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Glomerulonephritis: Types, Associations And Causes

Glomerulonephritis: Tipe (Jenis), Hubungan dan Penyebab

Histology Immune deposits Pathogenesis Association Clinical features
Minimal change Normal, except on electron microscopy, where fusion of podocyte foot processes is seen (occurs in many types of proteinuria) None Unknown Atopy, HLA-DR7 Drugs Acute and often severe nephrotic syndrome
Good response to corticosteroids
Dominant cause of idiopathic nephrotic syndrome in childhood
Focal segmental glomerulosclerosis (FSGS) Segmental scars in some glomeruli
No acute inflammation Podocyte foot process fusion seen in primary FSGS with nephrotic syndrome
Non-specific trapping in focal scars Unknown; in some, circulating factors increase glomerular permeability Injury to podocytes may be a common feature Healing of previous localglomerular injury HIV infection, heroin misuse, morbid obesity Primary FSGS presents as idiopathic nephrotic syndrome but is less responsive to treatment than minimal change; may progress to renal impairment, can recur after transplantation
Secondary FSGS presents with variable proteinuria and outcome
Focal segmental (necrotising) glomerulonephritis Segmental inflammation and/or necrosis in some glomeruli
May be crescent formation
Variable according to cause, but typically negative (or 'pauci-immune') Small-vessel vasculitis Primary or secondary small-vessel vasculitis Usually implies presence of systemic disease, and responds to treatment with corticosteroids and cytotoxic agents Check ANCA, ANA
Membranous nephropathy Thickening of GBM Progressing to increased matrix deposition and glomerulosclerosis Granular subepithelial IgG Antibodies to a podocyte surface antigen, with complement-dependent podocyte injury (presumed from animal model) HLA-DR3 (for idiopathic)
Heavy metals
Hepatitis B virus
Usually idiopathic; common cause of adult idiopathic nephrotic syndrome
One-third progress; may respond to chlorambucil/prednisolone
Associated HLA class II allele varies in different populations
IgA nephropathy Increased mesangial matrix and cells
Focal segmental nephritis in acute disease
Mesangial IgA Unknown Usually idiopathic
Liver disease
Very common disease with range of presentations, but usually including haematuria and hypertension (see text)
Mesangiocapillary glomerulonephritis (MCGN) (= membranoproliferative glomerulonephritis, MPGN)
Type I Mesangial cells interpose between endothelium and GBM Subendothelial Deposition of circulating immune complexes or 'planted' antigens Bacterial infection
Hepatitis B virus
Cryoglobulin-aemia (± hepatitis C virus infection)
Usually proteinuria, may be haematuria
Most common pattern found in association with subacute bacterial infection
No proven treatments except where cause can be treated
Type II Mesangial cells interpose between endothelium and GBM Intramembranous dense deposits Associated withcomplement consumption caused by autoantibodies C3 nephritic factor and partial lipodystrophy Also known as dense deposit disease
Post-infection Diffuse (uniformly in all glomeruli) proliferation of endothelial and mesangial cells
Infiltration by neutrophils and macrophages
May be crescent formation
Subendothelial Immune response to streptococcal infection Cross-reactive epitopes or other explanation Streptococcal and other infections Now rare in developed countries
Presents with severe sodium and fluid retention, hypertension, haematuria, oliguria
Usually resolves spontaneously
Goodpasture's disease (anti-GBM disease) Usually crescentic nephritis Linear IgG along GBM Autoimmunity to α3 chain of type IV collagen HLA-DR15 (previously known as DR2) Associated with lung haemorrhage but either may occur alone
Treat with corticosteroids, cyclophosphamide and plasma exchange to remove circulating autoantibodies
Lupus nephritis Almost any histological type Always positive and often profuse
Pattern varies according to type
Some anti-DNA antibodies also bind to glomerular targets Complement deficiencies
Complement consumption
Very variable presentation, sometimes as renal disease alone without systemic features
Responds to cytotoxic therapy in addition to prednisolone

Davidson's Principles and Practice of Medicine 20th Edition (Churchill Livingstone) 2007

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