GN Associated with Infections Flashcards
Four classic characteristics of acute nephritic syndrome
Sudden onset of 1) Gross hematuria 2) Edema 3) Hypertension 4) Renal insufficiency
Nephritogenic strains of GABHS that infect the throat
M1, M4, M25, some M12
Nephritogenic strains of GABHS that infect the skin
M49
Glomeruli appear enlarged and relatively bloodless and show diffuse mesangial cell proliferation, with an increase in mesangial matrix
APSGN
In APSGN, infiltration of ___ cells is common in glomeruli during the early stage of the disease
Polymorphonuclear leukocyte
In APSGN, immunofluorescence microscopy reveals a ___ pattern on the glomerular basement membrane and in the mesangium
“lumpy-bumpy”
Lumpy bumpy pattern in immunofluorescence of kidneys of patients with APSGN represent
Deposits of immunoglobulin and complement
On electron microscopy of kidneys affected by APSGN, electron-dense deposits, or “humps,” are observed on the ___ side of the glomerular basement membrane
Epithelial
Circulating immune complex formation with streptococcal antigens and subsequent glomerular deposition is thought likely to be a pathogenic mechanism of APSGN
F, LESS LIKELY
Poststreptococcal GN is most common in children ages ___ and uncommon before the age of ___
5-12 yr, 3 yr
Typical APSGN patient develops an acute nephritic syndrome ___ after an antecedent streptococcal pharyn- gitis or ___ after a streptococcal pyoderma
1-2 wk, 3-6 wk
T/F In APSGN, nephrotic syndrome develops in a minority (less than 5%) of childhood cases
T
In individuals who present with a purpuric rash and renal disease, it is difficult to distinguish APSGN from ___ without a renal biopsy
Henoch-Schönlein purpura
The acute phase of APSGN generally resolves within ___
6-8 wk
In APSGN, urinary protein excretion and hypertension usually normalize by ___ after onset
4-6 wk
In APSGN, persistent microscopic hematuria can persist for ___ after the initial presentation
1-2 yr
Anemia seen in APSGN
Mild normochromic
Mild normochromic anemia may be seen in APSGN due to
Hemodilution and low-grade hemolysis
In APSGN, the serum C3 level is significantly reduced in >90% of patients in the ___ phase
Acute
C3 levels in APSGN returns to normal ___ after onset
6-8 wk
T/F Serum CH50 is commonly depressed in APSGN
T
T/F C4 is most often depressed in APSGN
F, Normal or only mildly depressed
T/F Confirmation of the diagnosis of APSGN requires clear evidence of a prior streptococcal infection
T
A positive ___ might support the diagnosis of APSGN or might represent the carrier state
Throat culture report
A ___ confirms a recent streptococcal infection
Rising antibody titer to streptococcal antigen(s)
___ is commonly elevated after a pharyngeal infection but rarely increases after streptococcal skin infections
Antistreptolysin O titer
The best single antibody titer to document CUTANEOUS streptococcal infection is the ___
Antideoxyribonuclease B level
Measures multiple antibodies to different streptococcal antigens
Streptozyme screen
T/F Serologic evidence for streptococcal infections is more sensitive than the history of recent infections
T
T/F Serologic evidence for streptococcal infections is far more sensitive than positive bacterial cultures obtained at the time of onset of acute nephritis
T
MRI of the brain is indicated in APSGN patients with severe neurologic symptoms and can demonstrate ___
Posterior reversible encephalopathy syndrome in the parietooccipital areas on T2-weighted images
Renal biopsy in patients with APSGN should be considered only in the presence of (5)
1) Acute renal failure 2) Nephrotic syndrome 3) Absence of evidence of streptococcal infection 4) Normal complement levels 5) Hematuria and proteinuria, dimin- ished renal function, and/or a low C3 level persist more than 2 mo after onset
___ can indicate a chronic form of postinfectious GN or another disease such as membranoproliferative GN
Persistent hypocomplementemia
Acute postinfectious GN can also follow other infections with (3)
1) Coagulase-positive and coagulase-negative staphylococci 2) Streptococcus pneumoniae 3) Gram-negative bacteria
Viral etiologies that are particularly notable as causes of acute GN (2)
1) Influenza 2) Parvovirus
Acute complications of APSGN result from ___ and ___
1) Hypertension 2) Acute renal dysfunction
Hypertension is seen in ___% of patients with APSGN
60
Hypertension in APSGN is associated with Hypertensive encephalopathy in ___% of cases
10
T/F Early systemic antibiotic therapy for streptococcal throat and skin infections eliminates the risk of GN
F, Does not eliminate
T/F Antibiotic therapy (10-day course of penicilin) does NOT affect the natural history of APSGN
T
Complete recovery occurs in ___% of children with APSGN
> 95
T/F Recurrences of APSGN are extremely rare
T
Pathogenesis of HIV-associated nephropathy
Direct viral infection of nephrons occurs because renal cells express a variety of lymphocyte chemokine receptors that are essential for and facilitate viral invasion
Classic histopathologic lesion of HIV-associated nephropathy is ___
Focal segmental glomerulosclerosis
GN with no immune deposits
RPGN
GN with granular IgG and C3 on IF
PSGN
GN with linear IgG and C3 on IF
Goodpasture syndrome
GN with no deposits on electron microscopy
Goodpasture syndrome and RPGN
Treatment for Goodpasture syndrome
Plasma exchange, steroids, cyclophosphamide
Treatment for RPGN
Steroid pulse therapy
Common GN with decreased complement level
SLE, APSGN, MPGN
Common GN with normal complement level
HSP, Goodpasture, IgA nephropathy, RPGN, nonstreptococcal postinfectious GN
