 damage to glomerulus causes either nephrotic syndrome and nephritic syndrome. Glomerulus forms the filtering apparatus in the nephron and if we see the filtration barrier through which the filtration of substances occurs and the substances enter into the nephron this filtration barrier consists of three main layers. In this first layer is formed by these capillary endothelial cells which is basically the cells lining the capillary actually there is a capillary trough which forms the glomerulus so the walls of these capillaries are lined by endothelial cells. Then beneath these endothelial cells there is a layer of the basement membrane so here magnified version it is showing the layer of the basement membrane and third layer is that of epithelial cells and this epithelial cells basically consist to offer two types of epithelial cells so two layers are there one layer is reflected on the glomerulus which forms a filtration barrier and the other is part of the Bormins capsule so this layer which forms a part of the filtration apparatus that is visceral epithelial layer okay visceral epithelial cells and these cells are also known as podocytes okay so here a podocyte has been shown now you see these podocytes have lot of processes so these are known as food processes of podocytes and these food processes of different different podocytes they basically encircle these layers okay but you see there is some space between these food processes of the podocytes and this forms the slit diaphragm through which the filtration will take place now this slit diaphragm has certain proteins which are basically the proteins of the food processes of the podocytes only and very important one is nephrin then there is podosin we need to know all these proteins because there might be mutations in the genes which are responsible for the production of these proteins and these mutations will lead to problems in the slit diaphragm and hence the problems in the filtration of the substances across the glomerular filtration barrier now with this basic concept of the glomerular filtration membrane which basically consists of capillary endothelium the basement membrane and the visceral epithelial cells that is the podocytes let us go into what is this nephrotic syndrome and what is this nephritic syndrome just remember one thing here before we proceeded that i told about visceral epithelial cells there is another layer parietal epithelial cells and this parietal epithelial cell basically lines these bowman's capsule okay so there is parietal epithelial cells here why we need to know this because we will see one condition in which there is proliferation of this parietal epithelial cells as well so let us first move on to that what are the mechanisms which can cause glomerular injury because based on these mechanisms either the patient can present with nephrotic syndrome nephritic syndrome or maybe a mixed condition so first very important mechanism of glomerular injury is immune mechanisms actually most of the injuries which occur to the glomerulus are due to this immune mechanisms then the second one is podocyte injury so only the foot processes we were talking about the visceral epithelial cell that is the podocyte so that podocyte injury can occur and third one is the nephron loss so obviously when nephron loss is there the glomerulus will not be there and the filtration will be affected but let us focus here only these two mechanisms how this immune injury will occur and the podocyte injury will occur so as I told you that most of the injury is due to the immune mechanisms and this immune mechanisms means that there is antigen antibody complex formation so what happens that either there may be an antibody which reacts with the antigen of the glomerulus itself okay so it is an antigen which is inherent to the body antigen which is situated in the glomerulus itself okay then there may be an antibody against an external antigen but this external antigen goes and deposits itself first in the glomerulus and then the antibody goes and reacts with this antigen which is present in the glomerulus okay third one is that there may be external antigen and there is formation of this antigen antibody complex and this antigen antibody complex goes and deposits itself in the glomerulus so three mechanisms basically one antibody against the inherent antigen of the glomerulus then antibody against an external antigen which went and deposited in the glomerulus and then the formation of antigen antibody complex in the circulation itself and this antigen antibody complex goes and deposits in the glomerular walls now when we talk about the diseases we will see some features of the diseases then we will see that where this antigen antibody complex is forming is it forming in the sub epithelial membrane okay sub epithelial we will see what are these terms is it forming in the sub endothelial region okay or is it forming in the mesangium we didn't deal with mesangium when we were talking about our layers of the glomerular capillary wall actually there are mesangium cells which are situated in between the glomerular capillary so that is the mesangium and when we talk about these terms of epithelial sub endothelial and mesangium actually we saw that this is the basement membrane and here there are endothelial cells right and here there are that epithelial cells visceral epithelial cells food processes so when the deposition of the antigen antibody complex is here so these are endothelial cells so these are known as sub endothelial deposition when the deposition is here then it is known as sub epithelial deposition so this we can visualize in electron microscopy and it differs from diseases to diseases then next mechanism can be podocyte injury very important and this podocyte injury can be either because of antibodies to antigens of the podocytes right and second one can be due to some toxins or some cytokines okay so that can be another mechanism of glomerular injury which can lead to various presentation now we will go into specific nephrotic and nephritic syndromes but one concept I want you to note here is that especially if there is podocyte injury if there is podocyte injury then there will be presentation mainly as nephrotic syndrome okay and if there is the immune mechanisms mostly immune mechanisms which are causing the injury then this will mainly present as nephritic syndrome broad concept actually in clinical presentation what we see that there are certain diseases which present with the combination of nephrotic and nephritic syndrome as well then there are certain nephrotic syndrome diseases which are broadly classified in the nephrotic syndrome but sometimes they can present as nephritic syndrome also because what happens that this podocyte injury may be a milder form of the injury and as the disease progresses there will be activation of the immune mechanisms and ultimately the person will land up in nephritic syndrome so there may be that a disease classified under nephrotic syndrome may present with nephritic syndrome also so let us go into the pathophysiology first for nephrotic syndrome so first of all what is actually nephrotic syndrome see when we talk about nephrotic and nephritic syndrome we are not talking about specific diseases it is a kind of a clinical presentation of the patient that we classify as nephrotic and nephritic syndrome and then we go ahead and find what is the disease condition which is causing this condition so this clinical profile of the patient what is it in nephrotic syndrome first of all there is proteinuria proteinuria that means protein is being lost in the urine and this proteinuria when it is greater than 3.5 grams per day then only we call it as a proteinuria of nephrotic range understanding so heavy proteinuria daily protein loss greater than 3.5 grams or more that is known as nephrotic range proteinuria below this that is known as sub nephrotic range proteinuria then second because of this proteinuria there is development of decrease in proteins in blood especially there is decrease in albumin in blood okay because albumin is the first protein which starts filtering when there is damage to the glomerulus remember actually little bit albumin does filter in the glomerulus normally also but when this damage to the glomerulus occurs then more and more filtration of albumin starts so that causes decrease in the albumin levels in blood and decrease in albumin levels actually less than 3 gram per deciliter occur in blood now when there is only albumin loss in a urine that is known as selective proteinuria okay and when other proteins as well start filtering from the glomerulus then that is known as non-selective proteinuria so as I told you that albumin is the first protein which is filtering so obviously if it is the only protein which is filtering that means damage to the glomerulus is not that much when the damage increases then there will be non-selective proteinuria that means other proteins also will start filtering from the glomerulus third there will be presence of edema generalized edema what is known as anasarca we will see what is the pathophysiology of all this thing okay so just now we are seeing the features and fourth there is presence of hyperlipidemia so lipids are increased in blood hyperlipidemia and remember that in blood lipids are also in combination with the plasma proteins now when there is loss of the plasma protein so obviously the glomerulus will not be able to retain these lipids also in the blood and there will be presence of lipiduria also lipiduria okay so these are the main features of nephrotic syndrome so now let us see that what is the pathophysiology what are the changes happening in the body because of proteinuria because main thing is that damage to the glomerulus has caused proteinuria to occur that is the filtration of the proteins into the bromine space into the tibials and loss of these proteins in urine so what happens that there is damage to the glomerulus and the damages which we discussed which damage especially the damage to the podocytes okay remember so whenever you see the term that there is damage to the podocytes right what is specifically is used is effacement of the food processes of podocytes okay when there is damage to the glomerulus that is to the podocytes there will develop proteinuria okay and this proteinuria what it will do is that there will be decrease in the oncotic pressure now you know that proteins basically cause the development of the oncotic pressure is in the blood and the oncotic pressure is a pull force so suppose this is the capillaries okay and this is the interstitial space interstitial fluid will be here what happens that due to the hydrostatic pressure fluid movement occurs outside the capillaries and due to the oncotic pressure fluid comes back into the capillaries so there is a push force and there is a pull force now when this oncotic pressure decreases the pull force of fluid into the blood is falling so because of that the less fluid will enter back into the capillaries and in the venous end and that will lead to accumulation of fluid in the interstitial space so decrease in oncotic pressure will lead to edema okay so that is accumulation of more fluid into interstitial space also if fluid is going out of the circulation then where it will be less less fluid in the intravascular space so basically edema will cause decrease in fluid in intravascular space very important because that is important if intravascular space fluid is less then it will decrease the circulation to the various organs isn't it now this decrease in fluid in intravascular space leads to all of the changes the secondary changes in circulation and what are these this decrease fluid in intravascular space because of this there will be decrease in renal blood flow decrease renal blood flow that will lead to decrease in GFR okay because that is one factor which will affect the hydrostatic pressure in the glomerulus and if you see my video on factors affecting glomerular filtration rate you will understand that decrease renal blood flow will decrease GFR then decrease GFR will activate the tubular glomerular feedback very important again I have made another video on this you can have a look that this tubular glomerular feedback basically causes the activation of renin angiotensin aldosterone system actually it is known as renin angiotensin system but I remember it has renin angiotensin aldosterone system and sometimes one A more I add because of release of ADH also okay now what is happening that with activation of all these what happens that there is basically increased formation of angiotensin 2 increased release of aldosterone from adrenal cortex and also there is increased release of ADH and you see because fluid is moving out into the intravascular space there is hemo concentration here also hemo concentration so whatever substances are there more concentrated they are becoming and this leads to increase in osmolarity which ultimately also causes release of ADH so that is another stimulus for release of ADH now this angiotensin 2 will lead to what this is going to cause vasoconstriction and other actions also ways angiotensin 2 that is angiotensin 2 only which is causing release of aldosterone ADH then it activates a thirst mechanism also okay so vasoconstriction is very important because it leads to increase in blood pressure increase in blood pressure okay then aldosterone what it is doing that is causing increase in the sodium reabsorption from the kidney and whenever sodium is reabsorbed water moves along with that so basically it is trying to correct the intravascular space fluid volume fine but you see since proteins are not there will this fluid volume be corrected no because whatever extra fluid is being added that will again move out that is happening because as hydro static pressure increases the fluid keeps moving out but it needs to be brought back into the circulation but if on caustic pressure is less that is not happening so it will lead to more and more edema so body is trying to correct but it is becoming counterproductive similarly ADH ADH causes more water reabsorption so that is also an compensatory mechanism to increase fluid in intravascular space but is that helping no it will not help because it will lead to more and more edema so that is one aspect of the nephrotic syndrome secondly due to heavy proteinuria what happens that liver starts to compensate liver starts to produce more proteins but that compensation is not enough but due to this compensatory effect of the liver it starts producing other proteins also and with that liver compensation it produces lipoproteins and that means there will be increase in the lipids so that causes hyperlipidemia and as I told you that because the proteins are not being retained in the circulation this hyperlipidemia ultimately will result in lipiduria okay so that is another concept now lipiduria is occurring but are tubular cells after filtration what are tubular cells do they try to absorb the reabsorb the stuff which has been filtered so this fat also they try to reabsorb the protein also they reabsorb some of the proteins which is filtered is reabsorbed by endocytrosil but the capacity of the tubular cells is always overwhelmed so that is why so much loss of proteins is occurring now with the reabsorption of the lipids what happens these tubular cells become lipid laden lipid laden cells and these lipid laden cells when shed into the tubular fluid they are lost in urine that is why in urine analysis we get fat laden ovals cells in nephrotic syndrome so what we have discussed we have discussed one concept on anchotic pressure other concept on lipiduria hyperlipidemia and lipiduria and hawaii there is presence of fat laden cells then other changes are also occurring let us see what are those let me just rub all this make some space okay so third change which is occurring what we were talking about is non-selective proteinuria other proteins are also getting filtered so they will be decreased in globlins as well and what are the globlins responsible for these are gamma globlins which are produced from b-cells they are also getting lost in urine so what will happen the person there will be more chances of infection okay so resistance to infection is decreasing then say suppose other proteins are also lost and one very important protein is antithrombin 3 okay these are small proteins which are lost first like so antithrombin 3 when it is lost what will happen there will be more chances of coagulation antithrombin 3 is basically antithrombin that is it is preventing the excessive action of the thrombin so when that is being lost its concentration decreasing it increases the chances of coagulation in blood and ultimately it leads to one of the complications of nephrotic syndrome that is the deep vein thrombosis and also we said that because of the loss of fluid in the interstitial space the intravascular volume is decreasing and there is hemoconcentration so whenever there is hemoconcentration the blood flow the rate at which it is flowing slows down and that is known as stasis and that also promotes thrombus formation so loss of antithrombin 3 and stasis in the blood they all promote the thrombus formation with this now let us see some important diseases which lead to nephrotic syndrome I will not go into the full pathology of that but primary glomeral diseases the secondary one I will not talk about primary glomeral diseases which lead to nephrotic syndrome let us see in brief so we will talk about three diseases one is minimal change disease second is focal segmental glomerulus sclerosis and third is membranous nephropathy now tell me what will be the common thing in all of these see as I told you that the main thing which leads to nephrotic syndrome is a facement of the foot processes of the visceral epithelial cells that is the podocytes so that will be common to all so let us see how these diseases will be present how they are similar and how they differ from each other first of all let us talk about the presentation so this minimal change disease it is present generally present in children 2 to 6 years of age and they present with selective proteinuria selective proteinuria is what that is loss of only albumin selective proteinuria fsgs most common nephrotic syndrome cause in adults and there is non-selective proteinuria so non-selective proteinuria in membranous nephropathy also and this is the commonest cause in case of elderly for the nephrotic syndrome then let us move on to the cause cause of these so yes there is importance of immune mechanisms but immune mechanisms are not so much that it leads to inflammation in the glomerulus okay in fact in minimal change disease we don't even see any sign of immune mechanism in minimal change disease however because this disease is responding to steroids we say that yes there may be some immune mechanism involved then in focal segmental glomerous crosses there there may be many causes there may be secondary causes but I will just talk about that we discussed about the proteins nephrin podosin so genetic mutations genetic mutations of these proteins can lead to fsgs but there are many other causes that you see in pathology then in membranous nephropathy there is antibody to podocyte antigen as I told you that podocyte injury can occur due to antibody to a antigen which is present in the podocyte so antibody to podocyte antigen and the antigen is PLA2 receptor PLA2 receptor that will lead to membranous nephropathy now if we see the light microscopic findings light microscope you see in minimal change disease actually light microscopy is generally not required but still if there is confusion and we get biopsy and we see the sample under light microscopy what we see is that normal glomeruli normal glomeruli are there so we don't see any changes under light microscopy on the other hand in fsgs as the term suggests focal segmental glomerulo sclerosis so there is presence of sclerotic areas right and focal and segmental means that the biopsy specimen which we have taken if we observe all the glomeruli in that biopsy specimen we see that it is present in less than 50% of the glomeruli focal means that less than 50% of the glomeruli are affected in the biopsy sample which we are seeing so it is very important that the biopsy sample should have minimum 10 to 20 glomeruli and we have to examine all of them then what is segmental segmental means that the glomeruli which are affected they are not affected fully only some parts some segments of the glomeruli are affected so that is the meaning of focal segmental glomerulo sclerosis so as i told you there will be sclerotic areas plus what we see under light microscopy is something known as highly noses that is there is deposition of the plasma proteins along capillary valve so that is known as highly noses and in membranous nephropathy the term membranous means there is thickening of the membrane that is one hallmark of this membranous nephropathy there is diffuse thickening of the membrane okay then next is what we see under electron microscopy one common thing what we see is diffuse effacement of food processes that we see in all these and that is why they are presenting as nephrotic syndrome diffuse effacement of food processes in fact if you see in mcd we have not talked about any other change okay nothing is visible actually there is a neutralization of the charges which i present on the food processes there are basically negative charges in all the three layers of the glomerulus and there is loss of these charges but in electron microscopy what we see is that diffuse effacement of food processes is seen but in light microscopy nothing actually this is one hallmark of minimal change disease and the diagnosis of minimal change disease is based only when in light microscopy we see normal glomuli and in electron microscopy we see diffuse effacement of food processes then in fsgs what we see is diffuse effacement of food processes yes that will be there plus there is focally detachment of the epithelial cells right detachment of the epithelial cells so the food processes which are attached to the basement membrane we will see that they have been detached from that okay and also there is damage to the underlying basement membrane that is also damaged and in membranous nephropathy what we see we saw that the cause is antibody to podocyte antigen so this antibody goes and reacts on the podocyte antigen and what we see that deposits of this antibody are seen so that is seen as granular deposits granular deposits and this is basically granular deposits seen as very classical spikes and domes appearance spikes and domes appearance but whenever we talk about deposits remember that we have to think about where we have where they are present as I told you that there can be sub epithelial deposits some endothelial deposit and mesangial deposit so that also helps us in diagnosis and since the antigen is present on the podocytes right so again we will go to that diagram this is the endothelium so here this is sub endothelium and this is the food processes of the photosites so here it is the sub epithelial below the epithelium so here is the antigen right so where will be the deposits deposits will be in the sub epithelial region and that is seen is immunofluorescence immunofluorescence immunofluorescence means that we use tag the antibodies against specific substances so as I told you that the mechanism is basically the antigen antibody reaction so against what we have to use the tag substance against the antibodies against the complement substances so when we use that what we see here that we see immunoglobulin and complement deposition in which area in the sub epithelial region similarly in FSGS also we see some deposits and that is the IgM deposits and plus complement deposits we will see why this complement deposits we are seeing when we are we will talk about the nephritis syndrome because then we will talk about the pathophysiology anyways so these deposits are seen in the sclerotic region and also in mesangium okay so membranous nephropathy deposits seen in the sub epithelial region in FSGS deposits seen in the mesangium in MCD will there be any deposits no no deposits we don't see anything because basically here there is only neutralization of the charge of the foot processes with this let us move on to the nephritis syndrome so what are the features of nephritis syndrome in nephritis syndrome also we see proteinuria but it is sub nephrotic range proteinuria that is less than that in case of nephrotic syndrome that is 1 to 2 grams in 24 hours then we see hematuria that is loss of red blood cells in urine presence of red blood cells in urine and also there is presence of red cell cast okay yes there is a loss of WBCs also what is known as pyuria right then there is presence of hypertension very important and there is presence of esotemia that is increase in the blood urea and blood creatinine so that means now the kidney is not able to function properly and that is why we are getting decrease in blood urea and blood creatinine and when that happens that happens when there is decrease in GFR right so let us see that why all this thing is happening that is the pathophysiology of the nephritis syndrome in nephritis syndrome the damage to the glomerulus is extreme and why it is happening it is happening because of the formation of antigen antibody complex in the glomerulus and as I told you either it can be in situ formation in the glomerulus that is the antigen is there and antibody goes and reacts with the antigen there in the glomerulus or there may be deposition of this antigen antibody complex itself in the glomerulus and whenever there is antigen antibody complex formation always if you remember your immunology there is activation of the complement so this activates complements okay complement activation occur and complement activation there are certain factors like C3AC5A which cause chemotaxis so with chemotaxis there is infiltration of the leukocytes in the glomerulus and what are these leukocytes there is neutrophil there is macrophages all they will infiltrate in the glomerulus and this will lead to release of the cytokines also from the leukocytes and when there is presence of the cytokines there is proliferation of the cells which are present in the glomerulus so cellular proliferation occurs okay in the glomerulus and because of extensive damage which is going on in the glomerulus these leukocytes which have gone there they will also leak into the filtration space and there will be leakage of RBCs also but the shape of the RBCs will not be normal it will become distorted so what we see in urine is dysmorphic RBCs okay dysmorphic RBCs then why there is presence of cast cast is basically these RBCs which are getting filtered they become trapped in the tubules right so they kind of say suppose this is the tubule and all the RBCs become trapped like this what is happening the fluid which is coming the filtered fluid will push and ultimately they will land up in urine but you see they have formed a kind of cast where they were trapped that shape they will take so that is known as RBC cast now why does esotemia develop in nephritic syndrome see because of too much leukocyte infiltration and too much proliferation of the cells what happens that there is kind of reduction in filtration space and when that happen there will be decrease in GFR reduction infiltration space will lead to decrease in GFR and this decrease in GFR what will happen it will lead to activation of the tubulominal feedback and there will be again angiotensin activation angiotensin 2 formation aldosterone formation leading to hypertension but also the GFR reduces so much that the kidney is not able to perform its function and this leads to accumulation of urea and creatinine in blood understanding so what we saw the activation of RAS in nephrotics syndrome the reason was different what was the reason there is decrease in the intravascular volume primarily due to decrease in the oncotic pressure and that leads to decrease in renal blood flow and decrease in GFR but the damage to glomerulus per se was not the reason here what we are talking is that decrease in the glomerular filtration space itself that it is leading to decrease in GFR and that ultimately it causing hypertension and because of this the kidney is not able to function properly and there is accumulation of urea and creatinine now one may ask that why the protein loss is less if RBCs WBCs which are in like microns sizes in microns they can leak into the urine then why protein loss is less well we are telling that the glomerular filtration space itself is decreasing so yes protein will filter from those spaces but filtration area itself has decreased so the amount filtered will be less compared to that of the nephrotics syndrome but wherever damage has occurred damage is so much that obviously there will be non-selective protein urea and these cells will also start appearing in the urine now finally let us talk about some diseases which are responsible for nephrotics syndrome so as I told you that because of antigen antibody complex formation there will be activation of the complement leukocyte infiltration and cellular proliferation so what we see that in different diseases this cellular proliferation is occurring at various places and antigen antibody complex deposition is also occurring at different places so what are these diseases let us see based on that where the proliferation is occurring where that cellular proliferation is occurring so first is endocapillary proliferation okay endocapillary proliferation that is the cells within the capillary are proliferating second is mesangial proliferation third is very important that is a parietal cell proliferation that we have not discussed parietal cells are the cells which are lining the bomen space so that also can get proliferate and that is very dangerous actually so this endocapillary proliferation occurs in post-tropococcal glomerulonephritis and these proliferation of the cells is seen as hypercellular glomerulus in light microscopy so the glomeruli are large and we see the cellularity has increased because so much proliferation of the cells has taken place so this is under light microscopy and if we see under electron microscopy what will be the condition in electron microscopy we see these antigen antibody complex deposits in case of psg n we see it under in sub epithelial region sub epithelial region and the deposits are like granular deposits then coming to immunofluorescence when we are using tagged substances to identify various antibodies and complement what we see in psg n that various antibodies can be identified that is IgG IgM and various complement also can be identified C3 C4 in mesangium so various regions we are seeing actually this psg n disease first starts in sub endothelial region so actually initially these deposits are seen in sub endothelial region later they move on to the sub epithelial region so basically everything is like affected in immunofluorescence we see in mesangium these antibodies and complement factors and in electron microscopy we see granular sub epithelial deposits then mesangial proliferation that occurs in two diseases that is membranoproliferative nephritis and IgN nephropathy actually in all three we see all these endocapillary plus mesangial proliferation but this mesangial proliferation is more predominant is mpg n and IgN nephropathy but if we see under electron microscopy then the deposits we see at different places in psg n we see sub epithelial granular deposits in mpg n we see sub endothelial deposits sub endothelial deposits and in IgN nephropathy we see mesangial deposits okay mesangial deposits and in mpg n sub endothelial again the deposits are seen as granular while these IgN nephropathy deposits are linear plus in mpg n we see what is known as tram track appearance that is there is duplication of the basement membrane see when there is sub endothelial deposit and proliferation we see it appears that the basement membrane has duplicated so that is very classical of mpg n then in immunofluorescence what we see in mpg n is IgG plus C3 deposits complement deposit is there where again in the sub endothelial region okay and in IgN nephropathy what we see is deposition of IgA not IgG IgA deposits plus there is deposition of C3 plus proper DIN actually this IgA antibody activates alternate complement pathway so that is why we see the deposition of proper DIN as well and there is a special lack of C1 complement for this basically we have to make another video on complement what is this alternate pathway what is this classical pathway that is for another video okay finally coming to the parietal cell proliferation and that parietal cell proliferation basically the cells which are lining the bowman space they proliferate and they form crescents and that is responsible for rapidly progressive glomerulonephritis so that is one very classical that if parietal cell proliferation is seen forming the crescents that leads to rapidly progressive glomerulonephritis and again rapidly progressive glomerulonephritis causes can be many one is that there can be antibody against the glomerular basement membrane that is what we see in good pastures syndrome then there can be immune complex mediated RPGN and that can be due to other diseases like IgA nephropathies some patients may form rapidly progressive glomerulonephritis and there are many other diseases immune complex mediated diseases and finally there is posse immune where we hardly see any immune complex but there is presence of anti-nuclear cytoplasmic antibodies but the common thing is that in electron microscopy in all of them we see ruptures in glomerular basement membrane ruptures okay so there is parietal cell proliferation forming crescents ruptures in glomerular basement membrane and immunofluorescence in all the three the findings are different in a good pastures syndrome or anti-gbm antibody what we see is there is linear deposits of IgG and C3 in immune complex mediated the deposits are granular and in posse immune again there will be no deposits so this is similar to that of MCD the if we see under immunofluorescence but you see the presentation is totally different MCD we don't see any antigen antibody complex but there is no change in life microscopy also it is presenting as nephrotic syndrome RPGN it is very very serious disease and most of the cases move to end stage renal disease and that is very fast within weeks it can happen so in this brief video I have tried to tell what are the features of the nephrotic syndrome and nephrotic syndrome how they differ in pathophysiology and in some diseases I have tried to simplify what we see in light microscopy electron microscopy immunofluorescence and you can take these tables and use for memorizing what are the features of different diseases as well thanks for watching the video if you liked it do press the like button share the video with others and don't forget to subscribe to the 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