood because they are lost in urine. Only one protein increases in blood in nephrotic syndrome. And the name of that protein is fibrinogen. Fibrinogen level increases in nephrotic syndrome. So, I am teaching you right now nephrotic syndrome. Nephrotic syndrome. Nephrotic syndrome has six features. The first feature is proteinuria, which is massive. Massive or severe proteinuria. Proteinuria in which most of the protein is lost in urine. So, in the blood, less protein is there. In the blood, less protein is there. So, mainly mostly albumin is lost. So, patients have hypoalbuminemia. Albumin is reduced in the blood. That reduces because of which the patient has less osmotic pressure and patient has edema. These are the consequences. Not only this, patient has reduced immunoglobulin, which leads to infection. Not only this, patient has reduced thyroxine. So, because of which patients have hypothyroidism. Not only this, patient has hypothyroidism. I'm unable to write. Patients have reduced transferrin. Because of which patients have anemia. Or concerti. I just forgot. So, patient has, what other proteins were there? Patients have reduced antithrombin. Because of which patients have more chances of thrombus formation. So, all these proteins are lost in the urine. That's why their concentration is reduced, reduced, reduced, reduced, reduced. Only one protein in the blood increases in in nephrotic syndrome. The answer of that is fibrinogen. Fibrinogen. Fibrinogen increases in blood, not decreases. So, the combination of the two. Fibrinogen is the anti-a. Fibrinogen is a, you know, thrombolytic. Uh, thrombolytic protein. Uh, so, decreased antithrombin and increased fibrinogen. Both make the blood hypercoagulable. So, hypercoagulability of the blood is due to these two reasons. So, that is the nephrotic syndrome. Protein. Edema is there. Edema is severe. And it is due to fall in osmotic pressure, not due to sodium water retention like nephritic syndrome.

The next is hyperlipidemia. Now, why the lipid increases in blood and in urine in patient with nephrotic syndrome? What is the reason? Okay. So, you tell me from where protein comes in blood? You tell me from where protein comes in the blood. Let me draw a blood vessel. Okay. This is a blood vessel. Inside the blood vessel, can you tell me the source of the protein? From where protein comes? This is the protein present in our blood. This is a normal healthy human, healthy human blood protein. Cancer. There are two sources. You should tell me. My dietary protein, which we eat in the diet. We eat eggs, we eat pulses, we eat soya bean and meat. So, these are the sources of protein. So, whatever protein we take in diet, so that get absorbed from the intestine and come in blood. So, that is the first source, the dietary, the intestinal. The second source of protein is liver. Liver also synthesizes protein. Right? The second source of protein is liver. Here, you can see the liver synthesized protein and given the blood. So, see the two sources of protein in the blood. This is normal. We all know that. Why I'm telling you this? Let me give you a minute.

So, now let me draw a kidney. Normally, when this blood is going to the kidney, kidney do not excrete protein. In a normal healthy human kidney, do not excrete protein. But if the kidney has nephritic or especially nephrotic syndrome, there is massive proteinuria. So, all this currently I am talking about nephrotic syndrome. So, just suppose this kidney is not healthy kidney. This kidney is having nephrotic syndrome. So, whatever protein going in the kidney, that is excreted in urine. That is excreted in urine. So, the blood concentration of the protein falls, falls, falls, falls dramatically. Falls because the proteinuria here is massive. Massive proteinuria is there. Most of the protein is lost in urine. So, blood by protein concentration is false. So, liver will try to compensate. Liver will try to compensate this loss by trying to increase synthesis of protein. Trying to increase synthesis of protein. Not lipoprotein are one of the proteins. Yes or no? What are lipoproteins? Lipoprotein is VLDL, LDL. You know all these. So, liver will try to compensate the increase, the loss of the protein which is occurring in urine and nephrotic syndrome by causing increased synthesis of lipoprotein. So, basically, liver is increasing the synthesis of lipoprotein. Because there are more lipoprotein in the blood, lipid, lipid absorption will increase. So, patients have more lipid in the blood. That's why this patient has hyperlipidemia. That's why patients with nephrotic syndrome have hyperlipidemia. This is the reason because liver is trying to compensate the loss of the protein by causing increased synthesis of one of the protein, lipoprotein. So, lipoprotein is increased. That's why patients have hyperlipidemia. And the increase, increased lipid, will go in the kidney also and excreted in the urine also. And that's why patients have lipiduria, hyperlipiduria. So, lipid increases in the blood first and then increases in the urine. So, lipidemia and lipiduria, both are features of nephrotic syndrome. So, blood increased blood levels of total lipid, cholesterol, triglyceride, VLDL because liver is trying to compensate. Liver is responding to heavy proteinuria and trying to compensate by increasing synthesis of lipoprotein. So, that is the reason. And increase lipidemia followed by lipiduria, increased concentration of lipid in the blood, excreted in the urine. So, that is the thing.

And the last is hypercoagulability. I already taught you the reason for hypercoagulability. That is loss of antithrombin and increased fibrinogen. These both will contribute to hypercoagulability.

Now, name the, give me the examples of nephrotic syndrome. So, nephrotic syndrome, it is MCD. MCD is the most common example. Membranous glomerulonephritis. Membranoproliferative presents with both. Focal segmental glomerulosclerosis, it is nephrotic syndrome. And again, IgA present with both. Right? If you want to learn all, it's good. If you don't want to learn all, learn the most common. Most common cause of nephrotic syndrome in children, it is minimal change disease. In children, it is minimal change disease. And in adults, it is membranous glomerulonephritis. So, the answer is different in children and in adult. Let me give you the final summary. Full and final summary of nephritic and nephrotic. I am done. I am done with nephritic and nephrotic. And now I will teach you individual glomerulonephritis. Right? So, nephritic, please revise with me. Help me in revising. Nephritic, nephrotic. Please everyone, see here. It is I, here it is O. Nephritic and nephrotic. First, tell me the one, two, three, four, five symptoms here. And one, two, three, four, five, six symptoms here. Who will help me? Nimisha Malik? Anyone else? Fernando? Anyone would try to help me? The five symptoms of nephritic. Then we will come on the examples and most common. The second thing. First, tell me the five, five features. So, let me start with nephritic. The most important feature is hematuria. Hematuria, that is blood in urine. Hematuria is absent here. Hematuria is never seen here. Yes or no? The second feature here is proteinuria. Proteinuria, but this proteinuria is mild. Here also, the first feature I will write is proteinuria. But this proteinuria is massive. You know the specific cut-off? It is 3 grams per 24-hour urine. Less than 3 grams per 24-hour urine, mild proteinuria. More than 3 grams per 24-hour urine, it is massive proteinuria. So, it is three. If I say 2.9, it will go towards nephritic syndrome. If I say 3.1, it will go towards nephrotic syndrome. So, the cut-off is the three that you have to take into consideration. Give me a thumbs up. So, that is the proteinuria. The next feature is the edema. Edema again. Non-selective. Selective also, Malik. Very good. So, this side, the proteinuria is non-selective. That is all proteins are excreted. And this time, this, this side, more or less, it is selective, especially albumin is excreted. Edema again. Here, it is mild. And edema again, here, it is massive or severe or massive. Right? The cause of the edema is different in both of them. Who will tell me the cause of edema? The cause of edema here is sodium and water retention. Sodium, water retention. The cause of edema here is decreased osmotic pressure. So, please learn the cause of edema is different in nephritic and nephrotic syndrome. Right? The next two here is hypertension and oliguria. These are the features of nephritic only. These two are not common in nephrotic. Hypertension is mild. Oliguria, definition are less than 400 ml of urine per 24 hours. That is based on the volume of urine coming. Here, most of the protein is lost in urine. Massive proteinuria leads to hypo. So, less albumin in the blood. We understood that also. There is hyperlipidemia in the blood and hyperlipiduria in the urine. Hyperlipidemia, that is increased lipid in the blood. And hyperlipiduria, that is increased lipid in the urine. You know the reason for both of them, I guess. And last one, the blood become hypercoagulable. Hypercoagulable. Everyone, give me a thumbs up. Abdullah, there is no hypertension in nephrotic. Hypertension is a feature of nephritic, not nephrotic. You got my point, Abdullah? Yes. So, these are the five and six features of nephritic and nephrotic syndrome. Crystal clear in front of you, I guess. It's me. No student, none of the medical students should have even a slightest doubt here. You shouldn't have any doubt here. After that, I would like to move on the examples. Okay. I'm not writing all the examples. Tell me the most common cause of nephritic syndrome. And tell me the most common cause of nephrotic syndrome. Who will tell me? In nephritic syndrome, answer is very simple. Only one answer is there. RPGN. Rapidly progressive glomerulonephritis. Rapidly progressive glomerulonephritis. The most common cause of nephritic syndrome in children also, and adult also. But here, the answers will be different. Here, the answer will be different for children. And here, the answer will be different for adult. Who will tell me the two answers? In children and adults? Who will tell me the two answers? If I ask in children, the answer becomes minimal change disease. That is MCD. And if I ask in adult, the answer will become membranous glomerulonephritis. MG. And everyone, give me a thumbs up. This is the summary. Can you see the board? I guess you can see, right? So, this is the summary of nephritic and nephrotic syndrome. Right? We have done the nephritic and nephrotic syndrome. The same thing is written in front of you. You can read the thing. What it is written. You can see the most common cause of nephritic syndrome are nephrotic syndrome in adults, it is membranous glomerulonephritis. And if you ask about the children, it's minimal change disease. So, in children and adults, the answer is different. Everyone, give me a thumbs up. Shall I move ahead? Shall I move ahead? The reason for edema is different. The reason for edema in nephrotic syndrome is hypoalbuminemia. And the reason for edema in nephritic syndrome is sodium water retention. I have already explained you the two things. I guess we are done with nephritic and nephrotic. Does anyone have any doubt? You can read all the points. I have already explained you all the points. Which feature is common? Beer. So, we will see all the points one by one. See the proteinuria. This is nephritic and this is nephrotic. Proteinuria is mild here. And proteinuria is heavy here. The cut-off is 3 grams per 24-hour urine. And non-selective. Selective is also a part. Hypoalbuminemia is present here because most of the protein is lost. But not here. So, it is absent here. Edema. Again, both the things. Here, it is mild. And here, it is massive. The reason for the edema here is sodium water retention. And here, it is decreased osmotic pressure. The reason for the edema, right? Hematuria, hypertension, and oliguria. These three things are present here. Hematuria, hypertension, and oliguria. These three things are absent here. Absent, absent, and absent. Right? Now, the remaining three things. You can see the remaining three things. That is hyperlipidemia, hyperlipiduria, and hypercoagulability. These three things are present here. But absent here. You already know this, I guess. I have already crystal clear concept I have given to you. Everyone, give me a thumbs up. Shall I shall I move ahead? So, these are the differences between nephritic and nephrotic. I would like to ask few questions based on nephritic and nephrotic. If your concepts are clear, you please answer it. And please write your answer in the chat box. I want to see who is the first and who is the correct. Right? I want more things, accuracy and speed. Right? So, please don't rush. Read it. Give it a thought and then tell me what the correct answer. So, hypercoagulation in nephrotic syndrome is due to which reason? We know in nephrotic syndrome, the blood become hypercoagulable. Tell me the reason for that. I taught you two reasons. One of them is given in the option. The four options are in front of you. So, what is the correct answer? Abdullah Siddiqah Malik? What is the anchor? Who will tell me? What is the correct answer here? So, is that loss of antithrombin? Is it decreased fibrinogen? Is it decreased metabolism of vitamin K? Or is it increased protein C? What is the reason? Yes, absolutely right. Absolutely right. The correct answer is loss of antithrombin. I told you that in nephrotic syndrome, many proteins are lost in urine. Many proteins. So, the concentration of many proteins in the blood will fall. So, I have given you the list. So, albumin is the most common protein which is lost. And that's why less concentration in the blood. Apart from albumin, it is immunoglobulin. It is, uh, transferrin. It is thyroxine. It is ceruloplasmin. But the main protein is antithrombin 3, which is lost in urine. That's why blood concentration of antithrombin 3 is less. That leads to blood hypercoagulable. Only one protein increases in blood. The answer is fibrinogen. And the reason is liver compensation. The fibri. So, these are the two reasons of blood hypercoagulable in nephrotic syndrome. Loss of antithrombin in the urine. So, less antithrombin in blood because it is lost in urine. And increased fibrinogen in the blood. This option will also become correct. So, it is decreased antithrombin and increased fibrinogen. These are the two reasons for blood hypercoagulable. Everyone, give me a thumbs up. And you all are right. Very good. Very good. Deepam Malik, Abdullah, everyone is correct. So, moving ahead to the next question. This is the next question in front of you. Now, please read the question. All of the following are decreased in nephrotic syndrome except. The question contains except. So, one of them is not decreased, it is increased. So, tell me one protein which is increased. Rest all will decrease. I taught you specifically the name of the one protein which is increased in nephrotic. Rest all are decreased. Who will tell me the answer of that protein? Is it transferrin? Is it fibrinogen? Is it ceruloplasmin? Or is it albumin? Yes, yes, absolutely right. The correct answer is fibrinogen. So, only fibrinogen increases in blood. Rest all decrease. The reason for fibrinogen increase is the liver compensation. Liver tries to compensate the protein loss. And liver can increase only one protein, fibrinogen. Rest all will be lost in the urine. And liver cannot compensate it. So, correct answer here is B. Yes, absolutely right. Okay, I'm sorry. This is the next question. What is the reason for edema in nephrotic syndrome? Specific question, specific answer. Don't confuse. Don't do mistakes. Specific question, specific answer. Reason for edema, nephrotic syndrome. I'm not asking nephritic. I'm asking nephrotic syndrome. What would you like to say? What would you like to say? Yes, Balaji, absolutely right. What about others? What is the correct answer? Is it sodium water retention? Is it increased venous pressure? Is it hypoalbuminemia? Is it hyperlipidemia? Yes, absolutely right. Yada crease. It is hypoalbuminemia, which decreases oncotic pressure. So, decreased oncotic pressure due to hypoalbuminemia is the reason for, um, edema in nephrotic syndrome. The same question. I'm changing the question now. You tell me the answer. Answer C. Here, if this is the question, answer is I'm changing nephrotic to nephritic. I'm changing the spelling. Nephrotic to nephritic syndrome. Now, what is your answer from A, B, C, D? Who will tell me the answer? Change the question from nephrotic to nephritic. Now, what is your answer from A, B, C, D? Answer will change. So, answer in this case scenario will be A. You all are right. Absolutely right. Very good. In this scenario, answer will be coming. So, depending on the question, what is your answer? It depends, right? So, correct answer here is C, if it is asked for nephrotic. Right? Okay. The next question is in front of you. What is the most common cause of nephrotic syndrome? Nephrotic syndrome, most common cause of nephrotic syndrome in adults, not in children. In adults. Nephrotic syndrome in adults. So, yes, you all are right. In adults, the answer is membranous glomerulonephritis. Again, I'm changing the same question. Instead of adults, I'm asking children. So, most common cause of nephrotic syndrome, but not in adults, but in children. What is the answer now? What is the answer now? In children, it will be minimal change disease. Very good, Deep. Very good, very good. So, if I ask adult, answer is A. If I ask children, answer is B. So, you can say by changing the question, how the answer will become changed. So, same question is those most common cause of nephrotic syndrome in children. So, answer will become B. This time, I've already asked this question, right? I am done with the overview of glomerulonephritis. This was episode one, right? Now, I will teach you the primary glomerulonephritis, which are nine in number. We have already seen the classification. They are nine in number. I will teach you all nine in a comparative way. No one in this world will teach you in such a beautiful comparative way the nine types of glomerulonephritis. Right? First, I will teach you APGN, acute proliferative glomerulonephritis, or post-streptococcal glomerulonephritis. Then I will teach you RPGN. Then I will teach you MCD. Then MGN. Then MPG. Then focal segmental glomerulosclerosis. Focal segmental glomerulosclerosis. Then IgA nephropathy. Then chronic. So, these nine, I will teach you under following headings. I will teach you etiopathogenesis of all of them. Then the gross feature. Then three microscopy. In renal biopsy, we always say three types of microscopy: the light microscopy, the electron microscopy, the immunofluorescence microscopy. Right? So, you have to fill this table with me. Here, you have to draw the flow charts. Here, you have to draw the diagrams. The three types of diagrams you have to draw. Right? With this, it will require the next two hours. In the next two hours, we will finish all primary types of glomerulonephritis in a beautiful comparative manner. So, I request all my dear students to take a big sheet and divide the columns, the nine columns like this, and five columns like this, and one more you can add here, the clinical features. In the clinical features, you have to write either nephritic or nephrotic. I've already taught you which one of them are nephritic, which of them are nephrotic. Now, you know the meaning of nephritic, nephrotic. So, add one more column here. So, in this way, I will complete the nine glomerulonephritis. Are you people with me? But you have to give me a break for the 15 minutes. And after 15 minutes, join episode number two. So, give me a minute. Let me announce my next class. Then you people can go for a break of 15 minutes. Then we will connect again. Okay. Just a second. So, here I am. So, okay, my next class is just after 15 minutes. Right? That is sharp 10 a.m. Right? Now, sharp 10:10 a.m. Right? Just after 15 minutes, join episode number two of renal pathology, glomerulonephritis. It is episode number one currently going on since last two weeks. Two hours for the next two hours, we will connect on episode number two from 10 to 12. In 10 to 12, I will cover all primary glomerulonephritis. I want all the students to come back. Where is the class? It is on the same YouTube channel where you are attending now. That is Unacademy Live. You all have to come back on the YouTube only. On the same YouTube channel, you will find me live after 15 minutes. Right? Now, there are few announcements for you. On Unacademy, 2023 NEET PG batch is already launched. If you take the subscriptions, you will be eligible for the repeaters batch for NEET PG 2020. Freshers batch. Right? On Unacademy, we have five types of subscriptions available for the students. The Plus subscription, in which you will get only Unacademy live and recorded lectures. In Iconic, along with Unacademy, you will be having prep planner recordings also. In Live subscription, you will be having only test series. In MBBS Prep 1, you will get batches for Anatomy, Biochemistry, Physiology only. And in UPSC CMS subscription, you will be getting UPSC preparation batches. Right? You can see the various plans along with various prices, various durations. In each subscription, whatever plan fits to you, you can take that plan. You can purchase that plan. You can notice one thing. Longer the plan, cheaper it is. So, if you are a first crop, second class student, go with four year, three year, two year. Per month wise, it will be cheaper. But it's up to your choice, according to your wish, requirement. If you want to take any of these subscriptions, you are most welcome. If you are not sure, you can take as small as three months subscription for a trial. Right? Whatever subscription you are planning to take, before payment, please apply my code. Sachdev. My code is S-A-C-H-D-E-V. That is my surname. I am Dr. Priyanka Sachdev. So, Sachdev is my surname. Without space, 10. So, this is the code. If you apply my code on any of these subscriptions, you will get straight forward 10 percent discount. If you apply before payment. Thank you very much. I want all of you to join me back at 10 a.m. Right now, for episode 2 of renal pathology. Bye-bye. I'm ending it.