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12 Kidney Pathology > 12.3 Nephrotic Syndrome > Flashcards

12.3 Nephrotic Syndrome Flashcards

1
Q

which nephrotic syndrome is the only one with an effective treatment?

A
  • minimal change disease
  • tx with steroids (damage by cytokines of T cells)
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2
Q

Focal Segmental Glomerulosclerosis (FSGS)

-etiology, what associatd with?

A

-usu idiopathic. associated with HIV, heroin, sickle cell

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2
Q

diabetic nephropathy

-what drug slows its progression, how?

A
  • ACE-I, b/c it inhibits ATII’s constrictive effect on efferent arteriole.
  • remember, efferent arteriole is more affected by the hyaline arteriosclerosis of NEG
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3
Q

what is most common nephrotic and nephritic syndromes for SLE?

A

nephrotic: membranous nephropathy

nephritic (most common for SLE overall): Diffuse proliferative glomerulonephritis (causes rapidly progressive glomerulonephritis)

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4
Q

Focal Segmental Glomerulosclerosis (FSGS)

  • clinical findings
  • histology findings? IF?
A
  • nephrotic syndrome
  • effacement of podocytes (similar to MCD. if MCD does not respond to steroids, disorder progresses to FSGS)
  • focal (only certain glomeruli)
  • segmental (only part of glomerulus–becomes sclerosed)
  • negative IF (no immune deposits)
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5
Q

what is most common cause of nephrotic syndrome in whites?

A

Membranous nephropathy

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5
Q

Membranoproliferative glomerulonephritis

-tx

A

poor response to steroids, progresses to chronic renal failure

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6
Q

Amyloidosis on the kidney

-what happens

A
  • amyloid deposits in the mesangium, causing nephrotic syndrome
  • kidney is most commonly involved organ in systemic amyloidosis
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7
Q

Membranoproliferative glomerulonephritis

-what is each type associated with?

A

type 1: subendothelial

-assoc with HBV, HCV. (“tram track appearance”)

type 2: intramembranous (“dense deposit disease)

-assoc with C3 nephritic factor (autoAb that stabilizes C3 convertase, leading to overactivation of complement, inflammation, and low levels of circulating C3)

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8
Q

Nephrotic syndrome

-main clinical findings and their symptoms (5)

A
  1. proteinuria >3.5 g/day (liver makes 10-15 g/day, but tubular cells keep much of the protein that enters the tubules)
  2. hypoalbuminuria (pitting edema)
  3. hypogammaglobulinemia (increased infection risk)
  4. hypercoagulable state (loss of ATIII)
  5. hyperlipidemia, hypercholesterolemia (may result in fatty casts in urine)
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9
Q

Focal Segmental Glomerulosclerosis (FSGS)

-tx

A

-poor response to steroids, progresses to chronic renal failure

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10
Q

what is most common nephrotic syndrome in children?

A

minimal change disease

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11
Q

Membranous nephropathy

  • mech
  • what do you see on histology? (H&E, EM, IF)
A
  • immune complex deposition–subepithelial
  • H&E: thickened basement membrane
  • EM: ‘spike and dome’ appearance b/c BM grows over subepithelial deposits

IF: granular deposits

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12
Q

diabetic nephropathy

-what do you see on histology

A

Sclerosis of mesangium, (kimmelstiel-wilson nodules)

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13
Q

Membranoproliferative glomerulonephritis

-histology appearance

A
  • tram track appearance
  • mesangial cells are proliferating and slitting the immune complex depositions into two.
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15
Q

minimal change disease

  • clinical findings
  • tx
A
  • nephrotic syndrome
  • effacement of podocytes
  • selective proteinuria (albuminuria, not immunoglobulins)
  • Steroids, excellent response b/c damaged is from cytokines from T cells
15
Q

diabetic nephropathy

-stages of mech (3)

A
  • eventually nephrotic syndrome
    1. nonenzymatic glycosylation (NEG) of vascular BM, results in hyaline arteriosclerosis
    2. efferent arteriole more affected, leading hyperfiltration (microalbuminuria)
    3. eventually nephrotic syndrome from hyperfiltration damage
  • sclerosis of mesangium (kimmelstiel-wilson nodules)
17
Q

Nephrotic syndromes: List them (6)

A

remember by groups of 2:

  1. minimal change disease (MCD)
  2. focal segmental glomerulosclerosis (FSGS)
  3. Membranous nephropathy
  4. Membranoproliferative glomerulonephritis
  5. DM2
  6. Systemic amyloidosis
17
Q

minimal change disease

  • what do you see on histology (H&E stain, and electron microscopy)
  • what do you see in immunoflourescence (IF)
A
  • H&E light microscopy: normal glomeruli (may see thin filtration layer)
  • electron microscopy: effacement (flattening) of podocytes
  • IF: negative b/c no immune complex deposits
18
Q

Membranous nephropathy

-tx

A

poor response to steroids, progresses to chronic renal failure

19
Q

minimal change disease

  • etiology
  • mechanism
A
  • usu idiopathic, associated with Hodgkin’s Lymphoma
  • mech: damage to podocytes by cytokines from T cells
21
Q

C3 nephritic factor

A

-autoAb that stablizes C3 convertase, leading to overactivation of complement, inflammation, and low levels of circulating C3.

C3–> C3a + C3b

C3 convertase catalyzes this.

C3 nephritic factor stabilizes C3 convertase, overactivating it

22
Q

what is most common cause of nephrotic syndrome in Hispanics and blacks?

A

-focal segmental glomerulosclerosis (FSGS)

24
Q

Membranoproliferative glomerulonephritis

  • mech
  • types
A
  • mech: immune complex deposition (granular IF)
  • 2 types based on deposit location:

Type 1: subendothelial

Type 2: intramembranous

25
Q

Membranous nephropathy

  • etiology
  • associated with what other problems? (4)
A
  • usu idiopathic
  • associated with:
    1. Hep B, C
    2. solid tumors
    3. SLE
    4. drugs (NSAIDs, penicillamine)
26
Q

what is associated with C3 nephritic factor?

A

Type 2 Membranoproliferative glomerulonephritis

12 Kidney Pathology (12 decks)

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