Glomerulonephritis
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Basics
Description
- Glomerulonephritis presents with the nephritic syndrome: hematuria with RBC casts, hypertension, variable azotemia, and edema. Proteinuria and oliguria may also be present.
- Acute glomerulonephritis is associated with inflammation and cell proliferation in the glomerular tuft. It may be rapidly progressive.
- Chronic glomerulonephritis indicates permanent damage has occurred.
Epidemiology
- Postinfectious glomerulonephritis can occur after any infection; ~80% of cases are secondary to a streptococcal infection.
- Acute poststreptococcal glomerulonephritis (APSGN) can occur in anyone >2 years but is most frequently found in boys 5 to 15 years old. It can be sporadic or epidemic.
- Incidence of APSGN has declined over the last 2 decades.
- Chronic glomerulonephritis occurs more often at the end of the 1st decade of life and in adults.
Risk Factors
Exposure to nephritogenic streptococci
Genetics
Genetic predisposition: hereditary nephritis (e.g., X-linked Alport syndrome); C3 glomerulopathy, atypical HUS (complement regulation disorders)
Etiology
Can be categorized based on serum complement levels and presence of renal-limited versus systemic disease
- Low serum complement level: systemic diseases
- Vasculitis and autoimmune disease (e.g., systemic lupus erythematosus [SLE])
- Subacute bacterial endocarditis (SBE)
- Shunt nephritis
- Cryoglobulinemia
- Low serum complement level: renal diseases
- APSGN
- Membranoproliferative glomerulonephritis, C3 glomerulopathy
- Normal serum complement level: systemic diseases
- Microscopic polyangiitis (MPA)
- Granulomatosis with polyangiitis (GPA)
- Henoch-Schönlein purpura (HSP)
- Hypersensitivity vasculitis
- Anti-GBM disease (Goodpasture syndrome)
- Normal serum complement level: renal diseases
- IgA nephropathy
- Idiopathic rapidly progressive glomerulonephritis
- Pauci-immune glomerulonephritis (renal-limited ANCA vasculitis)
- Immune-complex disease
-- To view the remaining sections of this topic, please log in or purchase a subscription --
Basics
Description
- Glomerulonephritis presents with the nephritic syndrome: hematuria with RBC casts, hypertension, variable azotemia, and edema. Proteinuria and oliguria may also be present.
- Acute glomerulonephritis is associated with inflammation and cell proliferation in the glomerular tuft. It may be rapidly progressive.
- Chronic glomerulonephritis indicates permanent damage has occurred.
Epidemiology
- Postinfectious glomerulonephritis can occur after any infection; ~80% of cases are secondary to a streptococcal infection.
- Acute poststreptococcal glomerulonephritis (APSGN) can occur in anyone >2 years but is most frequently found in boys 5 to 15 years old. It can be sporadic or epidemic.
- Incidence of APSGN has declined over the last 2 decades.
- Chronic glomerulonephritis occurs more often at the end of the 1st decade of life and in adults.
Risk Factors
Exposure to nephritogenic streptococci
Genetics
Genetic predisposition: hereditary nephritis (e.g., X-linked Alport syndrome); C3 glomerulopathy, atypical HUS (complement regulation disorders)
Etiology
Can be categorized based on serum complement levels and presence of renal-limited versus systemic disease
- Low serum complement level: systemic diseases
- Vasculitis and autoimmune disease (e.g., systemic lupus erythematosus [SLE])
- Subacute bacterial endocarditis (SBE)
- Shunt nephritis
- Cryoglobulinemia
- Low serum complement level: renal diseases
- APSGN
- Membranoproliferative glomerulonephritis, C3 glomerulopathy
- Normal serum complement level: systemic diseases
- Microscopic polyangiitis (MPA)
- Granulomatosis with polyangiitis (GPA)
- Henoch-Schönlein purpura (HSP)
- Hypersensitivity vasculitis
- Anti-GBM disease (Goodpasture syndrome)
- Normal serum complement level: renal diseases
- IgA nephropathy
- Idiopathic rapidly progressive glomerulonephritis
- Pauci-immune glomerulonephritis (renal-limited ANCA vasculitis)
- Immune-complex disease
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