Glomerular Disease 3u6b58
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THE KIDNEY
GLOMERULAR DISEASES
Gopal
Dr.Venu 22/10/08
In primary glomerulonephritis, the kidney is the principal organ involved In secondary Glomerular diseases, the kidney is one of many organ systems damaged by a systemic disease. The chronic glomerulonephritis is the most common cause of chronic renal failure.
Acute diffuse proliferative glomerulonephritis
Post-streptococcal Non- Post streptococcal.
Rapidly progressive [ crescentric] glomerulonephritis. Membranous glomerulopathy. Minimal change disease. Focal segmental glomerulosclerosis Membrano - Proliferative glomerulonephritis Ig A nephropathy. Chronic glomerulonephritis.
SYSTEMIC DISEASE WITH GLOMERULAR INVOLVEMENT
Systemic lupus erythematosus. Diabetes mellitus Amyloidosis. Good pasture syndrome. Microscopic polyarteritis/Polyangitis. Wegener’s granulomatosis. Henoch-scholein purpura. Bacterial endocarditis.
HEREDITARY DISORDERS
Alport syndrome. Thin basement membrane disease. Fabry disease.
Pathogenesis of Glomerular Injury:
The immune mechanism predominate in Glomerular Injury.
IMMUNE MECHANISM The glomerular deposition of
antigen –antibody complexes is a major mechanism of glomerular injury. The antibodies can be directed against injury. Fixed intrinsic antigens .
Anti- glomerular basement membrane nephritis autoimmune disease in which antibodies are towards non- collagenous domain of the alpha3 chain of GBM type IV
This yields a linear immunofluroscence staining pattern. HEYMANN’S NEPHRITIS OF RATS: The antibodies react with a large 330KD megalin protein antigen expressed on visceral epithelial cells The resultant lesion exhibit sub epithelial deposits of antigen – antibody complexes resembling those in human membraneous glomerulonephritis. planted circulating exogenous [e.g:- infectious agent ] or endogenous
[ e.g:- DNA] antigens can occur.
CIRCULATING IMMUNE COMPLEXES Antigens may be endogenous
[e.g.:[e.g:-
thyroglobin] or exogenous infectious agent] Complexes are usually deposited subendothelially/ in the mesangium and yield a granular immunofluroscence pattern. Cytotoxic antibodies. Cell-mediated immune injury. Activation of alternative complement pathway.
Acute Proliferative [Post Streptococcal, Post-Infectious] Glomerulonephritis : Characterized by acute nephritic syndrome 1-4 weeks after streptococcal pharyngitis infection. Antibody mediated disease. Types 12,4,1 strains of group A BHemolytic streptococci are nephrotogenic .
Biopsy specimen show diffuse Glomerulonephritis and global hyper cellularity due to endothelial proliferation, mesangial and epithelial cell infiltration. Immunofluroscence show granular I gG, IgM and C3 deposition and electron microscopy show subepithelial hump like structures. The serum anti-streptococcal antibody levels are elevated and decrease of C3 serum complements level.
Characterised by cellular accumulation in bowman space in the form of crescents accompanied by a rapidly, Progressive decline in renal function.
The RPGN is divided into 3 broad groups.
Type I RPGN is an anti-GBM disease is Characterised by linear IgG deposits in the GBM.
In some,anti-GBM antibodies react pulmonary alveolar basement membraneous to produce pulmonary haemorrhages
The good pasture antigen is a peptide with in the noncollagenous domain of the 3 chain of type IV collagen. Type II RPGN is an immune-complex mediated disease: The immunofluroscence shows characterstic [lumpy bumpy] granular staining. Type III RPGN:- also called Pauci -immune Antineutrophilic cytoplasmic antibodies(ANCA) associated. Wegener granulomatosis. Microscopic polyarteritis nodosa.
MORPHOLOG Y
There is a distinctive crescents formed by parietal cell proliferation and monocyte and macrophage migration into bowman’s space. The electron microscopy discloses subepithelial deposits with rupture in GBM
Haematuria, moderate proteinuria and variable hypertension and oedema. Good pasture syndrome show recurrent haemoptysis. Serum analyses for anti-GBM antibodies and ANCA are helpful in diagnosis.
It is the major cause of nephrotic syndrome in adults. It show diffuse glomerular capillary wall thickening due to deposition of immunoglobulin containing electron dense material along the subepithelial side of G.B.M The disease is idiopathic in 85% of patients. The remaining 15% of membraneous G.N is associated with underlying malignant tumors SLE exposure to gold ,mercury, drug infections.
MORPHOLOG Y
There is diffuse thickening of the capillary wall, hence the term membraneous . Immunofluroscence there is diffuse granular staining pattern, there are subepithelial GBM deposits, which gets incorporated into GBM and assume intramembraneous location.
CLINICAL FEATURES:
This usually starts with the insidious onset of nephrotic syndrome. 40% of cases progress to renal insufficiency over an unpredictable time span of 2 to 20 years.
GLOMERULAR DISEASES
Gopal
Dr.Venu 22/10/08
In primary glomerulonephritis, the kidney is the principal organ involved In secondary Glomerular diseases, the kidney is one of many organ systems damaged by a systemic disease. The chronic glomerulonephritis is the most common cause of chronic renal failure.
Acute diffuse proliferative glomerulonephritis
Post-streptococcal Non- Post streptococcal.
Rapidly progressive [ crescentric] glomerulonephritis. Membranous glomerulopathy. Minimal change disease. Focal segmental glomerulosclerosis Membrano - Proliferative glomerulonephritis Ig A nephropathy. Chronic glomerulonephritis.
SYSTEMIC DISEASE WITH GLOMERULAR INVOLVEMENT
Systemic lupus erythematosus. Diabetes mellitus Amyloidosis. Good pasture syndrome. Microscopic polyarteritis/Polyangitis. Wegener’s granulomatosis. Henoch-scholein purpura. Bacterial endocarditis.
HEREDITARY DISORDERS
Alport syndrome. Thin basement membrane disease. Fabry disease.
Pathogenesis of Glomerular Injury:
The immune mechanism predominate in Glomerular Injury.
IMMUNE MECHANISM The glomerular deposition of
antigen –antibody complexes is a major mechanism of glomerular injury. The antibodies can be directed against injury. Fixed intrinsic antigens .
Anti- glomerular basement membrane nephritis autoimmune disease in which antibodies are towards non- collagenous domain of the alpha3 chain of GBM type IV
This yields a linear immunofluroscence staining pattern. HEYMANN’S NEPHRITIS OF RATS: The antibodies react with a large 330KD megalin protein antigen expressed on visceral epithelial cells The resultant lesion exhibit sub epithelial deposits of antigen – antibody complexes resembling those in human membraneous glomerulonephritis. planted circulating exogenous [e.g:- infectious agent ] or endogenous
[ e.g:- DNA] antigens can occur.
CIRCULATING IMMUNE COMPLEXES Antigens may be endogenous
[e.g.:[e.g:-
thyroglobin] or exogenous infectious agent] Complexes are usually deposited subendothelially/ in the mesangium and yield a granular immunofluroscence pattern. Cytotoxic antibodies. Cell-mediated immune injury. Activation of alternative complement pathway.
Acute Proliferative [Post Streptococcal, Post-Infectious] Glomerulonephritis : Characterized by acute nephritic syndrome 1-4 weeks after streptococcal pharyngitis infection. Antibody mediated disease. Types 12,4,1 strains of group A BHemolytic streptococci are nephrotogenic .
Biopsy specimen show diffuse Glomerulonephritis and global hyper cellularity due to endothelial proliferation, mesangial and epithelial cell infiltration. Immunofluroscence show granular I gG, IgM and C3 deposition and electron microscopy show subepithelial hump like structures. The serum anti-streptococcal antibody levels are elevated and decrease of C3 serum complements level.
Characterised by cellular accumulation in bowman space in the form of crescents accompanied by a rapidly, Progressive decline in renal function.
The RPGN is divided into 3 broad groups.
Type I RPGN is an anti-GBM disease is Characterised by linear IgG deposits in the GBM.
In some,anti-GBM antibodies react pulmonary alveolar basement membraneous to produce pulmonary haemorrhages
The good pasture antigen is a peptide with in the noncollagenous domain of the 3 chain of type IV collagen. Type II RPGN is an immune-complex mediated disease: The immunofluroscence shows characterstic [lumpy bumpy] granular staining. Type III RPGN:- also called Pauci -immune Antineutrophilic cytoplasmic antibodies(ANCA) associated. Wegener granulomatosis. Microscopic polyarteritis nodosa.
MORPHOLOG Y
There is a distinctive crescents formed by parietal cell proliferation and monocyte and macrophage migration into bowman’s space. The electron microscopy discloses subepithelial deposits with rupture in GBM
Haematuria, moderate proteinuria and variable hypertension and oedema. Good pasture syndrome show recurrent haemoptysis. Serum analyses for anti-GBM antibodies and ANCA are helpful in diagnosis.
It is the major cause of nephrotic syndrome in adults. It show diffuse glomerular capillary wall thickening due to deposition of immunoglobulin containing electron dense material along the subepithelial side of G.B.M The disease is idiopathic in 85% of patients. The remaining 15% of membraneous G.N is associated with underlying malignant tumors SLE exposure to gold ,mercury, drug infections.
MORPHOLOG Y
There is diffuse thickening of the capillary wall, hence the term membraneous . Immunofluroscence there is diffuse granular staining pattern, there are subepithelial GBM deposits, which gets incorporated into GBM and assume intramembraneous location.
CLINICAL FEATURES:
This usually starts with the insidious onset of nephrotic syndrome. 40% of cases progress to renal insufficiency over an unpredictable time span of 2 to 20 years.
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