glomrulonephritis

Glomerulionephritis
Acute G.N.
- chronic GNTypes of GN1
- associated with Nephrotic Syndrome
1- Membranous GN( 5% child., 30% adult)

2-MCD (65% child, 10% adult)3- FSGS (10% child, 35% adult)
4-membranoproliferative GN (10% child, 10% adult) 
5- IgA nephropathy (10% child, 15% adult)
2- associated with Nephritic Syndrome1-
Acute postinfectious (poststreptococcal) GN
2- IgA nephropathy (Berger Disease)
3- Rapidly progressive (crescentic) GN
Nephrotic Syndrome
Refers to a clinical complex that include the following:
1- massive protienuria with daily protein loss in the urine of 3.5 gm.
2- hpoalbuminemia, plasma albumin < 3 gm/dl
3- generalized edema
4- hyperlipidemia
Pathogenesis :
1- A derangement in the capillary walls of the glomeruli increased permeability to plasma protein serum albumin is
decreased plasma colloid osmotic pressure primary retention of salt and water by the kidney escape fluid from vascular tree into the tissue.
MININMAL – Change Disease(Lipoid Nephrosis):
Pathogenesis:
T-cell derived factor that cause podocyte damage and effacement of foot processes
Clinical pictures:
Insidious development of the nephritic syndrome, protein loss mainly albumin
Prognosis good (>90% respond to short course of corticosteroid therapy
FSGS(focal segmental glomerulosclerosis:
Pathogenesis:
Injury to the podocytes is thought to represent the initiating event of FSGS
Morphology:
1- focal: the disease affects only some of the glomeruli,
the lesion occurring in some tufts within a glomerulus and sparing of the others (segmental)
2-The affected glomeruli exhibit increased mesangial matrix, obliterated capillary lumens and deposition of hyaline masses and lipid droplets 
Clinically:
Primary FSGS accounts 20-30 % of nephrotic syndrome
The patient responses to corticosteroid therapy are usually poor
50% suffer from renal failure within 10 years.
Membranous glomerulonephritis:
Pathogenesis:
Is a form of chronic immune complex nephritis, exogenous Ag like hepatitis B or endogenous (DNA in SLE
so it is considered as autoimmune disease caused by Abs to renal auto antigens.
Morphology:
The basic change is diffuse thickening of the GBM, with further progression , the glomeruli can become sclerosed
Clinical course:
The MGN either idiopathic (primary) in 80%
Secondary include :
1- infection(syphilis, malaria, hepatitis B)
2- malignant tumor ca. of lung, colon and melanoma
3- SLE
4- drugs : pencillamine , captopril
Insidious development of the nephritic syndrome , non selective protienuria , not response to corticosteroid therapy, 40% progressive to renal failure.