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Kidneys Pathology Sample PDF (Hira - FJ)

Notes for renal system

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Minahil Shahid
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274 views11 pages

Kidneys Pathology Sample PDF (Hira - FJ)

Notes for renal system

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Minahil Shahid
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Big Robbins linical Manifestations of Renal Azotemia Uremia Nephritic Syndrome Nephrotic Syndrome Acute Kidney Injury Chronic Kidney Disease Glomerular Diseases Structure of Glomerulus Pathologic Responses of Glomerulus to Injury Mediators of Glomerular Injury NEPHRITIC SYNDROME Acute Proliferative (Postinfectious) Glomerulonephritis Pathogenesis * Morphology + Clinical Features Y Crescentic (Rapidly Progressive) Glomerulonephritis Pathogenesis + Morphology * Clinical Features NEPHROTIC SYNDROME Membranous Nephropathy Pathogenesis * Morphology + Clinical Features Minimal Change Disease * Pathogenesis + Morphology + Clinical Features Y Focal Segmental Glomerulosclerosis ‘© Pathogenesis + Morphology + Clinical Features Y HIV Associated Nephropathy * Pathogenesis + Morphology + Clinical Features a ae eke . * Tubular & interstitial Diseases ‘+ Acute Tubular Injury/ Necrosis Pathogenesis + Morphology + Glinical Features Tubulointerstitial Nephritis Pathogenesis * Morphology + Giinical Features Pyelonephritis and Urinary Tract Infection Acute Pyelonephritis Genetics & Pathogenesis Morphology Clinical Features Chronic Pyelonephri Nephropathy Genetics & Pathogenesis Morphology Clinical Features Nee ese & eee > Gystic Diseases of Kidney ‘Autosomal Dominant (Adult) Polycystic Kidney Disease Genetics & Pathogenesis Morphology Clinical Features Autosomal Recessive ( Kidney Disease Snag aan Cac Y Genetics & Pathogenesis ¥ Morphology ¥ Clinical Features > Urinary Tract Obstruction (Obstructive Uropathy) * Etiology ‘* Pathogenesis + Morphology * Clinical Features > Urolithiasis «Etiology & Pathogenesis + Morphology * Clinical Features > Neoplasms of Kidney © Benign Neoplasm Y Renal Papillary Adenoma © Pathogenesis * Morphology * Clinical Features Y Angiomyolipoma * Pathogenesis + Morphology © Giinical Features Y Oncocytoma ‘© Pathogenesis + Morphology + Glinicol Features Malignant Neoplasm Renal Cell Carcinoma Pathogenesis * Morphology * Clinica! Features Note: The topics over which I’ve mentioned extra, you can totally leave them, they're just. included for better understanding Priority List: > Post Strep GN > RPGN (Rapidly glomerulonephritis) > UTI & Pyelonephritis, > Renal Cell CA > Wilms Tumor iaboticlenbropathy Seria ae ees progressive > Clinical Manifestations of Renal Diseases © Azotemia > % Blood Urea Nitrogen (BUN ) & Creatinine > Due to LGFR |) Pre renal Azotemia: b/c of Kidney Hypoperfusion ii) Post Renal Azotemia: b/c of urine flow obstruction distal to kidney & Uremia Azotemia ~ Clinical signs = Uremia ‘ Nephritic Syndrome Inflammatory Glomerular Disease > Proteinuria, hematuria, HTN ‘ Nephrotic Syndrome > Heavy Proteinuria, Hypoalbuminemia, Severe Edema, Hyperlipidemia, Lipiduria ‘% Acute Kidney Injury Rapid W in GFR + electrolyte imbalance + Metabolic waste retention ‘ Chronic Kidney Disease GFR ¥ than 60ml/min/1.73m?/ 3 months ‘End Stage Renal Disease GFR < 5% of normal * Glomerular Diseases Table 204 Systemic Kidney Dhease and Uremia ‘stydraton tem ipertatemes Mtoe sadn a 73/296 — enna ee racers Cera Neen and vomiting ‘kedng Enophogets rcs, cols yp Fergal neropaiy oes ms =e ‘Table 20.2 Glomerular Diseases Acie proesove omer Poreecoun Slr ty progenies rt Minbrinosnapiopaiy Fo semen lomerdosderen Sepsis oer Dense dapont donne cA ratropaty ae pene ees eee eee eer eae ‘Alport syreme ‘Than barca membrane nephopahy Fabry dene ‘Table 20. Clinical Manifestations of Glomerular Diseases Nephre ymdrome —ematuraaotema warble protenur ‘Shuurtedera snd Fypertemon apy progressive ‘Acate repr, proten, and sete domersnephets ‘eval dure Nephroxcsdrome _>35 gay proteruria ypeabuminema. Iperipdems pera Cron ki Aastamis arom progresing or ‘dee ‘month 0 | tect ier lomerle hema andi ‘orate ‘bvepvon procera © Structure of Glomerulus GLOMERULUS apatay loops > GBM has Collagen Type IV Pathologic Responses of Glomerulus to Injury Hypercellularity: Increase in the number of cells in the glomerular tufts. This hypercellularity results from one or more of the following: 1) Proliferation _of_mesangial_or endothelial cells. 2) Infiltration of leukocytes 1+ 2= endocapillary proliferation 3) Formation of crescents. These are accumulations of cells composed of proliferating glomerular epithelial cells and infiltrating leukocytes. Pathogenesis of Crescent formation: Inflammation -> Plasma proteins leak into urinary space > Exposed to pro coagulants > i) Fibrin Deposition ii) Activation of coagulation factors > Crescent formation 4) Basement Membrane Thickening 5) Hyalinosis (Hyaline/plasma proteins deposition) and Sclerosis(Deposition of extracellular collagenous material). n NEPHRITICSYNOROME > tnfirymation i glomerul charaterited by 1) ematura i) Proteinuria i) azoteria Iv) Hypertension ‘cute Proifeatve (Postnfetious) ‘Glomerulonephrts~ Streptococcal Pathogenesis to Antigen Ab Complexes Hump uke Deposits Antigens planted ito glomerular eapilary wal Activate complex > Antigen Ab an ‘Morphology Enlarged, Hypercelular glomerut couse of Hypercellority: Loukoeytes{Nevtrophils & Monecytes) Proliferation of endothelial. mesangial els + > Global & Diffuse = Al lobules of Blomerultinvolved > Endothelial swaling > capilary lumen obstructed > Edema, Inftraton Wi) Crescent Formation Obiteration of glomerular capillary lumen: tt |s due to sweling and proliferation of endothelial and mesangla ells +inftration by leukocytes. 1 Tubules: may contain red call ast inthe lumen and the tubular epithelial cells may show degenerative changes. SOL aa Lac > 3 > > > 5 > > > > 3 tinico Features Young chia Malaise Fever, nausea Otigura (COLA COLORED URINE 12 weeks after recover from sore throat ematur ‘Mild Protelnurio( Blood vessel: Unvemarkable 9) Ammunofivorescence Microscopy: > Deposits of gs, C5 Andie > Focal & Sparse W) Hlecion Microscomy: Humps showing Antigen Ab complex Sub epithelial and sub endothelial deposits ‘Giomerulonephrits(Postinfectious ‘Giomerulonephrits) > Acute proliferative glomeruonephriis may ‘ako occur. in association with other Infections > Bacteria: Examples, staphylococcal ‘endocarditis, pneumococcal pneumonia, ‘and meningococcemia Virus: Examples, hepatitis (8 and Q), mumps, HIV. infection, varicla, and infectious ‘mononucleosis. Porosite: Examples, malaria, toxoplasmosis > The morphological changes ate sir to posttreptococcal glomeruloneptrits + Morphology > Gross 0 a) ineys Enlarged & Pale Petechial Hemorthage on cortical surtace > microscopy: 0 0 i» ‘Giomerul: Focal & Segmental necrosis Endothelal proliferation Mesangial proliferation Fiori strands b/w ayers of crescent ° ‘Components: Crescent are formed by: Proliferation ofthe parietal epithelial «ells ining Bowman capsule. a 5 VEN E TE capillary lumen obstructed -> Edema, Infitration Crescent Formation Obiiteraton of lmeular capilarylumen: it Is due to sweling and prolferation of endothelial and mesangial ells + infiltration by leukocytes. Tubues: It may contain red cll ast inthe lumen and the tubular epthelial cells may show degenerative changes Glico Features . Young Cid Malase Fever, navees| Olguria (COLA COLORED URINE 1-2 weeks after recovery from sore throat Hemature ‘Mid Proteinuria (<1g/éay) Petorital edems ‘Adults: P BUN ob Finaings: 1) TrAnt streprococal Ab titers y ve Crescentic (Rapidly ‘Glomerulonephits Crezcensin Glomeru formed by: Proliferation of epithelial Cells around bowman's capsule Infteation of monocytes & macrophages Pathogenesis Three Categories: ‘AniLGBM Ab mediated disease( Deposits of ye &c3) * Goodpasture syndrome: Anti GBM Ab oss react with pulmonary alveolar basement membrane > Pulmonary hemorrhage + renal faure ‘Antigen common to renal & pulmonary basement membrane = A peptide in Collagen type W Progressive) oe Interttiam aggf aang "aap eer also. occur in asociation with other infections: Bacterio: Examples, staphylococcal ‘endocarditis, pneumococcal pneumonia, and meringocoecemia Virus Examples, hepattis(8and C), mumps, HIV infection, varicella, and infectious ‘mononucleosis, Poraste: Examples, malaria toxoplasmasis. ‘The morphological changes ace similar to posttreptococcal lomerulonephrtis Morphology Gross 1) Kidneys Enlarged & Pale 4) Petcil"Hemomase on cont tee . oe 78/296 3 1) Glomeruli Focal & Sepmenea necrosis 1) Endothelial proliferation Ii) Mesangial proliferation Fin strands b/w layers of erescont Components: Crescent are formed by Proliferation ofthe parietal epithelial als ning Bowman capsule Intitration of monocytes and macrophages into the urinary space Stimulus: Fbvin leaked into the Bowmanspace is the stimulus and is found between the celular layers, Finis derived from fibrinogen, which escaped through the ruptured GBM into Bowman space Slgnfeance: it indcates severe ‘glomerular injury and does not represent any specific etiological factor. . . “Tubutes: The tubular lumen may show casts and it shows edema with inflammatory eal few Blood vessels: Norma. “ype Gocdpasture syndrome: 3 > > a » i 2) Immanofluorescence microscopy: Igand complements on GBM Electron Mie Rupture in GBM (lsjury_ that allowed ‘exudation and hence crescent formation) ‘clinica! Features homatura, proteinuria HIN, edema Goodpasture syndrome: recurrent hemoptysis / Pulmonary hemorrhage Diagnosis Serum analysis for Ant GBM Ab ANAS [Ani nuclear Ab and facial edema, Urine examination shows mild proteinurie, hemetura and RBC Casts diagnosis? a 4) ANCAS: i) Ant acter Ab Faised antistreptococal antibody terse. antstreptelysin 0 (ASO) titer Hypocomplmentemia: Significant reduction In serum concentration of complement (C3) components Ralsed blood urea and serum creatinine Urinary Findings Ofguria Mid (variable degree) proteinuria (usually Jess than t/a Hematutia (smoky or cola colored urine) Red cal asts of dysmorphic red cals red cals wth cellular protrusions or {ragmentation) FIMU Prof 2020 a) A mother ofS years od boy complains of his cola colored urine for afew days. She enve history of sore throat for 2 weeks . On ‘examination boy shows perl orbital puffiness examination report shows only proliferation of endothelial, mesangial and parietal cols with inflammstory cel Instrte 2} Whats the most appropiate diagnosis? eGN 1b) what is the basic underying pathogenic ‘mechanism for this condition? How this condition lassifed? [Annual 2017] 2. Approximately 10 days after an episode of jpharyngts, an. S-yearolé ri suddenly becomes lethargic, febrile and nauseous. a hb Ge a eee ae % and facial edema, Urine examination shows mild proteinuri, hematuria and RBC Casts 3) diagnosis? Post Strptococeal Glomerulonephrits 1) Describe te findings of Renal biopsy in this patient? ‘Nephiritic Syndrome LUHS prof 2006-2022 UHS Annual 2022 aus ‘A 8 year old gil was admited with [generalizes oedema, Her urine had become {rothy and laboratory investiestions shor hypernatremia, ir \/ Increased 791296 hypercholesterolem. hyperticerdemia, 24 hr urinary pote. ‘excretion was 12 What is the most thely diagnosis? Give ‘ological clasietion of thi syndrome, Nephrotc syndrome LUHS Annual 2021 0. A 14-year old previously healthy male ha been feeling tired for the past 5 days. He then passed derk-colour urine. His blood pressure is 160/80 mmMa. Laboratory tests show hie serum creatinine is 42 mg/dl and BUN 39 ma/dl. A rials reveals 6, specific gravity L011, no glucose, and no ketones, 3+ blood) 1+ protein and numerous RBCcass. The renal biopsy examination reveals omerular crescents, 2) Classify Rapidly Progressive (Crescentc) ‘Glomeruonephris on immunopathogenic base, 'UHS Supple 2024: a) Name and Interpret the Laboratory Tests performed to confirm favour the Diagnosis af“ Nephroti Syndrome”. 1.14 years ol previous healthy male has been feeling tired for the past 5 days. He ‘then passes dark coloced Urine. His blood pressure is 155/90 mm He Laboratory {este show his serum creatinine is 4.4 mg/dl and BUN is 41 mg/dL. Urine analysis feveale pi 6, specie gravity 1.013, 2 _lucose and no ketones, 3+bood, 1» protein and numerous RBC casts. The renal biopsy 5. Give the pathogenesis and morphology of cute proliferative poststreptococa ‘lomeruionephrits. (Annual 2006), ‘examination boy shows per orbital puffiness Se aac i " » ‘examination report shows nly proliferation of endothali, mesangial and Parietal celle with inflammatory calls intitrate. ‘Whats the most appropriate agnosis? RGN ‘What is the basic underiing pathogenic mechanism for ths condition? How Is this contion classified? [Annual 2017] ‘Approximately 10 days after an episode of pharyrats, an Byear-old gr! suddenly becomes letharglc, febrile and nauseous. er urine output is reduced and is ‘olacolored. Urine analysis shows mil proteinuria, hematuria and RBC cast. ASO teri ees ‘whats your clagnosis? Post streptococcal Glomerulonephrits Give ight microscopic Mndings of renal biopsy performed in sucha case ‘Give clinical course ofthis disease [Supple 2013 held in 2014], ‘A young male presents with nephritic syndrome. He s HCV #ve on serology. Renal biopsy was earied out which revealed on light microscopy an accentuation of lobular arrangement of glomerular ttt and 2 doubie contour of GBM ‘What wil be the electron mleoscopic and detailed ight microscopic picture of ‘this biopsy? [Supple 2009 held in 2010) Non Streptococcal (Acute Proliferative) ‘lomerulonephits 1 school going 7-year-old boy complains of few weeks of onset of gradual letharey, fatigue, and passage of small volume of dark colored urine following an episode of Upper respiratory tract infection. On examination, mild hypertension is present What wil be the characteristic ndings of Usine examination in his patent? Post Streptoccol GN Descrie the renal biopsy findings. {annual 2008) ‘4 NePHROTIC SYNDROME: | “<1 years: Lesion to kidney ‘Ait: Secondary to system disease ‘cline Features Massive Protelnuria (03 5e/day) Hypoalbuminemia Generalized Piting Edema (Ble proteins were maintaining Blood vessels ‘smotie Pressure) > _Hyperipidemia - Due to Synthesis, {4 catabolism, Abnormal Transport veurey glucose and no ketones, 3+ blood, 1+ protein fand numerous REC ests. The renal bopey 4 5. Give the pathogenesis and morphology of acute proliferative poststreptococcal ‘lomerulonephit: (Annual 2006), 80/296 a ena) > Spikes thicken > Produce dome tke protrusions > close over immune deposits > Bury them et Light microscopy 1. Glomeru Show uniform, difuse thickening of the ‘lomeruar caitary wall > Normeceluiar glomeruli: There is neither proliferation nor inflammation. 12. Tubules: The epithelial cells ofthe proximal ‘Post Streptoceoal GN ») Deserve the renal biopsy findings {éneual 2009] 4 NEPHROTICSYNOROME: > spices thicken > Produce dome tke + Pathogenesis protrasions > close aver immune deposits 3 AT years: Lesion to kidney > Bury them > Aduts: Secondary to systemic disease entra © clinical Features Massive Proteinuria 23 Se/day) Light Microscopy > Hypoabuminemia AL Glomeru: Generalized — Pitting Edema (6/c > Show uniform, diffuse thickening of the proteins were maintaining Blood vessels slomeruarcaptary wall ‘osmotic Pressure) > Normoceluiar glomeruli: There is nethy ‘3 Hyperipidemis ~ Due to 7 Sythe, pralferation nor ite { etaboism, Abnormal Wansport, 2 Tubules: The epithe! 81/296 > > Upicura| tubules show drop. son membranous Nephropathy protein Later tubules undergo atrophy. Deposition of Ig PThickening of glomerular 3 Interstium: it shows mononuclear cell ‘apilay wall Inflammatory cells and interstitial boss in ‘causes: late stages 1) rugs (NSA, Captopril) 4. Blood vessels: Early stages vessels appear 1) Maignant Tumors roma Ii) SLE/ Autoimmune clsorders + Pathogenesis Form of chronic immune mediated complex ’) mang Due to Autoimmune aiseace PUA = M Type Phospholipase = Antigen [Abbinds to PLAAR > Complement activation Deposits of immune complex along ‘omeruar basement membrane ‘Secondary: Either an endogenous (eg. ONA in SLE} oF ‘exogenous one (eg. hepaiis B virus, tumour antigen, treponema antigen, drug ‘therapy with peniilamine) ‘complement Detail: (CSb-c9 actwates glomerular epithelial & Mesangial cas > Induce them iberate proteases & oxidants > Capilry wall injury Electron croscopy > Thickening ofthe glomerular captary wall due to irregular electron-dense deposts of immune complexes between the basement membrane and the “overying veceral epithail cells (subepthai). The visceral epithelia els show effaced foot procesees. Fin between these immune deposi, basement membrane material aid down, hich appear as iregulr spikes protruding ‘rom the COM. Changes due to subepithelial Immune complexes are divided into stages > Stage I Copiary wals are normal or show mild thickening and subepithelial dense deposits Stage i: rejections of GBM material around dense deposits, which appear as spikes on ‘poten ea tae the ‘eoitheo surface of the Basement oncoce ermine membrane, which tin wither > Stage I! New basement membrane ‘of glomerular eapilay wall Electron Microscopy : Immune complexes botween basement memorane and ‘epithelial cals Basement membrane materia laid between ‘deposits: Spikes protrucing from GBM. feneircles the deposits and is ai over the Immune depast, which bury them within 2 ‘markedly thickaned, irragular membrane. In slner stain, they appear dome-the protrsions, > Stage IV: The immune deposits undergo degradation and iss Immunoftuorescence Microscopy > Focal: Sclerosis of SOME but NOT ALL Membrancus nephropathy: lomeru Ik shows granular deposits of both > Segmental: Only atutofapilaryisinvohed immunoglobulins and complement (6 and DO ONLY HIGHLIGHTED (Rest added for ‘GJinthe subepithelial (between the visceral understanding) ‘epithet cll and the GEM) region, There is Clefenn nape, gr poe also intense staining for membrane attack =e aera complen between basement membrane and ‘epithelial cls > Basement membrane material ai between ‘deposits: Spikes protruding from GBM. See a ey Immunetluorescence Microscopy > Membranous nephropathy: Ik shows granular deposits of both immunoglobulins and complement (i and ‘Ghinthe subepithelial between the visceral ‘epithelial cll and the GEM) region, There is ako intense staining for membrane attack complex ema gomear nice Features Hematuria HIN 4 Serum creatinine Biomarkers: PLAS, THSO7A Minimal Change Disease > Diffuse Efacoment(Fattaing) of foot processes of wera epithelia calle wees + pathogenesis Associated with respiratory infections ‘a Atopic disorders Due to immune dysfunction ‘Morphology ‘Glomerul normal GBM Normal (Only visceral epithelia cls abnormat: Show effacement of fot procesee Clinica Features 26 ys Massive proteinuria (Albumin*) NoHTN, No hematuria Significant Response to corticosteroid therapy" Focal Segmental Glomerulosclerosis voere weve 7 collapse of entire glomerular tut Light Microscopy ‘> The focal and segmental lesions invave only «2 minority ofthe glomeru. The glomerular ‘shows hyalinoss and seers > Myainosss It is choracterued by ‘evtacellar accumulation of homogeneous and eosinophil material inthe glomeruli represents leaked plasma proteins due to Leshan bervsrenedrepredeesidpenuerhenniaded ‘markedly thickened, irregular membrane. In siver stain, they appear dome-he protrusions > Stage IV: The immune deposits undergo degradation and iss > Focal: Sclerosis of SOME but NOT ALL omer > Segmental Only atuftof CapilaryisinvoWved DO ONLY HIGHUGHTED (Rest added for understanding) ‘etncecum ne tlowing ting pt ea sgt Soccer Erie matter tw nts hE af Riera 82/296 ts a on ater ‘Slane eg, ull age tp noajerangtd ees nt Shy tl nian ap oa ml htgpumne nto + Pathogenesis > Focal Disuption of Visceral Epithelial cels* > Entrapped Plasma proteins > Hyalinoss, Sclerone > Nut neHst INPHSI encodes nephrin > key component of sit daprragm > Nur NPHS2 NPHS2 encodes podocln Mut in podocyte atin binding protein alpha actin > Mut TRPCG Sequence of Events: |) Endotholal & visceral epithelia elinjury 1) Visceral epithelial cl oss GBM segments denuded of foot processes > petmeabilty > proteins in mesangial matri proliferation of mesangial cells, macrophage infiltration > sclerosis + Morphology sclerotic Segments: collapse of eapilry loops. Increased matrix, plasma protein ‘deposition along capilrywalliyalinosis) > ‘ccd caplary lumen > Eacement of foot processes Hyalinoss& Thickened afferent arterioles Special Pathology by Dr. Hira Maryam > Progression to CKOIChronie Kidney isease) Hiv Associated Nephropathy > APOLL gone + Morphology > Le Colapsing variant of FSGS 5 cystic tubular allaton(iled wth inflammation, fibrosis & proteinaceous therapy*? Focal Segmental Gomerulosclerosis > Effacement of foot processes > Hyalinoss& Thickoned afferent arterioles > Collapse of entre glomerular tut LUpht Microscopy ‘> The focal and segmental lesions involve only 2 minonty ofthe glomerul. The glomerular shows hyalinosis and sclerosis, > Myainasis itis characterized by ‘ertacellar accumulation of homogeneous ‘and eosinophilic material inthe glomerul it represents leaked plasma proteins due to ‘endothelial or capilry wal injury 1 Selerosss 1 an extracellular accumulation ‘of collagenous matriin the mesanglimorin the capllary ops, or bath Slomeral, which do not show segmental leslons appear nora on light microscopy Electron Microscopy Both sderotc and nonsclertic areas show fuse effacement of foot processes. FSGS: Epithelial damage consists of degeneration and focal. disruption of ‘visceral epithelial cells with effacement of foot processes is the hallmark of FSGS, Immunofiuorescence ‘microscopy lah and C3 may be seen in the sclerotic areas and/or in the mesangium Hematura Lore HON Proteinuria Poor response to corticosteroid therapy Blood vessels: During early stages appear normal but later may show changes due to hypertension Electron Microscopy and immunoflucrescence > Shaws discrete subendothalia electron dense deposts. > Immunatuorescence: ite appearance suggests actvation of cassie complement pathway by immune complex. me Tr eee ‘Progression to CKOIChronie kidney isease) tv asetated Nephropathy fro gene ‘orhotgy Ue cota vr of Fs Gre uber aatenFled with iatanton Ross "8 protect ne Talore sos Membranoprttertve ‘Someorepeis, Pethopeei Ben ene, 82296 Corsi & complement ‘pete eae Sport Sess (Marked by etn coranert Imre compet gous & beaten oeompiemen ptm very. sy voviver i ~ Large and hypercelllar glomeruli ve to © Proliferation of (mest endothli ols © nitration of leukocytes © Epithelial crescents are seen in many = Thickening of GBM: It may be segmental and most prominent In the Peripheral opilary loops. = Subendethelal immune complex ‘deposits stimulates > synthesis of now basement membrane produces cuplcation” "ofthe basement membrane (commonly called as splitingl produces"double-contour” oe ‘tramtrack" appearance due to slomerularcapilary wall. This is better appreciates with special tans such as ster or AS. TTubules: Epithelial cls of tubules may show vacuolation and dropets of hyaline Interstitium: tt may show mild focal chronic Inflammatory calls Pope sie in LGR Hw Proteinuria Poor response to corticosteroid therapy Blood vessels: During early stages appear normal but later may show changes due to hypertension Electron Microscopy and immunoflucrescence > Shows discrete subendothaial electron- dense deposi. > Immunofuorescence: ite appearance suggests sethation of cassie complement pathway by Immune ‘complex. + cline! Features Nephrotic & Nephi syndrome hematuria, proteinuria ¥ Dense Deposit Disease + Pathogenesis > Tyee PN > Excessive activation of complement > 4 C3, Ab factor, Properain 9 {GBM proper (cental zone named lamina dense}. Immunofluorescence Its appearance suggests activation of atternate complement pathway. > Gis present igs and early complement components (Clq and C8) are absent ther Glomerular Disease: i Sak Mantementine fihemrenribeoneeh. Lerbahinad Tubules: Epithelial cells of tubules may show vacuolation and droplets of hyaline. Inerstitium: it may show mild focal ehronie Inslammatory call, 0B, (ate patray 2 convertase) Propedin sate |) | iy CaNeF eae — ss 84/296 Sequence of Events Substances ike bacterial polysocharide, endotoxin, and aggregates of IgA cleave C3 toca Gab in the presence of factors 8 and ‘generates C3b6D (atternatve pathway C3 convertase), C3bAb sable and degraded by factors and H, but stabilized by properin Patients with type ll MPGN have an IgG. autoantioody against C3 convertase in the Serum known as C3 nephrite factor (C3NeF} GNeE acts atthe same step as properdin and sabies 3b» and pevent ts degradation. ‘This results in persistent and prolonged C3 activation ard hypocomplementemia. In addition, decreased synthesis of C3 by the Thee, also responsible for hypotomplementemia ‘Morphology ght microscopy Dense depasi slisease shows wide spectrum ‘of microscopic changes. Some cases of them show features of MPGN described earlier Majority show mainly mesangial proliferative pattern of injury, while fthers may show an inflammatory and focaly rescenticappearanc lection Microscopy Dit is characteristic and. shows regula, ribbonske depostion of electron-dense material of unknown compostion in the ne a nar Nephrote Syndrome b) what are the light microscopic, Immunofiuerescence and lectron microscopic findings of membranous nephropathy? (3) [Supple 2019 hel in 2020} 2. Mather ofa S-yearold boy noticed that he has been less active for about a week and progressive puffiness around the eyes for St a a ee aie, te toes

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