Types of Glomerulonephritis
Postinfectious acute glomerulonephritis is due to immune attack about the infecting organism in which there's cross-reactivity between an antigen from the infecting organism (e.
g.
, of group A beta-hemolytic streptococci) plus a host antigen.
The result is deposition of immune complexes and complement in glomerular capillaries and the mesangium.
Signs or symptoms and signs typically occur 7-10 days after onset of the acute pharyngeal or cutaneous infection and resolve more than weeks right after treatment from the infection.
Rapidly Progressive Glomerulonephritis: Immunofluorescence scientific studies permit distribution into subgroups correlating with other features from the disease.
Linear immunoglobulin deposits recommend antiglomerular basement membrane (GBM) antibody, which might coincident with pulmonary hemorrhage, characteristic of Goodpasture's syndrome.
Granular immunoglobulin deposits are suggestive of immune complexes due to an underlying systemic disease, such as IgA nephropathy, postinfectious glomerulonephritis, lupus nephritis, or mixed cryoglobulinemia.
Few or no immune deposits (pauci-immune) are frequently coincident with an autoantibody pattern (ANCA) common of Wegener's granulomatosis or microscopic polyangiitis.
ANCA-negative pauci-immune necrotizing glomerulonephritis is observed much less frequently but can also be a recognized clinical entity.
Immunofluorescence studies permit distribution into subgroups correlating with other functions of the disease.
From 5% to 20% of individuals have linear anti-GBM antibody deposits in glomeruli and a tendency to hemoptysis reminiscent of Goodpasture's syndrome.
Further, 30-40% have granular immunoglobulin deposits and an autoantibody pattern typical of Wegener's granulomatosis (antineutrophil cytoplasmic antibody).
The latter patients are usually older, with more systemic constitutional signs or symptoms.
Chronic Glomerulonephritis: Some patients with acute glomerulonephritis create chronic renal failure slowly over a period of 5-20 years.
Cellular proliferation, in either the mesangium or the capillary, is a pathologic structural hallmark in some of these cases, whereas other people are notable for obliteration of glomeruli (sclerosing chronic glomerulonephritis, which contains both focal and diffuse subsets), and yet other people display irregular subepithelial proteinaceous deposits with uniform involvement of individual glomeruli (membranous glomerulonephritis).
g.
, of group A beta-hemolytic streptococci) plus a host antigen.
The result is deposition of immune complexes and complement in glomerular capillaries and the mesangium.
Signs or symptoms and signs typically occur 7-10 days after onset of the acute pharyngeal or cutaneous infection and resolve more than weeks right after treatment from the infection.
Rapidly Progressive Glomerulonephritis: Immunofluorescence scientific studies permit distribution into subgroups correlating with other features from the disease.
Linear immunoglobulin deposits recommend antiglomerular basement membrane (GBM) antibody, which might coincident with pulmonary hemorrhage, characteristic of Goodpasture's syndrome.
Granular immunoglobulin deposits are suggestive of immune complexes due to an underlying systemic disease, such as IgA nephropathy, postinfectious glomerulonephritis, lupus nephritis, or mixed cryoglobulinemia.
Few or no immune deposits (pauci-immune) are frequently coincident with an autoantibody pattern (ANCA) common of Wegener's granulomatosis or microscopic polyangiitis.
ANCA-negative pauci-immune necrotizing glomerulonephritis is observed much less frequently but can also be a recognized clinical entity.
Immunofluorescence studies permit distribution into subgroups correlating with other functions of the disease.
From 5% to 20% of individuals have linear anti-GBM antibody deposits in glomeruli and a tendency to hemoptysis reminiscent of Goodpasture's syndrome.
Further, 30-40% have granular immunoglobulin deposits and an autoantibody pattern typical of Wegener's granulomatosis (antineutrophil cytoplasmic antibody).
The latter patients are usually older, with more systemic constitutional signs or symptoms.
Chronic Glomerulonephritis: Some patients with acute glomerulonephritis create chronic renal failure slowly over a period of 5-20 years.
Cellular proliferation, in either the mesangium or the capillary, is a pathologic structural hallmark in some of these cases, whereas other people are notable for obliteration of glomeruli (sclerosing chronic glomerulonephritis, which contains both focal and diffuse subsets), and yet other people display irregular subepithelial proteinaceous deposits with uniform involvement of individual glomeruli (membranous glomerulonephritis).
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