-podocytes defective
-Clinical features:
1.haematuria-rbc casts
2.hypertension
3.proteinuria<3.5g/24hr
4.Oliguria <400ml/day
5.uraemia
6.azotaemia
Diagnosis
.-Anti-streptolysin O titre/ASO titre(for post streptoccal infection only)
-renal biopsy
-focal--IgA nephropathy, Alport syndrome(hereditary nephritits, henoch scholein purpura, SLE,
-diffused
Causes:
1.Primary-minimal changes, RPGN, membranous GN,
-further divided into focal and diffused
-further divided into focal and diffused
2.Secondary--SLE, post streptococcal infection,
Proliferative basis:
Proliferative-thickening or thinning plus proliferation of mesangial cells.
- IgA nephropathy(upper GI and RS infection)-->IgA deposit and proliferation
-membrano-proliferative nephropathy..
Non Prolifrative -only thickenin and thinning
-minimal change-GN-podocyte abnormal in electron microscope, FSGN, membranous glomerulous nephritis
Pathology
After infection---Ag+Ab reaction--->immune complex--->lodged in glomerulus---->inflammation------->destruction BM
clinical features:
-haematuria--smoky brown urine, in severe case, blood
-oliguria<400ml/day
-hypertension
-oedema, pitting,--->generalised edema-->migratory edma
General features:
headache, fever, nausea,
signs of acute renal failure
Treatment.
antihypertensive
reduced salt intake
dialysis
corticosteroid
in certain case, penicillin prophylaxis
PATHOLOGY
antibodies against GBM or immune complex or the neutrophil are deposited in the bowman's space and rapidly deteriotes kidney function.
SIGNS
1. severe hameturia
2. RBC cast
3. Proteinuria(>3g/day)
4. odema
5.oligouria.
CLASSIFICATION(based on immunoflorescent pattern)
1. type 1(20%).. linear pattern
Ab against GBM esp collagen IV
eg. Good Pasture Syndrome
2. Type 2(25%).. granular pattern
Ab against immune complex deposition
eg. SLE, HSP, IgA nephropathy
3. Type 3(55%).. pauci immune
by neutrophil... no Ab
DIAGNOSIS
i. Renal biopsy
ii. Serum analysis..(anti GBM Ab, antinuclear Ab, ANCA)
TREATMENT
1. plasmapheresis
2. corticosteriod
3. cytotoxic
4. dialysis
5. transplant
Poststreptococcal Glomerulonrhritis
Pathology
After infection---Ag+Ab reaction--->immune complex--->lodged in glomerulus---->inflammation------->destruction BM
clinical features:
-haematuria--smoky brown urine, in severe case, blood
-oliguria<400ml/day
-hypertension
-oedema, pitting,--->generalised edema-->migratory edma
General features:
headache, fever, nausea,
signs of acute renal failure
Treatment.
antihypertensive
reduced salt intake
dialysis
corticosteroid
in certain case, penicillin prophylaxis
Rapidly Progressive Glomerulonephritis(creasent GN)
rapidly loss of kidney function(50% decline in GFR within 3 months with creasent seen in 50-75%)
antibodies against GBM or immune complex or the neutrophil are deposited in the bowman's space and rapidly deteriotes kidney function.
SIGNS
1. severe hameturia
2. RBC cast
3. Proteinuria(>3g/day)
4. odema
5.oligouria.
CLASSIFICATION(based on immunoflorescent pattern)
1. type 1(20%).. linear pattern
Ab against GBM esp collagen IV
eg. Good Pasture Syndrome
2. Type 2(25%).. granular pattern
Ab against immune complex deposition
eg. SLE, HSP, IgA nephropathy
3. Type 3(55%).. pauci immune
by neutrophil... no Ab
DIAGNOSIS
i. Renal biopsy
ii. Serum analysis..(anti GBM Ab, antinuclear Ab, ANCA)
TREATMENT
1. plasmapheresis
2. corticosteriod
3. cytotoxic
4. dialysis
5. transplant
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