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MHD V: Renal > 10.28: Renal III > Flashcards

10.28: Renal III Flashcards

1
Q

What is MCD?

A
  • Minimal change disease
  • Present with generalized and periorbital edema
  • Common in 2 - 6 yo: 95% of their nephROTIC synd.
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2
Q

What is FSGS?

A

Focal and Segmental Glomerulosclerosis

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3
Q

What is assumed diagnosis in child with nephrotic syndrome?

A
  • MCD
  • If course is normal and uncomplicated no biopsy is necessary
  • ***If it is determined that it is resistant steroids, biopsy performed
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4
Q

Is biopsy necessary in adults / kids for nephrotic syndrome?

A

Adults: Yes
Child: No, assumed MCD

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5
Q

Pathogenesis of MGD?

A
  • Reversible injury of unknown origin to podocytes of epithelial cells of basement membrane
  • No more more slit membranes allowing albumin leak
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6
Q

What type of immune complex is involved in MCD?

A
  • No IC involvement

- No inflammation

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7
Q

What does MCD disease usually occur after?

A
  1. NSAIDs
    2, Viral infection
  2. Hodgkins
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8
Q

What is podocyte effacement?

A
  • Injury to epithelial cells of basement membrane
  • Causes the feet to fuse losing slit membrane
  • Allows proteins to pass through: nephrotic syndrome
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9
Q

Prognosis of MCD?

A
  • Recurrent episodes of nephrotic syndrome
  • Stops at puberty
  • Treat with steroids to reverse podocyte injury
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10
Q

Treatment for membranous nephrotic syndrome?

A
  • Very hard to treat

- MCD is treated easily with steroids

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11
Q

General presentation of MCD?

A
  • Child
  • Proteinuria: foamy urine
  • ***Can be less than 3g in child
  • Periorbital and generalized edema
  • Lipiduria
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12
Q

What is effacement of podocytes characteristics of?

A

MCD

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13
Q

Differential diagnosis of 7-8 yo with nephrotic syndrome??

A
  1. 75% chance MCD

2. FSGS

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14
Q

Selective vs. nonselective proteinuria?

A

Selective: only albumin
Non selective: proteins other than albumin as well
**Usually indicative of greater degree of renal injury

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15
Q

FSGS presentation?

A
  • Nephrotic syndrome
  • Higher incidence of hematuria
  • Proteinuria is often non selective
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16
Q

DIfference in injury between FSGS and MCD?

A

MCD: Reversible injury to podocytes w. steroid treatment
FSGS: Injury is irreversible

17
Q

Progression of FSGS?

A
  • Initially only glomeruli in juxtmed. involved
  • Eventually all will be involved: global sclerosis leading to tubular atrophy and interstitial fibrosis
  • Will progress to renal failure
18
Q

Treatment of FSGS?

A
  • Initially responds to steroids

- Becomes dependant, then resistant

19
Q

Creatinine levels in FSGS?

A

Rising serum creatinine

20
Q

Possible etiologies of FSGS?

A
  1. Idiopathic
  2. HIV
  3. Parvovirus B19
  4. Heroin
  5. Sickle cell disease
  6. Obesity
  7. Low birthweight
  8. Bodybuilding steroids
  9. HTN
  10. Mutation in proteins for slit diaphragms
21
Q

What occurs in HIV associated FSGS?

A
  • Collapse of tuft and proliferation of visceral epithelium
  • Rapid progression to failure with very poor prognosis
    “Collapsing FSGS”
22
Q

When is immune complex seen in nephrotic syndrome?

A
  • Membranous nephropathy

- Autoimmune and resistant to steroids

23
Q

Two disease associated with nephrotic syndrome w/ hematuria?

A
  1. MPGN: Membranoproliferative glomerulonephritis

2. DDD: “Dense Deposit Disease”

24
Q

Etiology of MPGN?

A

Primary IC formation with complex activation, secondary to:

  1. Chronic immune disorders
  2. Hepatitis
  3. Endocarditis
  4. Chronic Bacterial infections
  5. Plasma cell monoclonal protein production
25
Q

What is thick basement memb. w/ “double contour or tram track” on silver stain indicative of?

A

MPGN

26
Q

Characteristics of MPGN?

A
  • Thick Basement memb. with IgG + complement
  • Low serum complement
  • Progression to renal failure
  • Try to treat underlying disease causing
27
Q

Etiology of DDD?

A
  • Sustained activation of complement via alt. pathway
  • No antibodies seen / no antigen antibody
  • Dense deposits in lamina densa
  • C3 convertase stabilization leading to comp. activation
28
Q

Determination of kidney needle biopsy?

A
  • Almost always needed in adults

- Usually only in kids if doesn’t respond to treatment

29
Q

What happens to glomeruli in diabetes?

A
  • Nonenzymatic glycosylation of vascular basement membrane leading to hyaline arteriosclerosis
    1. Narrows lumen
    2. Prevents nutrient diffusion through membrane
    3. Makes leaky and more porous
30
Q

Where is thickening of membrane in diabetes particular too?

A
  • Efferent artery

- Increases glomerular pressure

31
Q

What is amyloidosis?

A
  • Deposits of abnormally folded beta pleated sheets
  • Appears congo red positive and apple green under polarized light
  • Most often associated with multiple myeloma or plasma cells
32
Q

What is congo red positive indicative of?

A

Amyloidosis

33
Q

How is amyloidosis diagnosed?

A
  • Tissue biopsy of Fat of kidney tissue
34
Q

What is myeloma?

A

Cancer of plasma cells

35
Q

Who is lupus more common in?

A

Women

36
Q

Histology in early FSGS?

A

Parts of glomerular tufts obliterated capillaries

MHD V: Renal (28 decks)

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