glomerulonephritis pathology

1. 11

2. 22

3. 33

4. 44

5. 55

6. 66

7. 77

8. 88

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

11. Kidney Histology:Kidney Histology:
1111

12. Kidney Histology:Kidney Histology:
1212

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

27. Clinical effectsClinical effects
2727

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

31. 3131

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

56. Chronic GlomerulonephritisChronic Glomerulonephritis
5656

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

58. 5858