Pathology of Glomerulonephritis by sammyc2007

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									“To be a great champion you must believe you are the best. If you’re not, pretend you are….!”
– Muhammad Ali

The only place success comes before work is in a dictionary…!

Pathology of Glomerulonephritis
Dr. Venkatesh Murthy Shashidhar Associate Professor of Pathology Fiji School of Medicine.

Anatomy-Kidney

Anatomy of Kidney

Anatomy of Kidney
Note the positions of

Glomerulus Loop of Henley PCT, DCT, CT

Cortex, Medulla, Pelvis.

↓GFR  Renin Angiotensin Blood Pressure

JGA

Ultrastructure – Glom. capillary

Filtration Membrane – Electron Micro.
Capillary Space

GBM Endothelium

Urinary Space

Podocyte

Glomerular Filtration:
Blood Cells Proteins
3.6nm/70,000MW

Glomerular Capillary Lumen

Collagen IV Laminin Fibronectin Entactin etc.

L.R.I L.D. L.R.E
+

GBM

Plasma Proteins FILTRATE

Foot Process Podocyte (Visceral epithelium)

Bowman’s Capsule Space

Filtration Membrane

1. Fenestrated Endothelium 2. Lamina Rara Interna 3. Lamina Rara Densa 4. Lamina Rara Externa 5. Podocyte Slit membrane

Capillary Lumen

Normal Kidney:

Normal Glomerulus (PAS)

“The worst times in your life may contain seeds of the best. When you can see crisis as an opportunity, your life becomes not only easier, but more satisfying.”
–Joe Kogel

Disorders of Kidney:
 Congenital
 Malformations, ectopic, cysts, dysplasia.

 Acquired
 Glomerular diseases

 Tubulointerstitial diseases,
 Renal calculi.  Neoplasms – carcinoma.

Glomerular diseases:
 Primary
 Acute diffuse post streptococcal
 Lipoid nephrosis or minimal change  IgA nephropathy

 Secondary
 SLE, Diabetes, Hypertension etc.

 Immune, Toxins, Metabolic

Immune Glomerulonephritis:
 In-Situ immune complex deposition
 Tissue antigens - Goodpasture anti GBM Ag
 Planted antigens - infections, toxins, drugs.

 Circulating immune complex deposition.
 Endogenous - DNA as in SLE  Exogenous - infections.

 Cell mediated Immune injury

Diffuse Proliferative GN:
 Post streptococcal* common – (even others)  Primary infection - Pharynx, skin, ear etc..  Kidney damage – 1-4 weeks after infection.  Malaise, fever, nausea, edema*, ↑ASO, ↓C3  Resolution in 6-8 weeks.

Immune Glomerulonephritis:
1. Antigen or Antibody - Immune reaction

2. Activation of complements, Neutrophils…
3. destruction of glomerular structure

4. Inflammation, exudation  swelling.
5. ↓ blood flow, GFR, -

6. Oliguria, Proteinuria, Hematuria, Hypertension.

Neutrophil Activity
 Proteases  Reactive oxygen metabolites  Arachidonic acid metabolites

Other Mediators
 Cytotoxic antibodies  Macrophages  Platelets  Resident glomerular cells  Fibrin related products

Clinical Syndromes:
 Nephritic syndrome.
 Oliguria, Haematuria, Proteinuria, Oedema.

 Nephrotic syndrome.
 Gross proteinuria, hyperlipidemia,

 Acute renal failure (RPGN).
 Oliguria, loss of Kidney function - within weeks

 Chronic renal failure.
 Over months and years - Uremia

Nephritic Syndromes :
 Diffuse Proliferative GN
 Post Streptococcal.

 Rapidly Progressive GN (or Crescentic)
 Post Streptococcal, Goodpasture’s,

 Focal Glomerulonephritis
 Primary: Bergers disease (IgA Nephritis)  Secondary IgA nephritis, Henoch Schonlein purpura, SBE, Coeliac Disease etc.

Post Streptococcal GN (Prol.GN):
 1-4 weeks following streptococcal infection by nephritogenic strains (time for Ab formation)  Immune mediated  Granular deposits of IgG,IgM & C3 in GBM, (subepithelial location common)  Humps in GBM on EM or IF Microscopy

•Normal •Post Strepto GN

•Inflammation •Proliferation •Swelling. •Narrow capillary •↓GFR-Renin-BP

Diffuse Proliferative GN:
 Enlarged hypercellular glomeruli.  Hyperplasia of epithelium & endothelium. Cell Swelling.  Inflammatory cells.  Collapsed capillaries. Obstruction to blood flow.

IF- Diffuse Proliferative GN

Pathogenesis of Diffuse PGN:
 Streptococcal infection – Antibody attack GBM - inflammation & proliferation.  Glomerular capillary obstruction:
 J.G.A stimulation – Renin – high blood pressure  Reduced filtration – raised blood urea  Fluid retention – Oedema

 Damage to GBM:
 Unselective proteinuria (form Pr. casts in tubule)
 Haematuria (form RBC casts in tubule)

Progression of DPGN:
Poststreptococcal DPGN
Complete Healing

Focal segmental glomerulo sclerosis

CGN

Tubulo – Interstitial Damage

Diseases of Kidney: summary
Glomerulonephritis Glomerular diseases
Destruction of glomeruli by immune or infections.

Acute tubular necrosis Tubular diseases
Necrosis of tubules by toxins or infections.

Pyelonephritis Interstitial disease Infections

Nephrosclerosis Vascular diseases ––
thickening of blood vessels Hypertension leading to micro infarctions.

Clinical Syndromes:Summary
Nephritic syndrome.
 Oliguria, Haematuria, Proteinuria, Oedema.

Nephrotic syndrome.
 Gross proteinuria, hyperlipidemia,

Acute renal failure
 Oliguria, loss of Kidney function - within weeks

Chronic renal failure.
 Over months and years - Uremia

"It is our attitude at the beginning of a difficult task which, more than anything else, will affect its successful outcome."
William James 1842-1910, Psychologist and Author

Urine Microscopy :
 Cells Casts Crystals.  Cells - epithelial, inflammatory, malignant.  Casts – Protein cast of nephron – DCT/CT
 Suggest Kidney pathology – not URT.  Protein, lipid, cells or mixed.

 Crystals suggest high concentration or altered solubility.

WBC in Urine :

Urine Oxalate Crystals:

Granular Cast:

Epithelial Casts in Urine:

WBC Cast Urine:

Formation of Casts:

Red cell Casts in Urine:

What is an RBC cast?

Nephrolithiasis: stones.

Urolithiasis Hydronephrosis:

"If you tell the truth, you have infinite power supporting you; but if not, you have infinite power against you."
--Charles Gordon

Minimal Change Disease:

Loss of Foot processes

Membranous GN :

Crescentic GN - (RPGN)

Crescentic GN - (Trichrome Stain)

Goodpasture Syndrome:

Membranous GN :

Chronic Glomerulonephritis:

Urolithiasis:

Ooouuuch…!


								
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