Primary Glomerular Disease SHOKOUFEH SAVAJ ASSOCIATE PROFESSOR OF MEDICINE FIROOZGAR HOSPITAL,IUMS.
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Transcript of Primary Glomerular Disease SHOKOUFEH SAVAJ ASSOCIATE PROFESSOR OF MEDICINE FIROOZGAR HOSPITAL,IUMS.
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Primary Glomerular DiseaseSHOKOUFEH SAVAJ
ASSOCIATE PROFESSOR OF MEDICINE
FIROOZGAR HOSPITAL ,IUMS
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• Albumin has a negative charge with a physical radius of 3.6 nm.• GBM and slit-pore membranes have a radius of 4 nm• Albumin is reabsorbed in proximal tubule• Normal urine albumin :8-10 mg/d.
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Glomerulonephritis :Glomerular Injury with
Inflammation ( Leukocyte infiltration ,
Complement activation & Antibody deposition )
Primary :Limited to kidney
Secondary : Part of Systemic disorder
Acute :Injury occur in days or weeks
Subacute or rapidly progressive : in
Weeks or months
Chronic : Injury in years
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Nephrotic syndrome : > 3.5gr proteinuria in 24 hours/1.73 M2
Nephritic syndrome : proteinuria ,decrease in GFR,
hypertension,hematuria and cellular casts
Proliferative : Increase in glomerular cell number
( intracapillary & Extracapillary )
Sclerosis:Deposition of homogenous non fibrillar material
Fibrosis:Deposition of collagen type I and III
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Nephrotic Syndrome
Proteinuria
Hypoalbuminemia
Hyperlipidemia
hypercoagulable state
Hypertension
Decrease in GFR
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Minimal Change Disease
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Pathogenesis
T cell dysfunction
Permeability Factor : immune origin (IL13)
Genetic ??
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70–90% in childhood &10–15% of nephrotic syndrome in adults.
Acellular urinary sediment
Hypertension (30% in children, 50% in adults)
Microscopic hematuria (20% in children, 33% in adults)
Atopy or allergic symptoms (40% in children, 30% in adults)
Decreased renal function (<5% in children, 30% in adults).
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Causes of minimal change disease Allergy : bee stings, house dust, pollens..
Cancer :Lymphoma ,leukemia
Infection : syphilis, tuberculosis, HIV, Hepatitis C virus, and
Echinococcus
Drugs : NSAID, Lithium, ampicillin,rifampin pamidronate
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Membranous Nephropathy
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C5-9
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Neutral endopeptidase expressed by podocytes
Hepatitis antigens B/C
Helicobacterpylori antigens
Tumor antigens.
Autoantibodies against the M-type phospholipase A2 receptor
(PLA2R) circulate and bind to a conformational epitope present in
the receptor on human podocytes
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Primary/idiopathic membranous glomerulonephritis
Secondary membranous glomerulonephritis
Infection: Hepatitis B and C, syphilis, malaria, schistosomiasis,
leprosy, filariasis
Cancer: Breast, colon, lung, stomach, kidney, esophagus,
neuroblastoma
Drugs: gold, mercury, penicillamine, nonsteroidal anti-inflammatory
agents, probenecid
Autoimmune diseases: systemic lupus erythematosus, rheumatoid
arthritis, primary biliary cirrhosis, dermatitis herpetiformis, bullous
pemphigoid, myasthenia gravis, Sjögren's syndrome, Hashimoto's
thyroiditis
Other systemic diseases: Fanconi's syndrome, sickle cell anemia,
diabetes, Crohn's disease, sarcoidosis, Guillain-Barré syndrome,
Weber-Christian disease, angiofollicular lymph node hyperplasia
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30% of nephrotic syndrome Adult
The male to female ratio :2 to 1
80% nephrotic syndrome
Microscopic hematuria in 50%
Highest incidence of renal vein
thrombosis
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Focal segmental Glomerulosclerosis
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Primary focal segmental glomerulosclerosis
Secondary focal segmental glomerulosclerosis
Viruses: HIV/Hepatitis B/Parvovirus
Hypertensive nephropathy
Reflux nephropathy
Cholesterol emboli
Drugs: Heroin/analgesics/pamidronate
Oligomeganephronia
Renal dysgenesis
Alport's syndrome
Sickle cell disease
Lymphoma
Radiation nephritis
Familial podocytopathies
NPHS1 mutation/nephrin
NPHS2 mutation/podocin
TRPC6 mutation/cation channel
ACTN4 mutation/actinin
-Galactosidase A
deficiency/Fabry's disease
N-acetylneuraminic acid hydrolase
eficiency/nephrosialidosis
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Collapsing glomerulosclerosis
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Clinical Presentation
Hematuria
Hypertension
A level of proteinuria
Renal insufficiency
African-American raceare associated with a poor outcome, with
50% of patients reaching renal failure in 6–8 years
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Alport Syndrome
The most common hereditary nephrits
Genetic defect of α5 chain of type IV collagen
Gene on long arm of chromosome X
Males presented with :
Hematuria, Proteinuria, Progressive renal
insufficiency
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Immune Mechanisms of Glomerular Injury
Non inflammatory
• Podocyte
Inflammatory
• Neutrophil, Monocyte
• Proliferating glomerular cells
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Inflammatory Mechanisms of
Immune Glomerular Injury
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Antibody – Mediated Injury
1- Reactivity of circulatory autoantibodies with
intrinsic autoantigens
2-Insitu formation of immune Complex
( with extrinsic antigens )
3- Intraglomerular trapping of immune complex
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Generation of nephritogenic Antibodies :
1. Similarity with foreign antigen
2. Expression MHC II ( which were
invisible)
3. Problem in tolerance
Deposition of Nephritogenic antibodies within Glomerus
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Site of antibody deposition
Size
Charge
Quantity
Site of antigen
Local hemodynamics factor
Problem in clearance mechanisms for immune complexes
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Mechamism of glomerular Damage
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Post Streptococcal Glomerulonephritis
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Pathogenesis
Children 4-12 Decreased incidence rate Throat infections infection:1-3 weeks after
with M types of streptococci (nephritogenic strains) antedate glomerular disease and M types 1, 2, 4, 3, 25, 49, and 12 with pharyngitis
Skin: 2-6 weeks after infection ; M types 47, 49, 55, 2, 60, and 57 are seen following impetigo .
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IgA nephropathy
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Pathogeneis
Immune complex mediated GN with diffuse
mesangial IgA deposit
Abnormal IgA production
Abnormal IgA clearance (liver ,mesangial )
O-glycosylation of hinge region of IgA
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Clinical Presentation
Microscopic hematuria
Subnephrotic proteinuria
Nephrotic syndrome (rare)
Gross hematuria
Acute renal failure
Rapidly progressive GN
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Membranoproliferative GN type I
lobular appearance of the glomerular tuft with focal areas of increased glomerular cellularity (large arrows), mesangial expansion (*), narrowing of the capillary lumens, and diffuse thickening of the glomerular capillary walls
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Electron Microscopy In MPGN I
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Membranoproliferative Type II
Basement membrane thickening, double contour, mesangial
interposition
C3 deposition on capillary wall and
mesangium
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Electron microscopy in MPGN II DDD
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Pathogensis
Type I MPGN : secondary to glomerular deposition of
circulating immune complexes or their in situ formation
Types II and III MPGN :"nephritic factors," (autoantibodies
that stabilize C3 convertase).
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Clinical Findings
Proteinuria, hematuria, and pyuria (30%)
Systemic symptoms of fatigue and malaise
An acute nephritic picture with RPGN and a
Speedy deterioration in renal function in up to
25% of patients.
Low serum C3 levels are common
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Prognosis
50% with MPGN develop ESRD in10 years after
diagnosis,
90% have renal insufficiency after 20 years.
Nephrotic syndrome, hypertension, and renal
insufficiency all predict poor
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Rapidly Progressive Glomerulonephriris
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