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pathology > renal review > Flashcards

renal review Flashcards

1
Q

what are the typically proteinuria values of nephrotic and nephritic syndromes?

A

nephrotic > 3.5g/24h

nephritic < 3.5g/24h

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2
Q

do you have a problem making urine in nephrotic or nephritic syndromes?

A

nephritic

No problem in nephrotic, typically have an excess

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3
Q

what primary glomerular lesions lead to nephrotic syndrome?

A 
MCD
FSGS
membranous glomerulopathy
membranoproliferative glomerulonephritis (often nephritic)
IgA nephropathy (often nephritic)
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4
Q

what systemic diseases can lead to nephrotic syndrome?

A

diabetes mellitus
SLE
amyloidosis

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5
Q

how do we diagnose MCD (what do we see on LM, EM, and IF)?

A

LM: normal glomeruli
IF: no staining, looks normal
EM: diffuse effacement of foot processes

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6
Q

what are the clinical features of FSGS?

A

proteinuria: nephrotic or non-nephrotic range

hematuria, hypertension

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7
Q

patients with FSGS usually do not respond well to what type of medication?

A

steroids

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8
Q

is FSGS rapidly or slowly progressing?

A

slowly

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9
Q

what population is most susceptible to FSGS?

A

black african american

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10
Q

how many of the glomeruli are damaged in FSGS?

A

<50%

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11
Q

what is the worst variant of FSGS?

A

collapsing glomerulopathy

idiopathic or HIV associated

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12
Q

how do we tell the difference between MCD and FSGS on LM?

A

you can see segmental sclerosis in FSGS

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13
Q

what is the hallmark of membranous glomerulopathy histologically?

A

GBM spikes on silver stain (jones)

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14
Q

what do you see on IF in membranous glomerulopathy?

A

granular IgG

C3 on capillary wall

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15
Q

what do you see on EM in membranous glomerulopathy?

A

subepithelial deposits regularly distributed along GBM

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16
Q

what is the typical presentation of glomerulonephritis (MPGN)?

A

proteinuria - typicaly nephrotic, but may be mild
hematuria, may be accompanied by nephritic syndrome
hypocomplementemia (low serum C3)

proliferation and thickening of capillary wall

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17
Q

most common form of MPGN

A

type 1 - lupus, hep C

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18
Q

what causes type II MPGN?

A

c3 nephritic factor

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19
Q

what is pathological about MPGN Type I?

A

hypercellular glomeruli: increased mesangial and infiltrating mononuclear cells in global distribution

thick-walled capillary loops: double contour or “tram track”

crescents (Rare)

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20
Q

what do we see on IF of MPGN type I?

A

granular C3 along capillary walls at the periphery of lobule (central sparing) often with IgG and IgM

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21
Q

what do we see on EM of MPGN type I?

A

immune deposits in subendothelial and mesangial locations

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22
Q

what two diseases are common etiologies of MPGN type I?

A

HCV and lupus

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23
Q

what is MPGN type II?

A

dense deposit disease

autoimmune disease with autoantibodies (C3 nephritic factor) directed at C3bBb

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24
Q

what are the clinical symptoms of acute nephritic syndrome?

A

hematuria +/- RBC casts
hypertension
azotemia, oliguria (usually transient)
edema, proteinuria variable (<3g/24h)

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25
Q

what are the etiologies of acute nephritic syndrome?

A

typically immune mediated

post-infection GN (post-strep)
primary glomerular disease (IgA nephropathy, MPGN - lupus)

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26
Q

what are the clinical features of acute post-infectious glomerulonephritis?

A

abrupt onset oliguria, elevated BUN and creatinine
anti-streptolyin O (ASO) in serology (for post-strep)
decreased serum C3 (this is how they monitor kids)

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27
Q

what do you see on histological slides for acute post-infectious glomerulonephritis?

A

diffuse proliferative glomerulonephritis (TONS of neutrophils)

hypercellular: proliferation of mesangial and other cells
exudative: neutrophils and mononuclear cells present

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28
Q

what do you see in IF of acute post-infectious glomerulonephritis?

A

coarsely granular deposits of IgG and C3

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29
Q

what do you see in EM of acute post-infectious glomerulonephritis?

A

subepithelial humps

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30
Q

what is the second most common cause of kidney failure in the world?

A

IgA nephropathy

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31
Q

what is pathological in IgA nephropathy?

A

they make IgA immunoglobulin incorrectly (only IgA1, not IgA2)

can look like a lot of diff things on LM, but if they diagnose they use IF: IgA strong staining within mesangium

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32
Q

what do you see in IF for IgA nephropathy?

A

strong IgA staining within mesangium

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33
Q

what is the clinical presentation of rapidly progressive GN?

A

acute nephritis with oliguria, RBC casts, hypertension
rapid loss of renal function (acute renal failure)

**really rapid creatinine increase and almost all associated with crescents.

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34
Q

what are the three types of glomerular injury that contribute to the pathogenesis of rapidly progressive GN?

A

type I: anti-glomerular antibody (anti-GBM)*
type II: immune complex
type III: anti-neutrophil cytoplasmic antibodies (ANCA)*

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35
Q

what causes the formation of a crescent?

A

proliferation of parietal epithelial cells forming layer >2 cells thick, involving >50% circumference

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36
Q

what syndrome often leads to anti-GBM disease?

A

goodpasture syndrome (if lung hemorrhage also present)

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37
Q

what do you see on IF for anti-GBM disease?

A

linear IgG along capillary wall (nothing else looks like this in kidney disease!)

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38
Q

what antibodies are found in Wegener Granulomatosis?

A

ANCA (know that this exhibits as little to no staining on IF)

39
Q

how does Wegener Granulomatosis appear on IF?

A

it’s pauci-immune (not much staining for ANCA pathologies)

you see some crescent formation otherwise

40
Q

do you see crescents in Wegener Granulomatosis?

A

yes

41
Q

what antibodies are present in SLE?

A

all he wants us to know is ANA present in essentially all patients

42
Q

when you see a patient presenting with clots and multiple miscarriages what pathology would you be suspicious of?

A

SLE

*due to anti-phospholipid antibodies

43
Q

what type of stain do you typically see for SLE?

A

FULL HOUSE STAIN

44
Q

what are the three renal syndromes attributable to diabetic neuropathy?

A

microalbuminuria or non-nephrotic proteinuria
nephrotic proteinuria
chronic renal failure

45
Q

what is kimmelstiel-Wilson disease?

A

nodular glomerulosclerosis due to diabetic neuropathy

46
Q

what do you see within the arterioles of patients with diabetic neuropathy?

A

hyaline deposits

47
Q

what do you see on EM of diabetic neuropathy?

A

thickened GBM with no deposits and mesangial expansion

48
Q

amyloid on congo red stain presents with what?

A

apple-green birefringence (due to characteristic ß-pleated sheets

49
Q

how does amyloid appear on EM?

A

non-branching fibrils

50
Q

what is characteristic of myeloma cast nephropaty (in staining)?

A

fractured casts

51
Q

cryoglobulinemia is typically associated with what disease?

A

HCV

52
Q

what are the causes of acute tubular necrosis?

A

ischemic: shock
antibiotics
radio-contrast agents

53
Q

NSAID nephropathy is the cause of what type of renal disease?

A

tubulointerstitial disease

54
Q

what is allergic tubulointerstitial nephritis?

A

hypersensitivity reaction to drug especially antibiotics

55
Q

what is a hallmark of allergic tubulointerstitial nephritis?

A

fever, rash, peripheral blood eosinophilia
acute renal failure
urine contains RBC, WBC (especially eosinophils)

typically appears about 2 weeks after drug started

56
Q

what do we see on IF for myeloma cast nephropathy?

A

exclusively one light chain isotype (typically kappa light chain) because of monoclonal proliferation

57
Q

what is characteristic about the group of disorders categorized as thrombotic microangiopathies?

A

microthrombosis of arterioles and capillaries

58
Q

what is the most common etiology of thrombotic microangiopathy?

A

hemolytic-uremic syndrome

59
Q

hemolytic-uremic syndrome typically follows what illness?

A

respiratory or GI distress (very common after E.Coli infection)

clinically often seen after person eats hamburger gets infected with O157:H7

60
Q

what happens to the kidneys after a patient takes immunosuppressants over time?

A

damage to the kidney

tacrolimus, cyclosporine used in allograft rejection prevention

61
Q

what causes hyperacute rejection?

A

preformed antibodies

minutes to hours after vascular anastamosis

62
Q

what is the clinical renal picture of acute cellular rejection?

A

sudden azotemia (elevated creatinine, BUN)

63
Q

what is the renal pathology seen in acute cellular rejection?

A

interstitial inflammation: lymphocytes

64
Q

what primary diseases are most likely to recur?

A

MPGN
anit-GBM disease
IgA nephropathy
FSGS

65
Q

what are the causes of urinary tract obstruction?

A

BPH
tumors
calculi (stones)
congenital abnormalities (typically seen in children)

66
Q

what is hydronephrosis?

A

dilation of renal pelvis, calcyes, and ureter due to obstruction

when urine can’t get out (dilation of renal pelvis, calyces, and ureter due to obstruction)

67
Q

what forms the largest type of stone (urolithiasis)?

A

struvite (magnesium ammonium phosphate)

68
Q

when do struvite stones form?

A

after infection with a urea-splitting bacteria (typically Proteus)

69
Q

stones of what type result in staghorn calculi?

A

struvite

70
Q

most common stone

A

calcium (oxalate and phosphate)

71
Q

what are the two types of polycystic kidney disease?

A

AD PKD

AR PKD

72
Q

what is unique about ADPKD?

A

cysts everywhere (berry aneurysms in circle of willis, hepatic cysts, cysts in pancreas lung and spleen, kidneys enlarged bilaterally, slowly overtime this replaces the entire kidney)

73
Q

does ADPKD cause slow or rapid progression to renal failure?

A

slow

74
Q

what is the molecular pathogenesis of ADPKD?

A

they make polycystin-1 inappropriately

75
Q

when does ARPKD usually present?

A

typically in childhood

30% die as neonates due to lung hypoplasia

76
Q

what macropathology do you see in patients with ARPKD (renal related)?

A

enlarged kidneys with smooth surface (cysts are small and enlongated perpendicular to surface)

77
Q

what is the hallmark of oncocytoma?

A

grossly tan or brown encapsulated stellate scar and large eosinophils

**benign, but can still grow large enough that you need to remove the entire kidney

78
Q

what is the most common cause of kidney cancer?

A

renal cell carcinoma

79
Q

is renal cell carcinoma familial or sporadic?

A

sporadic

80
Q

where do you typically find clear cell carcinoma (what pole of the kidney)?

A

upper pole

81
Q

what mutation causes wilm’s tumor?

A

WT1

82
Q

is wilm’s tumor encapsulated or non-encapsulated?

A

encapsulated

83
Q

what is the most common primary renal tumor in children?

A

wilm’s tumor

84
Q

What is the normal BUN:creatinine ratio?

A

15

85
Q

Patients exposed to ethylene glycol show development of what in the urine

A

oxalate crystals

86
Q

What is one of the highest yield findings of acute (allergic) interstitial nephritis?

A

Eosinophils in urine

87
Q

IF- shows coarsely granular deposits of IgG and C3, EM- shows subepithelial “humps.” What do u think they have?

A

acute post-infectious glomerulonephritis

88
Q

SLE kidney disease *buzzwords?

A
  • full house stain
  • mesangial deposits
  • subendothelial deposits
89
Q

_________ pattern most common for hep C and lupus

A

MPGN…..

specifically MPGN type 1 for hep C

90
Q

cracked casts, dif colors in the cast, cellular reaction =

A

myeloma cast nephropathy

91
Q

pathogenesis of malignant nephrosclerosis

A

renal failure, death if not treated immediately

92
Q

thrombotic microangiopathy is a group of disorders characterized by

A

microthrombosis of arterioles and capillaries, which is caused by microangiopathic hemolytic anemia test q

93
Q

hemolytic-uremic syndrome can cause ________________, which can often lead to acute renal failure & death in 1/2 adults who get this

A

thrombotic microangiopathy

94
Q

Hemolytic-Uremic syndrome clinical finidings

A

acute renal failure,
thrombocytopenia,
hemolytic anemia

pathology (8 decks)

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