hello class welcome to our john patlab session so for today i will be discussing the renal pathology so let's begin let's review class the basic histology of the kidney as it is helpful later on in diagnosing the diseases the renal tissue has four main compartments we have here the glomerulus which consists of a tuft of capillaries and functions to filter the blood and we also have here the renal tubules which functions to reabsorb the substances such as electrolytes we also have the blood vessels and the last compartment that supports the tissue such as the two pills is called the interstitium so again you have the glomerulus the interstitium the adrenal tubules and the blood vessels renal diseases are usually manifested by a limited number of symptoms that are grouped into clinical syndromes class such as nephrotic syndrome nephritic syndrome acute and chronic renal failure etc so so why is it important glass to know these compartments that is because any injury to the kidney can result in damage to those one or more compartments thus the accurate diagnosis of renal disease entails detailed knowledge of the structure and function of the normal kidney as well as an understanding of the clinical morphologic and isopathologic aspect of the disease and i think by this time those were already emphasized in the lecture also i would like to stress class that aside from the clinical and laboratory information the light microscopic findings should be also correlated with immunofluorescence and electron microscopy findings however in our pre-lab we will only be seeing the light microscopy findings so i would like to emphasize class that you correlate each slide with the textbook so here class we have a an image of the glomerulus and the labels of the part of the glomerulus the glomerulus is a vascular structure which is composed of a tuft of specialized fenestrated capillaries that arise from the afferent arteriole to form globules and rejoin the vascular pole to drain into the afferent arteriole so each lobule class consists of a cluster of capillaries and it's supported by a message which forms the health framework of naglomerulus this stuff of capillaries class lies within the lumen and it's called the bowman's space as you can see here so the spaces line on its parietal aspect by a simple squamous layer of epithelial cells and this overlays a basement membrane together forming the woman's capsule also seen here are epithelial cells of the visceral layer of the capsule which is called podocytes so these podocytes glass have numerous tiny food processes that can be seen on electron microscopy and also the messenger supports the glomerulus and is composed of cells which are which has functions similar to parasites and smooth muscle cells so these cells class possess contractile properties and are also phagocytic in nature these images were taken from the textbook so these are electron microscopy findings so this is a cut section of the glomerulus note the the capillary lumen the messenger cell and the endothelial cell and this is a high magnification of the food processes of the podocytes along with the filtration sleet so this is the epithelial side and the endothelial side and it's separated by a basement membrane so you have here the lamina densa and you have here the laminar internal and this one is the lamina rara externa so the positive class can either be on the on the editorial side or in the sub-epithelial side of the basement membrane our first slide class is hydropic change of the kidney i think you've already seen this slide on uh during the first semester semester in in cell injury so hydropic change is a form of reversible cell injury that is commonly due to natural toxicity so if you can still remember class in the first semester the response of cells to injury would be cellular swelling or fatty change so in this slide this is an example of cellular swelling the compartment affected here are the renal tubules so you can see that the tubules are swollen and hydropic change class refers to the accumulation of water inside the cell and almost all of the tubules here are affected on a higher magnification you can see the pale appearance of the tubular cells which is due to vacuolar degeneration brought about by the influx of water so so why does this happen class so this happened because the damaged cells are incapable of maintaining the fluid and electrolyte homeostasis so this leads to the influx of water inside the cell causing it to swell and this form of injury is reversible still you can uh applicate the presence of the nucleus and there are no features of necrosis such as carrier axes cardiolysis and hypnosis so this injury is still reversible so do not forget this class as it is very easy to identify the slide our next slide is acute kidney infarct so infarction class occurs when a blood supply of an organ is diminished or totally cut off so most renal infarcts are due to embolism moisture which commonly arises from the left atrium or ventricle following a myocardial infarction other causes can include atherosclerosis and vasculitis so grossly kidney infarcts are classified as a white infarct which occurs with arterial occlusions of organs with an arterial supply hydrologically acute kidney infraclass is seen as coagulative necrosis so it's a form of necrosis in where the architecture is preserved for a span of days as the enzymes that would normally digest the dead cells are also denatured so here class you can see the vessels are congested note this hypodemic area in the middle which is due to the congestion you can also appreciate the pale areas that are also infected in this left and in the right area so let's have a higher modification for the higher modification you can appreciate here congestion note the presence of numerous red blood cells in the interstitium and lomarulus the there's also presence of cognitive necrotic changes as you can see the outlines of the glomerulus and tubules are preserved note the absence of nucleus and the increased eosinophilia of the cell so those are features class of coagulative necrosis on other areas note the extensive coagulative necrotic change the outlines of the glomerulus and the tubules can be clearly seen so there's absence of nucleus on some of the cells and there's lots of basically of the nucleus and an increased aeosinophilia of the cytoplasm of the cells these are all features class of your coagulative necrosis so our next slide class is acute glomerulonephritis or also called as post-streptococcal glomerulonephritis so this disease class is characterized by diffuse endocapillary proliferation of glucometer cells associated with dicositic infiltrates and this is brought about by the deposition of immune complex so this is a type 3 hypersensitivity reaction the antigen class can be exogenous or endogenous and the most common cause of this disorder will be due to a septococcal infection it usually appears one to four weeks after a pharyngeal or skin infection with a group a beta hemolytic streptococci such as cytococcus pyogenes hildren class are commonly affected by this disease the antigen antibody complex are deposited in the chromerulus in where it elicits an acute inflammatory response this disease would manifest as nephritic syndrome so clinical features would include hematuria proteinuria asotemia and hypertension here you can see that the glomeruli are globally and diffusely and large the hyper cellularity of the glomerulus is due to the infiltration of inflammatory cells and the proliferation of messaging and endothelial cells so why would there be hypercellularity remember class that the glomerulus response to injury is characterized by either the process of hypercellularity thickening of the glomerular basement membrane or hyalinosis and sclerosis so here in acute glomerulonephritis there's proliferation of the mesangial and endothelial cells along with the infiltration of nucleocytes giving it a cellular appearance on light microscopy also this can develop into crescentic glomerulonephritis specifically the immune complex type the type 2 the deposition class of immune complexes in the glomerulus leads to local inflammatory reaction that produces injury so the antibodies may activate the complement system which in turn activate the leukocytes messenger cells and endothelial cells so again this would lead to hypercellularity so if we do immunofluorescence staining hair class there will be a glandular appearance due to the presence of the position of your igg and c3 in the glomerular basement membrane and mesangium in electron microscopy the electron dense deposits are localized in the sub-epithelial location the so-called sub-epithelial humps so again these are that is the feature of your acute glomerulonephritis our next slide is good posture syndrome with crescents good pasture syndrome is an autoimmune disease characterized by auto antibodies against the glomerular basement membrane this auto antibody class can also cross react with alveolar basement membrane so patients can also present with pulmonary symptoms and hemoptysis the auto antibodies here are against the non-collagenous portion of the alpha 3 chain of collagen type 4. in the kidneys good pasture syndrome produces a crescentic glomerulonephritis and a linear deposition of igg and c3 along the basement membrane so let's have a higher modification on a higher modification class you can see the presence of crescent formation within the bowman's space so this is due to the proliferation of the epithelial cells lining the bowman capsule and the migration of monocytes and macrophages good pasture syndrome is a type one presenting glomerulonephritis the other types of presenting glomerulonephritis includes type 2 which is due to immune complex supposition such as post-infectious glomerulonephritis and ij nephropathy you also have the type 3 which is called possy immune type so this is typically associated with anka or antiotrophilic cytoplasmic antibodies so going back to the slide you can see the crescent formation so what stimulates the formation of these crescents so it is belief class that plasma proteins click into the woman's space and exposure to tissue factor leads to the deposition of fibrin if we do staining for fibrin fibrin strands can be seen in the cellular layer of these crescents so if we do immunofluorescence it will show a linear deposition of ig and complement along the basement membrane electromicroscopy class will show ruptures in the basement membrane and the rupture will allow the leakage of plasma proteins and inflammatory mediators that trigger the crescent formation eventually in chronic cases there will be obliteration of the urinary space as you can see here and there's mark sclerosis of the glomerulus patients class with presenting glomerulonephritis present with hematuria proteinuria hypertension and edema so our next slide class is member news glomerulopathy so in general class membranes nephropathy is the most common cause of nephrotic syndrome in adults whereas minimal change disease is more common in children in the united states the most common cause of nephrotic syndrome is in adults is focus segmental glomeruloskelerosis or fsgs membranous appropriate class is characterized by the presence of diffuse glomerular wall thickening due to the presence of deposits containing immunoglobulins on the sub-epithelial side of the basement membrane majority of the cases are idiopathic whereas the remaining cases class are due to secondary causes such as systemic disease infections and drugs the primary membranous nephropathy class in most cases is due to the presence of an auto antigen called the phospholipase a2 receptor and the binding of an auto antibody causes complement activation which leads to the deposition of immunoglobulins so this is his class is an example of a type 3 hypersensitivity reaction those patients class with membranous nephropathy present with a nephrotic syndrome so there will be massive protein area of 3.5 grams or more daily there will be also presence of hypoalbuminemia anazarka hyperlipidemia and lipiduria hematuria and hypertension glass can also be present on light microscopy class what is seen is the presence of diffuse thickening of the glomerular capillary wall note the absence of hyper cellularity absence of sclerosis in the messenger and absence of inflammatory cells so so what is the thickening of the capillary so remember class that this is an immune complex injury and the deposition of immunoglobulins will lead to activation of complement which leads to capillary wall injury and plasma protein leakage the deposition of plasma proteins can be appreciated as hyaline doses on light microscopy so hyalinosis class refers to the accumulation of homogeneous and eosinophilic material so it's composed of plasma proteins that have deposited in the glomerulus and is usually a consequence of capillary injury immunofluorescence will show a granular appearance of immunoglobulins and complement electron microscopy will show that the deposits are located on the sub-epithelial side of the basement membrane along with a placement of the food processes of the podocytes silver stains class will show presence of spikes which represents basement membrane in the deposits we have also a disease class called membrano proliferative glomerulonephritis so unlike membranous nephropathy mpgn is characterized by the presence of hyper cellularity due to messenger activation proliferation of your uh glomerular cells and infiltration of inflammatory cells the deposits are located on the sub-endothelial side and there will also be presence of a double contour or tram track appearance of the basement membrane which is due to the duplication of the basement membrane so make sure class to review the textbook as it is explained there much better the pathogenesis of these glomerular diseases so here class we have a higher modification of a glomerulus in a patient with membranous glomerulopathy so note the thickening of the capillary wall and there's an asynophilia of the capillary vessel that is highly no system so when you say hyalinosis again it refers to the accumulation of homogeneous and aesthetic material and is and it is composed of plasma proteins so again if you do immunofluorescence there will be presence of a granular appearance due to the deposition of immunoglobulins and complement and in electron microscopy those deposition is localized in the sub-epithelial side of the basement membrane our next slide class is iga nephropathy or also called as burger disease ig nephropathy is the most common cause of glomerulonephritis worldwide it's characterized class by the presence of deposits in the messenger regions of the glomerulus the deposits are composed of immunoglobulin a that are fully glycosylated auto antibodies produced against these apparently glycosylated iga form immune complexes with the iga molecules and these are then deposited in the mesanjoub thus leading to the messenger proliferation also the immune complexes activate the alternative pathway of the complement which also plays a role in the inflammation in ige nephropathy class this presents with hematuria after an infection in the respiratory gastrointestinal tract and urinary tract it also occurs in those individuals with celiac disease and liver disease so our slide class is somewhat a sub optimal so it's it's poorly stained so but what you can appreciate here is the presence of glomerular hypercellularity so again in ige nephropathy class the presence of glomerular hypercellularity is due to messenger proliferation note the presence of hyalinosis in the messenger which is caused by the deposition of plasma proteins if we do immunofluorescence it will show messaging deposition of immunoglobulin a and sometimes c3 these messenger deposits can be confirmed by electron microscopy