1. Acute poststreptococcal glomerulonephritis.
De ntion: Poststreptococcal (or postinfectious) glomerulonephritis (PSGN) refers to acute
glomerular in ammation that results from a preceding infection with nephritogenic strains of
streptococci. Although most commonly seen in children following group A streptococcal
tonsillopharyngitis, skin infections such as impetigo may trigger PSGN as well. Deposition of
immune complexes containing the streptococcal antigen within the glomerular basement
membrane results in complement activation and subsequent damage to the glomeruli.
Etiology:
- occurs ca. 10-30 days after an acute infection
- group A beta- hemolytic streptococci
- mouth and pharynx: tonsillitis, pharyngitis
- soft tissue infections: erysipelas ( bacterial infection of the upper dermis), impetigo
- osteomyelitis
- immune complex glomerulonephtritis can also manifest during an acute infection ( e.g. in
endocarditis or soft tissue abscesses)
Pathophysiology: Infection with nephritogenic strains of group A beta-hemolytic streptococci →
immune complexes containing the streptococcal antigen deposit within the glomerular basement
membrane (likely involves molecular mimicry) → complement activation → destruction of the
glomeruli → immune complex-mediated glomerulonephritis and nephritic syndrome (see
glomerular diseases for more information).
Clinical features
- 50% remain asymptomatic
- nephritic syndrome
- hematuria
- hypertension
- edema
- oliguria
- in uenza like symptoms
- ank pain
Diagnostics
- lab
- normocytic, normochromic anemia
- elevated BUN and creatinine
- elevated antistreptolysin O titer
- elevated anti DNase B antibody
- decreased C3 complement
- urinalysis: nephritic sediment
- US: enlarged kidneys
- renal biopsy:
- indication: suspected rapidly progressive GN
DD: IgA nephropathy, thin basement membrane disease
Treatment
- mostly self limiting and only supportive treatment focused on the complications of volume
overload is necessary
- Monitor electrolytes, renal function parameters, and blood pressure
- For edema: low-sodium and low-protein diet, loop diuretics
- For hypertension: ACE-inhibitors/ARBs, calcium channel blockers (see "Treatment" in the
learning card on hypertension)
- If persisting streptococcal infection: antibiotic therapy (penicillin G benzathine)
- If severe course/complications: glucocorticoids, temporary need for dialysis
Complications: ARF, rapidly progressing GN, nephrotic syndrome
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,2. Idiopathic nephrotic syndrome.
, 3. Membranous GN.
De nition: MGM is a slowly progressive disease of the kidney a ecting mostly people between
ages of 30 and 50 years. It is the second most common cause of nephrotic syndrome in adults.
Etiology:
- primary/ idiopathic
- secondary
- autoimmune conditions ( e.g. SLE)
- infections ( e.g. syphillis, malaria, hep. B and C, HIV)
- drugs ( e.g. captopril, NSAIDS, penicillamine)
- inorganic salts
- tumors
Pathogenesis and Pathophysiology
- caused by immune complex formation in glomerulus
- formed by bidding of Ab to Ag in glomerular basement membrane
- Ag may be part of the basement membrane or deposited from elsewhere by the systemic
circulation
- triggers response from complement system-> formation of MAC on glomerular epithelial
cells-> stimulates release of proteases and oxidants by mesangial and epithelial cells
imaging capillary walls and causing them to become leaky
Diagnosis:
- urinalysis
- blood test
- creatinine
- protein
- lipid
- urine albumin
- BUN
- creatinine clearance
- biopsy
- antinuclear Ab test
- antidouble strand DNA test
- testing: Hep. B and C, malaria, syphillis, complement levels, cryoglobulin
Treatment:
- treatment of original disease
- immunosuppressive drugs: corticosteroids, chlorambucil, cyclosporine, tacrolimus,
cyclophosphamide, mycosphenolalte mofetil, rituximab
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De ntion: Poststreptococcal (or postinfectious) glomerulonephritis (PSGN) refers to acute
glomerular in ammation that results from a preceding infection with nephritogenic strains of
streptococci. Although most commonly seen in children following group A streptococcal
tonsillopharyngitis, skin infections such as impetigo may trigger PSGN as well. Deposition of
immune complexes containing the streptococcal antigen within the glomerular basement
membrane results in complement activation and subsequent damage to the glomeruli.
Etiology:
- occurs ca. 10-30 days after an acute infection
- group A beta- hemolytic streptococci
- mouth and pharynx: tonsillitis, pharyngitis
- soft tissue infections: erysipelas ( bacterial infection of the upper dermis), impetigo
- osteomyelitis
- immune complex glomerulonephtritis can also manifest during an acute infection ( e.g. in
endocarditis or soft tissue abscesses)
Pathophysiology: Infection with nephritogenic strains of group A beta-hemolytic streptococci →
immune complexes containing the streptococcal antigen deposit within the glomerular basement
membrane (likely involves molecular mimicry) → complement activation → destruction of the
glomeruli → immune complex-mediated glomerulonephritis and nephritic syndrome (see
glomerular diseases for more information).
Clinical features
- 50% remain asymptomatic
- nephritic syndrome
- hematuria
- hypertension
- edema
- oliguria
- in uenza like symptoms
- ank pain
Diagnostics
- lab
- normocytic, normochromic anemia
- elevated BUN and creatinine
- elevated antistreptolysin O titer
- elevated anti DNase B antibody
- decreased C3 complement
- urinalysis: nephritic sediment
- US: enlarged kidneys
- renal biopsy:
- indication: suspected rapidly progressive GN
DD: IgA nephropathy, thin basement membrane disease
Treatment
- mostly self limiting and only supportive treatment focused on the complications of volume
overload is necessary
- Monitor electrolytes, renal function parameters, and blood pressure
- For edema: low-sodium and low-protein diet, loop diuretics
- For hypertension: ACE-inhibitors/ARBs, calcium channel blockers (see "Treatment" in the
learning card on hypertension)
- If persisting streptococcal infection: antibiotic therapy (penicillin G benzathine)
- If severe course/complications: glucocorticoids, temporary need for dialysis
Complications: ARF, rapidly progressing GN, nephrotic syndrome
fl flfi fl
,2. Idiopathic nephrotic syndrome.
, 3. Membranous GN.
De nition: MGM is a slowly progressive disease of the kidney a ecting mostly people between
ages of 30 and 50 years. It is the second most common cause of nephrotic syndrome in adults.
Etiology:
- primary/ idiopathic
- secondary
- autoimmune conditions ( e.g. SLE)
- infections ( e.g. syphillis, malaria, hep. B and C, HIV)
- drugs ( e.g. captopril, NSAIDS, penicillamine)
- inorganic salts
- tumors
Pathogenesis and Pathophysiology
- caused by immune complex formation in glomerulus
- formed by bidding of Ab to Ag in glomerular basement membrane
- Ag may be part of the basement membrane or deposited from elsewhere by the systemic
circulation
- triggers response from complement system-> formation of MAC on glomerular epithelial
cells-> stimulates release of proteases and oxidants by mesangial and epithelial cells
imaging capillary walls and causing them to become leaky
Diagnosis:
- urinalysis
- blood test
- creatinine
- protein
- lipid
- urine albumin
- BUN
- creatinine clearance
- biopsy
- antinuclear Ab test
- antidouble strand DNA test
- testing: Hep. B and C, malaria, syphillis, complement levels, cryoglobulin
Treatment:
- treatment of original disease
- immunosuppressive drugs: corticosteroids, chlorambucil, cyclosporine, tacrolimus,
cyclophosphamide, mycosphenolalte mofetil, rituximab
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