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Acute Glomerulonephritis
Soumya Ranjan Parida
Basic B.Sc. Nursing 4th
year
Sum Nursing College
Efferent arteriol
Distal tubule
Endothelial cell
Mesangial cell
Mesangial matrix
Viscaral epithelial cell
Proximal; tubule
Lamina densa
Parietal epitheal cell
Afferent arteriol
Bowman’s capsule
Bowman’s space
GLOMERULUS
Pathogenesis of glomerular diseases
Genetic –
• Mutations in exons of DNA
• Mutations in the regulatory genes controlling DNA transcription
• Abnormal post transcriptional modification of RNA transcripts
• Abnormal post translational modifications of proteins
Immunological injury –
• AG – Ab – Glomerulus – complement activation – chemtactic and
anaphylatoxin-like factors
Coaglation system activation –
• Direct or indirect
• Activation of kinin system- chemtactic and anaphylatoxin-like factors
Pathology
• Proliferation of glomerular cells –
Generalized – all glomeruli
Focal – some glomeruli
Diffuse – all parts of glomeruli
Segmental – some parts of glomeruli
Endothelial, mesangial cells, mesangial matrix proliferation
Increased glomerular size – norrow the lumens of glomerular
capillaries – renal insufficiency
• Crescent formation in bowman capsule –
Proliferation of parietal epithelial cells
Composition – Fibrin, epithelial cells, BM-like material
macrophages
Fibroepithelial crescent – invasion of connective tissue
Crescent – glomerular cell death – eosinophilic appearance
• Exudation of blood cells –
Neutrophils, eosinophils, basophils, mononuclear cells
• Increase in the width of the BM
• Tubulo interstitial fibrosis –
Injury to the renal tubules – MNC infiltration – soluble factors –
fibrosis – destruction of renal tubules and peritubular capillaries
Pathology
Acute poststreptococcal GN
It is characterized by sudden onset of gross hematuria, edema,
hypertension and renal insufficiency
Etiology and epidemiology –
• Nephritogenic strains of group-A β hemolytic streptococci –
• Throat serotype – 1,3, 4, 12,25
• Skin serotype – 2, 49, 55, 57, 60
•
• Pharyngitis - ( cold weather )
• Pyoderma - (warm weather )
Pathogenesis & Pathology
Pathogenesis –
Immune complex mediated injury
Alternate pathway activation
Pathology -
• Light microscopy –
All glomeruli enlarged,
Bloodless
Mesanchymal cell proliferation
Mesanchymal matrix proliferation
PMN cell infiltration
Crescent formation
• Immunofluorescence microscopy –
Lumpy-bumpy deposits of Ig and complements in BM & mesangium
• Electrone microscopy –
Electrone dense deposits or ‘humps’ on epithelial side of BM
Clinical manifestations
• Age – 5-12 yrs, uncommon before 3 yrs
• Pharyngitis – 1-2 wks
• Pyoderma – 3-6 wks
• Asymptomatic microscopic hematuria, normal RFT to
ARF
• Edema, HT, oliguria, encephalopathy, CHF,nephrotic
syndrome(10 20%)
• Malaise, lethargy, abdominal pain, fever, acute subglottic
edema, air way obstruction
• Acute phase – 6-8 wks
• Proteinuria and HT – 4-6 wks
• Microscopic hematuria – 1-2 yrs
Diagnosis
Normal urine examination -
No cast,except hyaline 1/hpf
RBC – 1-2/hpf
WBC – Male – 0-3/hpf
Female -0-5/ hpf
Epithelial cell few
Bacteria – no organism/oif : unspun
<20/hpf : spun
Urine in AGN –
RBC,
RBC cast,
proteinuria,
PMN cells
Diagnosis
Blood –
Normochromic anemia
C3 level decreased
ASLO – throat infections
2-5 yrs – 120-160 todds unit
6-9 yrs – 240 todds unit
10-12 – 320 todds unit
> 13 yrs - 320 todds unit
DNase B – skin infection
Positive throat culture
Diagnosis
Streptozyme test –
( SLO, DNase B, Hyaluronidase, Streptokinase, NADase )
Renal biopsy –
- ARF
- Nephrotic syndrome
- Absence of evidence of streptococcal infection
- Normal complement level
- Hematuria, proteinuria and low C3 >2 months
Complications
• Hypertension
• Encephalopathy
• CHF
• Hyperkalemia
• Hyperphosphatemia
• Hypocalcemeia
• Acidosis
• Seizures
• Uremia
Treatment & Prognosis
Treatment –
Diet – Protein, sodium, potassium restricted
Penicillin – 10 days
Fluid restriction
Diuretic
Antihypertensive – CCB, Vasodilators, ACE inhibitors
Prognosis –
95% complete recovery
Recurrences are extremely rare
Membranous Glomerulonephritis
Etiology –
SLE, chronic ITP, neuroblastoma, gonadoblastoma,
syphilis,HBV infection, gold .penicillamine.
Pathology –
LMC – Diffuse thickening of GBM without significant proliferative
changes.
Deposition of membrane-like material by visceral epithelial
cells
Resembles ‘spikes’ on epithelial side of GBM.
IFM – Granular deposits of IgG & C3 on epithelial side.
EMC – Linear staining of IgG,IgA,C3 on tubular BM
Clinical features –
Most common in 2nd
decade, nephrotic syndrome (2-6%),
microscopic or gross hematuria, HT (20%).
Diagnosis –
C3 normal except SLE.
Kidney biopsy –
Nephrotic syndrome > 10yrs, Unexplained hematuria and
proteinuria, increased risk of RVT.
Treatment –
Salt restriction, diuretic, prednisone+cyclophosphamide or
chlorombucil
Prognosis –
CRF (20%), Active disease (40%)
Membranous Glomerulonephritis
Pathogenesis –
C3 nephritic factors- activates alternative complement pathway
Pathology –
Type 1 –
LMC - most common
- Accentuation of lobular pattern
- Generalized increased in mesangial cells & matrix
- GBM splitting from interposition of mesangial cytoplasm & matrix b/w
- endothelial cell and GBM
- Formation of crescent
IFMC – C3 & lesser amount of Ig in mesangium and along the peripheral
capillary in a lobular pattern
EMC – immune complex-like deposits in mesangial and subendothelial
regions
Type 2 –
-less common, irregular ribbon-like thickening of GBM,
crescent common, splitting rare.
Membranoproliferative (mesangiocapillary)
Glomerulonephritis (MPGN)
Type 3 –
Similar to type 1 in LMC & IFMC
EMC – subepithelial and subendothelial
Clinical features –
Most common in 3rd decade, nephrotic syndrome, acute
nephritic syndrome, RFT-normal to decreased, HT.
Diagnosis –
C3 decreased
Renal biopsy – Nephrotic syndrome >10yrs, significant proteinuria
with microscopic hematuria, decreased C3 >8wks.
Treatment –
Long term prednisone EOD
Prognosis –
ESRD (50%), type 2 worst prognosis, recurrent MPGN in kidney
transplant, type 1(13%), type 2(90%)
Membranoproliferative (mesangiocapillary)
Glomerulonephritis (MPGN)
SLE Nephritis
Immune complex mediated injury, both T cell and B cell function alteration
WHO classification –
Type 1 – No abnormality
Type 2 – Mesangial lupus nephritis
2a – mild deposit
2b – moderate deposit
Type 3 – FSGN, subendothelial & mesangeal deposits,
necrosis,crescent, sclerosis.
Type 4 – Most common, most severe, diffuse proliferative lupus
nephritis, subendothelial & mesangeal deposits, ‘wire loop
lesions’ necrosis,crescent, sclerosis.
Type 5 – Membranuous lupus nephritis, least common, resembles
membranuous GN except mild to moderate mesangial
proliferation, decreased C3 level.
Clinical features –
• Adolescence , female
• All type 2 and some type 3 – hematuria, normal RFT, proteinuria <1g/day.
• Some type 3 and all type 4 - hematuria, decreased RFT, proteinuria,
nephrotic syndrome, ARF
• Type 5 – nephrotic syndrome.
Diagnosis –
ANA, antibody to double stranded DNA, C3-C4 level decreased.
Treatment –
• All patients – prednisone 4-6 months
• Type 3 & 4 – 6 monthly IV cyclophosphamide 500-1000mg/m2
followed by
every 3 monthly dosing for 18-36 months.
• Type 1 & 2 – azathioprine single dose daily, 1.5-2mg/kg/day
Prognosis –
Highest risk of progression in type 4
SLE Nephritis
Henoch-schonlein purpura nephritis
Pathology and pathogenesis –
• Immune complexes containing IgA1 deposition within the capillaries of the
skin, intestine and glomerulus.
• Crescent formation more common and extensive
Clinical manifestations –
• 1-3 wks after URI
• Gross hematuria (20-30%),
• Isolated microscopic hematuria
• Hematuria and proteinuria
• Acute nephritic syndrome
• Nephrotic syndrome
• Renal insufficiency
• Ureteritis
Prognosis –
Best - Isolated microscopic hematuria
Poor - Acute nephritic syndrome, Nephrotic syndrome
Rapidly Progressive (crescentic) GN
Classification –
1. Immune comlex mediated GN – PSGN, MPGN, lupus, HSP and IgA
nephritis.
2. Anti-GBM mediated GN – Goodpasture disease.
3. ANCA mediated GN –Microscopic PAN, Wegner granulomatosis.
Crescent formation.
Goodpasture disease –
-Pulmonary hemorrage and GN with antibody against type 4
collagen of alveolar BM and GBM.
-Continuous linear pattern of IgG along the GBM.
Diagnosis –
ANA, Normal C3, anti DNase B,
ANCA to MPO or proteinase-3
Treatment -
According to cause
THANKS

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Acute glomerulonephritis

  • 1. Acute Glomerulonephritis Soumya Ranjan Parida Basic B.Sc. Nursing 4th year Sum Nursing College
  • 2. Efferent arteriol Distal tubule Endothelial cell Mesangial cell Mesangial matrix Viscaral epithelial cell Proximal; tubule Lamina densa Parietal epitheal cell Afferent arteriol Bowman’s capsule Bowman’s space GLOMERULUS
  • 3. Pathogenesis of glomerular diseases Genetic – • Mutations in exons of DNA • Mutations in the regulatory genes controlling DNA transcription • Abnormal post transcriptional modification of RNA transcripts • Abnormal post translational modifications of proteins Immunological injury – • AG – Ab – Glomerulus – complement activation – chemtactic and anaphylatoxin-like factors Coaglation system activation – • Direct or indirect • Activation of kinin system- chemtactic and anaphylatoxin-like factors
  • 4. Pathology • Proliferation of glomerular cells – Generalized – all glomeruli Focal – some glomeruli Diffuse – all parts of glomeruli Segmental – some parts of glomeruli Endothelial, mesangial cells, mesangial matrix proliferation Increased glomerular size – norrow the lumens of glomerular capillaries – renal insufficiency • Crescent formation in bowman capsule – Proliferation of parietal epithelial cells Composition – Fibrin, epithelial cells, BM-like material macrophages Fibroepithelial crescent – invasion of connective tissue Crescent – glomerular cell death – eosinophilic appearance
  • 5. • Exudation of blood cells – Neutrophils, eosinophils, basophils, mononuclear cells • Increase in the width of the BM • Tubulo interstitial fibrosis – Injury to the renal tubules – MNC infiltration – soluble factors – fibrosis – destruction of renal tubules and peritubular capillaries Pathology
  • 6. Acute poststreptococcal GN It is characterized by sudden onset of gross hematuria, edema, hypertension and renal insufficiency Etiology and epidemiology – • Nephritogenic strains of group-A β hemolytic streptococci – • Throat serotype – 1,3, 4, 12,25 • Skin serotype – 2, 49, 55, 57, 60 • • Pharyngitis - ( cold weather ) • Pyoderma - (warm weather )
  • 7. Pathogenesis & Pathology Pathogenesis – Immune complex mediated injury Alternate pathway activation Pathology - • Light microscopy – All glomeruli enlarged, Bloodless Mesanchymal cell proliferation Mesanchymal matrix proliferation PMN cell infiltration Crescent formation • Immunofluorescence microscopy – Lumpy-bumpy deposits of Ig and complements in BM & mesangium • Electrone microscopy – Electrone dense deposits or ‘humps’ on epithelial side of BM
  • 8. Clinical manifestations • Age – 5-12 yrs, uncommon before 3 yrs • Pharyngitis – 1-2 wks • Pyoderma – 3-6 wks • Asymptomatic microscopic hematuria, normal RFT to ARF • Edema, HT, oliguria, encephalopathy, CHF,nephrotic syndrome(10 20%) • Malaise, lethargy, abdominal pain, fever, acute subglottic edema, air way obstruction • Acute phase – 6-8 wks • Proteinuria and HT – 4-6 wks • Microscopic hematuria – 1-2 yrs
  • 9. Diagnosis Normal urine examination - No cast,except hyaline 1/hpf RBC – 1-2/hpf WBC – Male – 0-3/hpf Female -0-5/ hpf Epithelial cell few Bacteria – no organism/oif : unspun <20/hpf : spun Urine in AGN – RBC, RBC cast, proteinuria, PMN cells
  • 10. Diagnosis Blood – Normochromic anemia C3 level decreased ASLO – throat infections 2-5 yrs – 120-160 todds unit 6-9 yrs – 240 todds unit 10-12 – 320 todds unit > 13 yrs - 320 todds unit DNase B – skin infection Positive throat culture
  • 11. Diagnosis Streptozyme test – ( SLO, DNase B, Hyaluronidase, Streptokinase, NADase ) Renal biopsy – - ARF - Nephrotic syndrome - Absence of evidence of streptococcal infection - Normal complement level - Hematuria, proteinuria and low C3 >2 months
  • 12. Complications • Hypertension • Encephalopathy • CHF • Hyperkalemia • Hyperphosphatemia • Hypocalcemeia • Acidosis • Seizures • Uremia
  • 13. Treatment & Prognosis Treatment – Diet – Protein, sodium, potassium restricted Penicillin – 10 days Fluid restriction Diuretic Antihypertensive – CCB, Vasodilators, ACE inhibitors Prognosis – 95% complete recovery Recurrences are extremely rare
  • 14. Membranous Glomerulonephritis Etiology – SLE, chronic ITP, neuroblastoma, gonadoblastoma, syphilis,HBV infection, gold .penicillamine. Pathology – LMC – Diffuse thickening of GBM without significant proliferative changes. Deposition of membrane-like material by visceral epithelial cells Resembles ‘spikes’ on epithelial side of GBM. IFM – Granular deposits of IgG & C3 on epithelial side. EMC – Linear staining of IgG,IgA,C3 on tubular BM
  • 15. Clinical features – Most common in 2nd decade, nephrotic syndrome (2-6%), microscopic or gross hematuria, HT (20%). Diagnosis – C3 normal except SLE. Kidney biopsy – Nephrotic syndrome > 10yrs, Unexplained hematuria and proteinuria, increased risk of RVT. Treatment – Salt restriction, diuretic, prednisone+cyclophosphamide or chlorombucil Prognosis – CRF (20%), Active disease (40%) Membranous Glomerulonephritis
  • 16. Pathogenesis – C3 nephritic factors- activates alternative complement pathway Pathology – Type 1 – LMC - most common - Accentuation of lobular pattern - Generalized increased in mesangial cells & matrix - GBM splitting from interposition of mesangial cytoplasm & matrix b/w - endothelial cell and GBM - Formation of crescent IFMC – C3 & lesser amount of Ig in mesangium and along the peripheral capillary in a lobular pattern EMC – immune complex-like deposits in mesangial and subendothelial regions Type 2 – -less common, irregular ribbon-like thickening of GBM, crescent common, splitting rare. Membranoproliferative (mesangiocapillary) Glomerulonephritis (MPGN)
  • 17. Type 3 – Similar to type 1 in LMC & IFMC EMC – subepithelial and subendothelial Clinical features – Most common in 3rd decade, nephrotic syndrome, acute nephritic syndrome, RFT-normal to decreased, HT. Diagnosis – C3 decreased Renal biopsy – Nephrotic syndrome >10yrs, significant proteinuria with microscopic hematuria, decreased C3 >8wks. Treatment – Long term prednisone EOD Prognosis – ESRD (50%), type 2 worst prognosis, recurrent MPGN in kidney transplant, type 1(13%), type 2(90%) Membranoproliferative (mesangiocapillary) Glomerulonephritis (MPGN)
  • 18. SLE Nephritis Immune complex mediated injury, both T cell and B cell function alteration WHO classification – Type 1 – No abnormality Type 2 – Mesangial lupus nephritis 2a – mild deposit 2b – moderate deposit Type 3 – FSGN, subendothelial & mesangeal deposits, necrosis,crescent, sclerosis. Type 4 – Most common, most severe, diffuse proliferative lupus nephritis, subendothelial & mesangeal deposits, ‘wire loop lesions’ necrosis,crescent, sclerosis. Type 5 – Membranuous lupus nephritis, least common, resembles membranuous GN except mild to moderate mesangial proliferation, decreased C3 level.
  • 19. Clinical features – • Adolescence , female • All type 2 and some type 3 – hematuria, normal RFT, proteinuria <1g/day. • Some type 3 and all type 4 - hematuria, decreased RFT, proteinuria, nephrotic syndrome, ARF • Type 5 – nephrotic syndrome. Diagnosis – ANA, antibody to double stranded DNA, C3-C4 level decreased. Treatment – • All patients – prednisone 4-6 months • Type 3 & 4 – 6 monthly IV cyclophosphamide 500-1000mg/m2 followed by every 3 monthly dosing for 18-36 months. • Type 1 & 2 – azathioprine single dose daily, 1.5-2mg/kg/day Prognosis – Highest risk of progression in type 4 SLE Nephritis
  • 20. Henoch-schonlein purpura nephritis Pathology and pathogenesis – • Immune complexes containing IgA1 deposition within the capillaries of the skin, intestine and glomerulus. • Crescent formation more common and extensive Clinical manifestations – • 1-3 wks after URI • Gross hematuria (20-30%), • Isolated microscopic hematuria • Hematuria and proteinuria • Acute nephritic syndrome • Nephrotic syndrome • Renal insufficiency • Ureteritis Prognosis – Best - Isolated microscopic hematuria Poor - Acute nephritic syndrome, Nephrotic syndrome
  • 21. Rapidly Progressive (crescentic) GN Classification – 1. Immune comlex mediated GN – PSGN, MPGN, lupus, HSP and IgA nephritis. 2. Anti-GBM mediated GN – Goodpasture disease. 3. ANCA mediated GN –Microscopic PAN, Wegner granulomatosis. Crescent formation. Goodpasture disease – -Pulmonary hemorrage and GN with antibody against type 4 collagen of alveolar BM and GBM. -Continuous linear pattern of IgG along the GBM. Diagnosis – ANA, Normal C3, anti DNase B, ANCA to MPO or proteinase-3 Treatment - According to cause