1.glomerulonephritis
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This document discusses various topics related to kidney function and disease. It begins with the microscopic anatomy of the kidney filtration membrane. It then covers kidney functions, histology, diseases like azotemia and uremia, types of glomerular diseases including primary and secondary glomerular diseases. It discusses clinical presentations like nephrotic syndrome and acute nephritic syndrome. Pathogenesis, mediators of injury, and specific conditions like acute glomerulonephritis are described. Laboratory findings for acute glomerulonephritis and characteristics of nephrotic syndrome are also summarized.
1.glomerulonephritis
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- 9. Capillary SpaceCapillary Space EndotheliumEndothelium UrinaryUrinary SpaceSpace GBMGBM PodocytePodocyte Filtration Membrane – ElectronFiltration Membrane – Electron Micro.Micro. 99
- 10. Functions of Kidney – PhysologyFunctions of Kidney – Physology Kidney Function Test – study BiochemistryKidney Function Test – study Biochemistry 1010
- 13. AzotemiaAzotemia Refers to an elevation of blood urea nitrogen and creatinine levelsRefers to an elevation of blood urea nitrogen and creatinine levels and is largely related to a decreased glomerular filtration rate (GFR).and is largely related to a decreased glomerular filtration rate (GFR). UremiaUremia When azotemia becomes associated with a constellation of clinicalWhen azotemia becomes associated with a constellation of clinical signs & symptoms & biochemical abnormalitiessigns & symptoms & biochemical abnormalities 1313
- 14. Glomerular DiseasesGlomerular Diseases Destruction of glomeruli by immune or infections.Destruction of glomeruli by immune or infections. A. Primary Glomerular Diseases – Histological typesA. Primary Glomerular Diseases – Histological types Includes diseases where the glomerulus is primarily involvedIncludes diseases where the glomerulus is primarily involved 1.1. Acute glomerulonephritis (Acute diffuse proliferative glomerulonephritis)Acute glomerulonephritis (Acute diffuse proliferative glomerulonephritis) * Poststreptococcal* Poststreptococcal * Non-poststreptococcal* Non-poststreptococcal 1.1. Rapidly progressive (crescentic) glomerulonephritisRapidly progressive (crescentic) glomerulonephritis 2.2. Membranous glomerulopathyMembranous glomerulopathy 3.3. Minimal-change disease(nil disease,kidnay disease cause nephrotic )Minimal-change disease(nil disease,kidnay disease cause nephrotic ) 4.4. Focal segmental glomerulosclerosis(cause of nephrotic syndrome child)Focal segmental glomerulosclerosis(cause of nephrotic syndrome child) 5.5. Membranoproliferative GNMembranoproliferative GN 6.6. IgA nephropathy(abnormal deposite of a protein)IgA nephropathy(abnormal deposite of a protein) 7.7. Chronic GNChronic GN 1414
- 15. Diffuse lesions:Diffuse lesions: Relatively uniform, involve most or all glomeruliRelatively uniform, involve most or all glomeruli Focal lesions:Focal lesions: Involve only some glomeruli; others normalInvolve only some glomeruli; others normal Segmental-local:Segmental-local: Involve only one part of the glomerulusInvolve only one part of the glomerulus Mesangial:Mesangial: Deposits of immunoglobulins in mesangial matrixDeposits of immunoglobulins in mesangial matrix Membranous:Membranous: Thickening of BMThickening of BM Proliferative lesions:Proliferative lesions: Increased number of glomerular cellsIncreased number of glomerular cells Sclerotic lesions:Sclerotic lesions: Glomerular scarring from previous glomerular injuryGlomerular scarring from previous glomerular injury Crescent lesions:Crescent lesions: Accumulation of proliferating cells in Bowman's spaceAccumulation of proliferating cells in Bowman's space 1515
- 16. B. Secondary GD-B. Secondary GD- associated with Systemic Diseasesassociated with Systemic Diseases 1.1. Lupus nephritis (systemic lupus erythematosus)Lupus nephritis (systemic lupus erythematosus) 2.2. Diabetic nephropathyDiabetic nephropathy 3.3. AmyloidosisAmyloidosis 4.4. Goodpasture syndromeGoodpasture syndrome 5.5. Microscopic polyangiitis/polyarteritisMicroscopic polyangiitis/polyarteritis 6.6. Wegener's granulomatosisWegener's granulomatosis 7.7. Henoch-Schönlein purpuraHenoch-Schönlein purpura 8.8. Bacterial endocarditis-related GNBacterial endocarditis-related GN 1616
- 17. C. Hereditary DisordersC. Hereditary Disorders Alport syndromeAlport syndrome Defect in the synthesis of collagen (important structural componentDefect in the synthesis of collagen (important structural component of basement membranes in the kidney, inner ear, and eye)of basement membranes in the kidney, inner ear, and eye) Thin basement membrane disease (benign familialThin basement membrane disease (benign familial hematuria)hematuria) The only abnormal finding in this disease is a thinning of the BMThe only abnormal finding in this disease is a thinning of the BM Fabry diseaseFabry disease Accumulate of glycolipid within the blood vessels and organs. ThisAccumulate of glycolipid within the blood vessels and organs. This accumulation leads to an impairment of their proper functionaccumulation leads to an impairment of their proper function 1717
- 18. Clinical presentations (Glomerulo syndromes)Clinical presentations (Glomerulo syndromes) Nephrotic syndromeNephrotic syndrome Acute nephritic syndromeAcute nephritic syndrome Acute renal failure -Acute renal failure - loss of Kidney function - within weeksloss of Kidney function - within weeks Chronic renal failure -Chronic renal failure - Over months and years – UremiaOver months and years – Uremia Asymptomatic hematuria or proteinuriaAsymptomatic hematuria or proteinuria, or a combination of these two,, or a combination of these two, Is usually a manifestation of subtle or mild glomerular abnormalities.Is usually a manifestation of subtle or mild glomerular abnormalities. HypertensionHypertension It may be the first findings in some pt with certain glomerular diseaseIt may be the first findings in some pt with certain glomerular disease 1818
- 19. Pathogenesis of glomerular injuryPathogenesis of glomerular injury A. Antibody-mediated immuneA. Antibody-mediated immune 1.1. Circulating Immune Complex DepositionCirculating Immune Complex Deposition Injury resulting from deposition of soluble antigen-antibody complex inInjury resulting from deposition of soluble antigen-antibody complex in the glomerulusthe glomerulus Endogenous antigens (e.g. DNA in SLE, tumor antigens)Endogenous antigens (e.g. DNA in SLE, tumor antigens) Exogenous antigens (e.g. infectious products - streptococci)Exogenous antigens (e.g. infectious products - streptococci) There is type III hypersensitivity reactionThere is type III hypersensitivity reaction This is the most commonThis is the most common
- 20. 2. In Situ Immune Complex Deposition2. In Situ Immune Complex Deposition Injury by antibodies reacting in situ within the glomerulus either withInjury by antibodies reacting in situ within the glomerulus either with 1.1. Insoluble fixed (intrinsic) glomerular antigensInsoluble fixed (intrinsic) glomerular antigens Glomerular basement membrane/anti-GBM nephritis - GoodpastureGlomerular basement membrane/anti-GBM nephritis - Goodpasture syndromesyndrome Heymann antigen - Membranous glomerulopathyHeymann antigen - Membranous glomerulopathy Mesangial antigensMesangial antigens Others – unknown antigenOthers – unknown antigen 1.1. Planted antigen within the glomerulusPlanted antigen within the glomerulus ExogenousExogenous – drugs, infectious– drugs, infectious agentsagents Endogenous – DNA,Endogenous – DNA, IG AIG A
- 21. 3. Cytotoxic Antibodies3. Cytotoxic Antibodies CA directed against glomerular cell components like mesangial cell,CA directed against glomerular cell components like mesangial cell, endothelial cell or visceral epithelial cell glycoproteinendothelial cell or visceral epithelial cell glycoprotein B. T Cell-Mediated Immune InjuryB. T Cell-Mediated Immune Injury It is suggestiveIt is suggestive C. Activation of Alternative Complement PathwayC. Activation of Alternative Complement Pathway
- 22. Mediators of Glomerular injuryMediators of Glomerular injury CellsCells Chemical mediatorsChemical mediators 2222
- 23. Acute Nephritic Syndrome (acute glomerulonephritisAcute Nephritic Syndrome (acute glomerulonephritis syndrome )syndrome ) It is a clinical manifestation in which several different renal diseasesIt is a clinical manifestation in which several different renal diseases giving rise to a group of specific symptomsgiving rise to a group of specific symptoms It is the classical presentation of acute glomerulonephritis/AGNIt is the classical presentation of acute glomerulonephritis/AGN Characterized byCharacterized by Hematuria – grossly visible. Urine is smokeyHematuria – grossly visible. Urine is smokey Variable proteinuria – usually less than 1gVariable proteinuria – usually less than 1g Oliguria and edemaOliguria and edema AzotemiaAzotemia HypertensionHypertension 2323
- 24. Acute GlomerulonephritisAcute Glomerulonephritis (Acute proliferative GN, Acute diffuse proliferative GN, Acute Nepritis)(Acute proliferative GN, Acute diffuse proliferative GN, Acute Nepritis) This is a group of glomerular disease characterized anatomically byThis is a group of glomerular disease characterized anatomically by inflammatory alterations in the glomeruli & clinically by the syndromeinflammatory alterations in the glomeruli & clinically by the syndrome of acute nephritisof acute nephritis TypesTypes Acute poststreptococcal glomerulonephritisAcute poststreptococcal glomerulonephritis Non streptococcal glomerulonephritisNon streptococcal glomerulonephritis 2424
- 25. Acute poststreptococcal (prolferative) glomerulonephritisAcute poststreptococcal (prolferative) glomerulonephritis It appears 1-3 weeks after streptococcal infection most commonly ofIt appears 1-3 weeks after streptococcal infection most commonly of the skinthe skin Occurs most commonly in children – 6- 10 years but adults can beOccurs most commonly in children – 6- 10 years but adults can be affectedaffected Mostly presents as acute nephritis syndromeMostly presents as acute nephritis syndrome Aetiology –Aetiology – Group A beta hemolytic streptocociGroup A beta hemolytic streptococi 2525
- 26. PathogenesisPathogenesis Strep infection of the throat or skinStrep infection of the throat or skin Antibody formed against streptococciAntibody formed against streptococci AG-Ab complex formationAG-Ab complex formation Deposition of Ag-Ab complex in glomerular basement membraneDeposition of Ag-Ab complex in glomerular basement membrane Compliment fixationCompliment fixation Type III hypersensitivity reactionType III hypersensitivity reaction Endothelial & mesangial cell(around the blood vessels) proliferationEndothelial & mesangial cell(around the blood vessels) proliferation AGNAGN 2626 Normal
- 28. Non streptococcal glomerulonephritisNon streptococcal glomerulonephritis AetiologyAetiology Bacteria – S. Aureus (endocarditis), pneumococcus (pneumonia),Bacteria – S. Aureus (endocarditis), pneumococcus (pneumonia), meningococcusmeningococcus Viruses – Hepatitis B virus, mumps virus, varicella virus & Epstein-Viruses – Hepatitis B virus, mumps virus, varicella virus & Epstein- Barr virus (infectious mononucleosis)Barr virus (infectious mononucleosis) Protozoa – plasmodium malarie, toxoplasmaProtozoa – plasmodium malarie, toxoplasma 2828
- 29. MorphologyMorphology Naked EyeNaked Eye May show no particular gross abnormalities.May show no particular gross abnormalities. In severe cases, the cut surface of the renal cortex may show aIn severe cases, the cut surface of the renal cortex may show a petechial (red or purple spot)petechial (red or purple spot) 2929
- 30. MicroscopicMicroscopic GlomeruliGlomeruli Changes are diffuse i.e. all lobules of all glomerulai are affectedChanges are diffuse i.e. all lobules of all glomerulai are affected Enlarged, hypercellular & relatively bloodlessEnlarged, hypercellular & relatively bloodless (Hypercellularity is due to proliferation of endothelial & mesangial cells.(Hypercellularity is due to proliferation of endothelial & mesangial cells. Neutrophil & monocyte infiltration. Endothelial cells are swollen )Neutrophil & monocyte infiltration. Endothelial cells are swollen ) 3030
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- 32. MicroscopicMicroscopic TubulesTubules May show reversilble cell injury & red cell casts(composed of matrixMay show reversilble cell injury & red cell casts(composed of matrix containing RBC in various stage of degeneration and visibility,chare.containing RBC in various stage of degeneration and visibility,chare. Renal bleeding.)Renal bleeding.) InterstitiumInterstitium Shows oedema & inflammatory cellsShows oedema & inflammatory cells 3232
- 33. Two patterns of deposition of immune complexes as seen by immunofluorescence microscopy: granular,characteristic of circulating and in situ immune complex nephritis (D) and linear, characteristic of classic anti- GBM disease
- 34. Laboratory findings of AGNLaboratory findings of AGN Physical findingsPhysical findings Urinary findingsUrinary findings Scanty urine (oliguria)Scanty urine (oliguria) Red or smoky or cocola coloured (hematuria)Red or smoky or cocola coloured (hematuria) Microscopic findingsMicroscopic findings RBCRBC PUS cellsPUS cells Epithelial cellsEpithelial cells Casts – red cell casts (diagnostics), granular castsCasts – red cell casts (diagnostics), granular casts 3434
- 35. The Nephrotic SyndromeThe Nephrotic Syndrome The Nephrotic syndrome refers to a clinical complex that includes theThe Nephrotic syndrome refers to a clinical complex that includes the following:following: Massive proteinuria - 3.5 gm or more/day (24hours)Massive proteinuria - 3.5 gm or more/day (24hours) Hypoalbuminemia, with plasma albumin levels less than 3 gm/dlHypoalbuminemia, with plasma albumin levels less than 3 gm/dl Generalized edemaGeneralized edema Hyperlipidemia – lipoprotein & choesterol is increasedHyperlipidemia – lipoprotein & choesterol is increased 3535
- 36. Initially - derangement in the capillary walls - resulting in increasedInitially - derangement in the capillary walls - resulting in increased permeability to plasma proteins.permeability to plasma proteins. Protein to escape from the plasma into the glomerular filtrate -Protein to escape from the plasma into the glomerular filtrate - hypoalbuminemiahypoalbuminemia drop in plasma colloid osmotic pressure and primary retention of saltdrop in plasma colloid osmotic pressure and primary retention of salt and water by the kidney - generalized edemaand water by the kidney - generalized edema Hypoalbuminemia triggers increased synthesis of lipoproteins in theHypoalbuminemia triggers increased synthesis of lipoproteins in the liver and impairment of peripheral breakdown of lipoproteins.liver and impairment of peripheral breakdown of lipoproteins. The lipiduria - reflects the increased permeability of the GBM toThe lipiduria - reflects the increased permeability of the GBM to lipoproteins.lipoproteins. 3636
- 37. 3737 Acute nephritic syndrome Nephrotic syndrome Common cause Acute GN Minimal change disease, membranous GN Oedema Local edema Anasarca Urinary changes •Amount •Hematuria •Proteinuria •Red cell cast Oliguria Grossly visible Less than 1g/24 hrs Present Oliguria Absent Massive proteinuria Absent Blood •Protein •Cholesterol Normal Normal Decreased (albumin) Raised Hypertension Mild to moderate Absent
- 38. Causes of Nephrotic syndromeCauses of Nephrotic syndrome Primary Glomerular DiseasePrimary Glomerular Disease Minimal-change diseaseMinimal-change disease Membranous GNMembranous GN Focal segmental glomerulosclerosisFocal segmental glomerulosclerosis Membranoproliferative GNMembranoproliferative GN 3838
- 39. Causes of Nephrotic syndromeCauses of Nephrotic syndrome Systemic Diseases with Renal ManifestationsSystemic Diseases with Renal Manifestations Diabetes mellitus Diabetes mellitus Systemic lupus erythematosus Systemic lupus erythematosus AmyloidosisAmyloidosis Drugs (gold, penicillamine, "street heroin")Drugs (gold, penicillamine, "street heroin") Infections (malaria, syphilis, hepatitis B, HIV)Infections (malaria, syphilis, hepatitis B, HIV) Malignancy (carcinoma, melanoma)Malignancy (carcinoma, melanoma) 3939
- 40. Minimal change Disease (Lipoid Nephrosis)Minimal change Disease (Lipoid Nephrosis) Most common cause nephrotic syndrome in childhoodMost common cause nephrotic syndrome in childhood Aetiology & PathogenesisAetiology & Pathogenesis Unknown. Probably there is some immune dysfunction asUnknown. Probably there is some immune dysfunction as MCD may follow a respiratory infections or recent immunizations, andMCD may follow a respiratory infections or recent immunizations, and because of the response of the disease to steroid therapy.because of the response of the disease to steroid therapy. There is presumably an alteration in the electrical charge of the GBMThere is presumably an alteration in the electrical charge of the GBM that makes some proteins, especially albumin permeable.that makes some proteins, especially albumin permeable. The glomerular capillaries (though structurally intact) are no longer ableThe glomerular capillaries (though structurally intact) are no longer able to retain albumin in the vascular space and so albuminuria results.to retain albumin in the vascular space and so albuminuria results. 4040
- 41. HistologyHistology Normal, except on electron microscopy, where fusion of podocyteNormal, except on electron microscopy, where fusion of podocyte foot processes is seenfoot processes is seen Tubules – lipoprotiens pass through glomeruli & are reabsorbed.Tubules – lipoprotiens pass through glomeruli & are reabsorbed. Cells of proximal tubules are usually laden with lipid & thus calledCells of proximal tubules are usually laden with lipid & thus called lipoid nephrosislipoid nephrosis Clinical AspectClinical Aspect Pt present as nephrotic syndromePt present as nephrotic syndrome 4141
- 42. Membranous glomerulonephritis (membranous Nephropathy)Membranous glomerulonephritis (membranous Nephropathy) Most common cause of nephrotic syndrome in adultsMost common cause of nephrotic syndrome in adults Characterised by diffuse thickening of glomerular capillary wall &Characterised by diffuse thickening of glomerular capillary wall & accumulation of immune complex along the subepithelial side ofaccumulation of immune complex along the subepithelial side of basement membranebasement membrane 4242
- 43. EtiologyEtiology Idiopathic (85%) – taken as autoimmune diseaseIdiopathic (85%) – taken as autoimmune disease Secondary to systemic diseaseSecondary to systemic disease Malignant epithelial tumoursMalignant epithelial tumours SLESLE Infections – chronic nephritisInfections – chronic nephritis Plasmodium malariaPlasmodium malaria DrugsDrugs Other autoimmune diseaseOther autoimmune disease 4343
- 44. PathogenesisPathogenesis It is taken as a chronic antigen antibody disease, immune complex isIt is taken as a chronic antigen antibody disease, immune complex is formed in situ or in circulation which fixes complementformed in situ or in circulation which fixes complement 4444
- 45. MorphologyMorphology The glomeruli show uniform, diffuse thickening of Glomerular capillaryThe glomeruli show uniform, diffuse thickening of Glomerular capillary basement membrane due to immune complex depositionbasement membrane due to immune complex deposition 4545
- 46. Clinical effectsClinical effects Presents as nephrotic syndrome (85%) or insidious onset or non-Presents as nephrotic syndrome (85%) or insidious onset or non- nephrotic protienuria (15%)nephrotic protienuria (15%) PrognosisPrognosis May progress to renal failure in about 50%May progress to renal failure in about 50% 4646
- 47. Rapidly progressive (crescentic) glomerulonephritis (RPGN)Rapidly progressive (crescentic) glomerulonephritis (RPGN) Crescents are formed in Bowman’s space by proliferating parietalCrescents are formed in Bowman’s space by proliferating parietal epithelial cells with infiltrating monocytes & macrophage &epithelial cells with infiltrating monocytes & macrophage & sometimes neutrophils & lymphocytessometimes neutrophils & lymphocytes ClinicallyClinically It is rapidly progressive state with declining renal function withIt is rapidly progressive state with declining renal function with severe oliguria & anuria(fail urine production)severe oliguria & anuria(fail urine production) It usually passes to irreversible renal failure in weeks or monthsIt usually passes to irreversible renal failure in weeks or months 4747
- 48. Causes, types & pathogenesisCauses, types & pathogenesis Type I (Anti – GBM antibody)Type I (Anti – GBM antibody) IdiopathicIdiopathic Goodpasture syndrome – it is due to anti GBM antibodies evoked byGoodpasture syndrome – it is due to anti GBM antibodies evoked by antigens present in Glomerular & pulmonary basement membraneantigens present in Glomerular & pulmonary basement membrane (goodpastures antigen)(goodpastures antigen) There is renal failure & pulmonary haemorrahgeThere is renal failure & pulmonary haemorrahge 4848
- 49. Causes, types & pathogenesisCauses, types & pathogenesis Type II (Immune complex)Type II (Immune complex) IdiopathicIdiopathic Post infectionPost infection SLESLE Henoch-Schönlein purpura(small hemorrhages)Henoch-Schönlein purpura(small hemorrhages) Type III RPGN (Pauci –immune)Type III RPGN (Pauci –immune) ANCA(anti neutrophil cytoplasmic antibodies)(autoimmune disorder)ANCA(anti neutrophil cytoplasmic antibodies)(autoimmune disorder) IdiopathicIdiopathic Microscopic polyangiitis(autoimmune dis.necrotizing small vessels,noMicroscopic polyangiitis(autoimmune dis.necrotizing small vessels,no evidence)evidence) Wegener's granulomatosis(same likeWegener's granulomatosis(same like Polyangiits,it effects lungs and kidney)Polyangiits,it effects lungs and kidney) 4949
- 50. Ig A Nephrotpathy (Berger’s Disease)Ig A Nephrotpathy (Berger’s Disease) Is named for the deposits of IgA in the glomerulus (Mesangium)Is named for the deposits of IgA in the glomerulus (Mesangium) Common in children & young adultsCommon in children & young adults AetiopathogenesisAetiopathogenesis Ig A synthesis is increased and evoked by antigens (e.g. viruss,Ig A synthesis is increased and evoked by antigens (e.g. viruss, bacterai, food protein)bacterai, food protein) There is deposition of immune complexes in the mesangiumThere is deposition of immune complexes in the mesangium They activate the complement pathway & initiate glomerular injuryThey activate the complement pathway & initiate glomerular injury 5050
- 51. ClinicallyClinically Recurrent gross or microscopic painless, hematuria ocursRecurrent gross or microscopic painless, hematuria ocurs Proteinuria is mildProteinuria is mild Sometimes nephrotic or rarely Crescentic GN may developSometimes nephrotic or rarely Crescentic GN may develop Slowly progressive & may lead to CRFSlowly progressive & may lead to CRF 5151
- 52. Membranoproliferative Glomerulonephritis (MPGN)Membranoproliferative Glomerulonephritis (MPGN) (mesangiocapillary GN)(mesangiocapillary GN) Occurs in older children & young adultsOccurs in older children & young adults Presents clinically as Nephrotic, Nephritic or mild proteinuriaPresents clinically as Nephrotic, Nephritic or mild proteinuria Characterized byCharacterized by There is thickening of GBMThere is thickening of GBM Splitting of BM occurs due to inclusion of processes of mesangialSplitting of BM occurs due to inclusion of processes of mesangial cellscells Proliferation of glomerular cells & mesangial cellsProliferation of glomerular cells & mesangial cells 5252
- 53. Types & pathogenesisTypes & pathogenesis 1. Primary or idiopathic MPGN1. Primary or idiopathic MPGN SubtypesSubtypes Type I MPGNType I MPGN In most of the cases immune complexes are present in theIn most of the cases immune complexes are present in the glomerulusglomerulus Type II MPGNType II MPGN Most cases are autoimmune diseaseMost cases are autoimmune disease 2. Secondary MPGN – associated with certain systemic disorders2. Secondary MPGN – associated with certain systemic disorders 5353
- 54. Focal proliferative glomerulonephritisFocal proliferative glomerulonephritis Focal is used when some but not all glomeruli are involved & segmentalFocal is used when some but not all glomeruli are involved & segmental is used when a portion of the capillary tuft of the affected glomeruli isis used when a portion of the capillary tuft of the affected glomeruli is involvedinvolved Presented usually with microscopic or gross haematuria or nonPresented usually with microscopic or gross haematuria or non nephrotic proteinnephrotic protein It may occurIt may occur In Systemic disease like subacute bacterial endo carditis , heochIn Systemic disease like subacute bacterial endo carditis , heoch schonlein purpura SLEschonlein purpura SLE IG A nephropathyIG A nephropathy IdiopathicIdiopathic 5454
- 55. Focal Segmental glomerulosclerosis (hyalinosis)Focal Segmental glomerulosclerosis (hyalinosis) Presents with nephrotic syndrome or heavy proteinuriaPresents with nephrotic syndrome or heavy proteinuria It may be primary or secondary disorderIt may be primary or secondary disorder There is visceral epithelial damage, hyalinosis & sclerosis of involvedThere is visceral epithelial damage, hyalinosis & sclerosis of involved segmentssegments 5555
- 57. 5757 Histological types of glomerulonephritis Most common types of clinical presentation Acute GN Acute Nephritic Syndrome Minimal change disease Nephrotic syndrome in children Membranous glomerulonephritis Nephrotic syndrome in Adult Ig A nephropathy Astmptomatic hematuria Rapid progressive GN (crescentric GN) Acute nephritic syndrome, progressive renal failure Focal Segemental GN Hematuria , proteinuria Mesangiocapillary GN Hematuria, proteinuria, nephritic or nephrotic syndrome Focal glomerulosclerosis Proteinuria or nephrotic syndrome Chronic GN Progressive renal failure
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