12.3 - Nephrotic syndrome Flashcards

1
Q

why does nephrotic syndrome result in a hypercoagulable state?

A

loss of antithrombin III

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2
Q

how does nephrotic syndrome lead to fatty casts?

A

due to hyperlipidemia and hypercholesterolemia

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3
Q

minimal change disease is associated with what type of cancer?

A

hodgkin lymphoma

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4
Q

what is seen on EM in minimal change disease?

A

effacement of foot processes

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5
Q

what is the IF finding in minimal change disease?

A

normal

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6
Q

is minimal change disease responsive to steroids?

A

yes - excellent response

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7
Q

which type of nephrotic syndrome is associated with HIV, heroin, and sickle cell disease?

A

FSGS

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8
Q

what are the H&E findings in FSGS?

A

focal and segmental sclerosis

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9
Q

what is seen on EM in FSGS?

A

effacement of foot processes

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10
Q

what are the IF findings in FSGS?

A

normal

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11
Q

is FSGS responsive to steroids?

A

no

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12
Q

which type of nephrotic syndrome is associated with hep B, hep C, solid tumors, SLE, drugs?

A

membranous

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13
Q

thick glomberular BM on H&E (no tram tracks) - diagnosis?

A

membranous nephropathy

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14
Q

what are the EM findings in membranous nephropathy?

A

subepithelial deposits with “spike and dome” appearance

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15
Q

subepithelial deposits with “spike and dome” appearance on EM - diagnosis?

A

membranous nephropathy

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16
Q

is membranous nephropathy responsive to steroids?

A

no

17
Q

thick glomberular BM on H&E with tram tracks - diagnosis?

A

membranoproliferative glomerulonephritis

18
Q

what is the IF appearance of membranous nephropathy?

A

granular

19
Q

what is the IF appearance of membranoproliferative glomerulonephritis?

A

granular

20
Q

where are the deposits in type I membranoproliferative glomerulonephritis? what diseases is it associated with?

A
  • subendothelial

- associated with HBV, HCV

21
Q

where are the deposits in type II membranoproliferative glomerulonephritis?

A

intramembranous

22
Q

which type of membranoproliferative glomerulonephritis is associated with C3 nephritic factor? what does it do?

A
  • type II
  • autoantibody that stabilizes C3 convertase, leading to overactivation of complement, inflammation, low levels of circulating C3
23
Q

low levels of C3 and intramembranous deposits - diagnosis?

A

type II membranoproliferative glomerulonephritis

24
Q

what is the end result of the nonenzymatic glycosylation of the vascular BM seen in DM?

A

hyaline arteriolosclerosis

25
Q

which glomerular arteriole is affected more by nonenzymatic glycosylation? what is the result?

A
  • efferent

- high GFR and hyperfiltration injury leading to microalbuminemia

26
Q

what is the cause of the high GFR and hyperfiltration injury leading to microalbuminemia seen in DM?

A

selective nonenzymatic glycosylation of the efferent arteriole

27
Q

what drug can slow the progression of hyperfiltration induced damage in DM? why?

A
  • ACE inhibitors

- via prevention of efferent vasoconstriction from angiotensin II

28
Q

what is the organ most involved in systemic amyloidosis? where does the deposition occur? what is the end result?

A
  • kidneys
  • mesangium
  • nephrotic syndrome