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CRRAB II > Renal Path 10/28 (lots of Glomerular Nephritis) > Flashcards

Renal Path 10/28 (lots of Glomerular Nephritis) Flashcards

1
Q

Autosomal dominant PCKD?

A

Adult

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2
Q

Berry aneurysms

A

Adult PCKD

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3
Q

Mitral valve prolapse

A

Adult PCKD

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4
Q

Autosomal recessive PCKD?

Enlarged, smooth kidneys

A

Childhood

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5
Q

7% of dialysis patients with acquired cystic develop?

A

renal cell carcinoma

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6
Q

The BIG feature of glomerulonephritis?

A

IMMUNE MEDIATED

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7
Q

complement C5a molecule does what?

A

chemotactic for neutrophils

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8
Q

“Diffuse” GN means:

A

all glomeruli involved

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9
Q

“focal” GN means:

A

a portion of glomeruli involved

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10
Q

“Global” GN means:

A

entire single glomerulus involved

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11
Q

“Segmental” GN means:

A

part of single glomerulus involved

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12
Q

some component of the kidney is the antigen?

A

in situ immune complex deposition

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13
Q

antigens and antibodies form complex before deposit in kidney:

A

circulating immune complex deposition

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14
Q

LINEAR, homogenous, diffuse pattern on IF:

A

Anti-GBM GN

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15
Q

Pulmonary alveoli involvement GN

A

Goodpastures

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16
Q

NC1 domain of alpha 3 chain of type IV collagen is antigen

A

Anti-GBM GN

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17
Q

Granular, interrupted pattern on IF

M-type Phospholipase A2 antigen

A

Membranous GN

Heymann

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18
Q

Inflammatory and Proliferative GN

A

Nephr-I-tic syndrome

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19
Q

Proteinuria > 3.5 g/24 hrs

A

Nephr-O-tic syndrome

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20
Q

Low serum C3

Large hypercellular glomeruli

subEPIthelial “Camel Humps” on EM

A

Acute Poststreptococcal GN

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21
Q

“smoky” urine

periorbital edema

children

A

Acute poststreptococcal GN

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22
Q

Crescents (fibrinous proliferations) of parietal epithelial cells of Bowman’s capsule mixed with inflammatory cells

A

Rapidly Progressive GN

23
Q

RPGN

LINEAR deposits in IF

A

Type I

anti-GBM

24
Q

RPGN

“lumpy-bumpy” granular pattern on IF

A

Type II

Immune complex mediated

25
Q

RPGN

lack of IF staining

pANCA or cANCA

A

Type III

Pauci-immune

26
Q

Time frame for RPGN

A

Weeks

27
Q

Complement mediated damage to GBM

“SPIKES” on silver stain

A

Membranous GN

28
Q

Most common cause of nephrotic syndrome in children

A

Minimal Change Disease

29
Q

Atopy (prone to allergic rxn)

Hodgkin Lymphoma

A

Minimal Change Disease

30
Q

Tx for minimal change disease?

A

corticosteroids

**responds well!!!

31
Q

Diffuse Effacement of Foot Processes and no deposits on EM

no IF staining

normal glomeruli

A

Minimal Change Disease

32
Q

Main lab finding in MCD?

A

MASSIVE proteinuria

33
Q

sclerosis of SOME (not all) gloms

HIV
HEROIN
Sickle cell
Morbid Obesity

A

Focal Segmental Glomerulosclerosis

FSGS

34
Q

Pathogenesis of FSGS:

A

damage to visceral epithelial cells

35
Q

On light microscopy:

Collapsed GBM

increased mesangial matrix

hyalinization

+/- foam cells

A

FSGS

36
Q

proteinaceous material and inflammation

tubuloreticular inclusions in endothelial cells

A

HIV nephropathy

37
Q

leukocyte infiltration

mixed nephrotic/nephritic

A

Membranoproliferative Glomerulonephritis

38
Q

SLE

Hep B/C

Endocarditis

Infx vetriculoarterial shunts

Hematologic malignancy

A

Membranoproliferative Glomerulonephritis

39
Q

“tram track” on silver stain

A

MPGN

40
Q

SUBENDOTHELIAL deposits on EM

Alternative complement pathway

A

Type I MPGN

41
Q

“Dense deposit disease”

-lamina densa of GBM is “RIBBON LIKE”

A

Type II MPGN

42
Q

Most common glomerulonephritis worldwide

A

IgA Nephropathy

43
Q

recurrent hematuria

maybe gluten enteropathy or liver disease related

A

IgA Nephropathy

44
Q

Site of IgA deposition in IgA Nephropathy?

A

mesangium

45
Q

MESANGIAL DEPOSITS OF IGA ON I.F.

A

IgA nephropathy

46
Q

Hematuria following respiratory, GI, or urinary tract infx:

A

IgA nephropathy

47
Q

Nephritis

nerve deafness

eye disorders

A

Alport Syndrome

48
Q

Irregular “thick and thin” GBM

splitting of lamina densa

A

Alport Syndrome

49
Q

COL4A5

defective GBM synthesis

A

Alport Syndrome

50
Q

Diffuse thinning of GBM

A

Thin Membrane Disease

51
Q

Small, diffusely granular kidneys

Globally hyalinized glomeruli

A

Chronic GN

52
Q

Disease most likely to progress to Chronic GN?

A

RPGN (crescentic)

53
Q

“Full house” – IF stains with everything

“Wire loop” lesions

A

Lupus Nephritis

54
Q

IgA in mesangium

Purpuritic skin lesions

A

HSP

CRRAB II (28 decks)

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