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Flashcards in GN Associated with Infections Deck (52):
1

Four classic characteristics of acute nephritic syndrome

Sudden onset of 1) Gross hematuria 2) Edema 3) Hypertension 4) Renal insufficiency

2

Nephritogenic strains of GABHS that infect the throat

M1, M4, M25, some M12

3

Nephritogenic strains of GABHS that infect the skin

M49

4

Glomeruli appear enlarged and relatively bloodless and show diffuse mesangial cell proliferation, with an increase in mesangial matrix

APSGN

5

In APSGN, infiltration of ___ cells is common in glomeruli during the early stage of the disease

Polymorphonuclear leukocyte

6

In APSGN, immunofluorescence microscopy reveals a ___ pattern on the glomerular basement membrane and in the mesangium

“lumpy-bumpy”

7

Lumpy bumpy pattern in immunofluorescence of kidneys of patients with APSGN represent

Deposits of immunoglobulin and complement

8

On electron microscopy of kidneys affected by APSGN, electron-dense deposits, or “humps,” are observed on the ___ side of the glomerular basement membrane

Epithelial

9

Circulating immune complex formation with streptococcal antigens and subsequent glomerular deposition is thought likely to be a pathogenic mechanism of APSGN

F, LESS LIKELY

10

Poststreptococcal GN is most common in children ages ___ and uncommon before the age of ___

5-12 yr, 3 yr

11

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

12

T/F In APSGN, nephrotic syndrome develops in a minority (less than 5%) of childhood cases

T

13

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

14

The acute phase of APSGN generally resolves within ___

6-8 wk

15

In APSGN, urinary protein excretion and hypertension usually normalize by ___ after onset

4-6 wk

16

In APSGN, persistent microscopic hematuria can persist for ___ after the initial presentation

1-2 yr

17

Anemia seen in APSGN

Mild normochromic

18

Mild normochromic anemia may be seen in APSGN due to

Hemodilution and low-grade hemolysis

19

In APSGN, the serum C3 level is significantly reduced in >90% of patients in the ___ phase

Acute

20

C3 levels in APSGN returns to normal ___ after onset

6-8 wk

21

T/F Serum CH50 is commonly depressed in APSGN

T

22

T/F C4 is most often depressed in APSGN

F, Normal or only mildly depressed

23

T/F Confirmation of the diagnosis of APSGN requires clear evidence of a prior streptococcal infection

T

24

A positive ___ might support the diagnosis of APSGN or might represent the carrier state

Throat culture report

25

A ___ confirms a recent streptococcal infection

Rising antibody titer to streptococcal antigen(s)

26

___ is commonly elevated after a pharyngeal infection but rarely increases after streptococcal skin infections

Antistreptolysin O titer

27

The best single antibody titer to document CUTANEOUS streptococcal infection is the ___

Antideoxyribonuclease B level

28

Measures multiple antibodies to different streptococcal antigens

Streptozyme screen

29

T/F Serologic evidence for streptococcal infections is more sensitive than the history of recent infections

T

30

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

31

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

32

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

33

___ can indicate a chronic form of postinfectious GN or another disease such as membranoproliferative GN

Persistent hypocomplementemia

34

Acute postinfectious GN can also follow other infections with (3)

1) Coagulase-positive and coagulase-negative staphylococci 2) Streptococcus pneumoniae 3) Gram-negative bacteria

35

Viral etiologies that are particularly notable as causes of acute GN (2)

1) Influenza 2) Parvovirus

36

Acute complications of APSGN result from ___ and ___

1) Hypertension 2) Acute renal dysfunction

37

Hypertension is seen in ___% of patients with APSGN

60

38

Hypertension in APSGN is associated with Hypertensive encephalopathy in ___% of cases

10

39

T/F Early systemic antibiotic therapy for streptococcal throat and skin infections eliminates the risk of GN

F, Does not eliminate

40

T/F Antibiotic therapy (10-day course of penicilin) does NOT affect the natural history of APSGN

T

41

Complete recovery occurs in ___% of children with APSGN

>95

42

T/F Recurrences of APSGN are extremely rare

T

43

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

44

Classic histopathologic lesion of HIV-associated nephropathy is ___

Focal segmental glomerulosclerosis

45

GN with no immune deposits

RPGN

46

GN with granular IgG and C3 on IF

PSGN

47

GN with linear IgG and C3 on IF

Goodpasture syndrome

48

GN with no deposits on electron microscopy

Goodpasture syndrome and RPGN

49

Treatment for Goodpasture syndrome

Plasma exchange, steroids, cyclophosphamide

50

Treatment for RPGN

Steroid pulse therapy

51

Common GN with decreased complement level

SLE, APSGN, MPGN

52

Common GN with normal complement level

HSP, Goodpasture, IgA nephropathy, RPGN, nonstreptococcal postinfectious GN