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CRAAB II > Renal Pathology Lecture 3 > Flashcards

Renal Pathology Lecture 3 Flashcards

1
Q

Classic presentation of IgA Nephropathy

A

hematuria following a respiratory, GI or UTI

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2
Q

IgA Nephropathy often occurs

A

Post transplantation

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3
Q

Alport syndrome presentation

A

Nephritis
Nerve deafness
eye disorders (lens dislocations, cataracts, corneal dystrophy)
X linked dominant inheritance

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4
Q

Pathology of Alport?

A

EM: irregular thick and thin GBM

  • splitting of lamina densa
  • charges are widespread
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5
Q

Mutation of Alport?

A

alpha 5 chain of type IV collagen (COL4A5)

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6
Q

Clinical pearls of Alport?

A

Hematuria at age 5-20
proteinuria (sometimes)
Renal failure by age 20-50

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7
Q

Thin membrane disease

A

thinning of GBM (normal is 300 to 400 nm, thinned is 150-225 nm)

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8
Q

Prognosis of thin membrane disease

A

excellent prognosis; homozygous may progress to renal failure

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9
Q

What does this membrane disease present with?

A

Hematuria

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10
Q

Gross presentation of chronic glomerulonephritis

A

small, diffusely granular kidney

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11
Q

micro presentation of chronic glomerulonephritis

A

globally hyalinized glomeruli, atrophy and fibrosis of tubules

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12
Q

What conditions statistically progresses to chronic GN most commonly?

A

PRGN (crescentic)

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13
Q

Nearly all SLE patients show kidney involvement. True or False?

A

True. Full house on IF (stains with everything). Wire loop lesion (thickening of capillary)

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14
Q

Henoch-Schonlein Purpura presentaiton

A

Purpuric skin lesions on arms, legs, buttocks
Abodominal pain, vomitng, bleeding
arthralgia
Renal abnormalties (1/3 patients)

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15
Q

Henoch-Schonlein Purpura population

A

Most common in children 3-8 years old

Onset after URI

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16
Q

Henoch-Schonlein Purp. path

A

IgA in mesangium

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17
Q

Diabetic nephropathy

A
  • 40% of diabetics
  • Early proteinuria
  • Capillary membrane thickening
  • Diffuse mesangial sclerosis
  • Nodular glomerulosclerosis
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18
Q

Hemodynamic effects in early diabetic nephropathy

A

increased GRF and glomerular hypertrophy in early disease - results in glomerulosclerosis

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19
Q

Kimmelstiel Wilson is also know as

A

Nodular glomerulosclerosis

Hyaline masses at periphery of glom.

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20
Q

EM detects this in diabetic nephropathy

A
  • Capillary basement membrane thickening

- Diffuse mesangial scerlosis

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21
Q

Ischemic and toxic injury to the tubules leads to these three things…

A
  1. ATN ( acute tubular necrosis)
  2. ATI (acute tubular Injury)
  3. ARF
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22
Q

Inflammatory reactions of the tubules and interstitium lead to

A

Tubulointerstitial nephritis

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23
Q

MOST COMMON CAUSE OF ACUTE RENAL FAILURE

A

ATN

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24
Q

Define ATN

A

Destruction of tubular epithelial cells which clinically presents as acute loss of renal function

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25
Q

What causes ATN?

A

Ischemia or nephrotoxicity

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26
Q

Pathogenesis of ATN

A

tubular injury

Persistent and severe changes in blood flow

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27
Q

Pathology of ATN

A

-Tubular epithelial necrosis
-Sloughing of tubular cells into the lumen
-Hyaline and granular casts
-Interstitial edema and increased lymphocytes
-Toxic ATN may show specific changes
(Ethylene glycol poisoning has calcium oxalate crystals in tubular lumens)

28
Q

Prognosis for ATN

A

nephrotoxic: 95% if survive initial event

shock/multiorgan failure: 50%

29
Q

Difference between acute and chronic tubulointerstitial nephritis

A

Acute has PMNs/Eos and edema

Chronic has fibrosis and tulular atrophy

30
Q

Causes of tubulointerstitial nephritis?

A

LOTS! Infections, toxins, metabolic, neoplasms, physical factors or immuno reactions

31
Q

What is vesicoureteral reflux

A

Incompetence of the vesicoureteral valve allows bacteria to enter ureter and renal pelvis
Usually due to congenital shortening of the intravesicle portion of the ureter
Bladder infection, spinal cord injury increases reflux

32
Q

Complications of Acute Pyelonephritis

A

Papillary necrosis (diabetics, obstruction)
Pyonephrosis
Perinephric abcess

33
Q

What is a perinephric abscess

A

suppurative inflammation extended through renal capsule and adjacent tissue

34
Q

What does papillary necrosis look like?

A

Yellow necrosis of papillary tips with coagulative necrosis

35
Q

Acute pyelonephritis morphology?

A

PMNs
Intratubular aggregates of neutrophils
Tubular necrosis
Heals by scarring (tubular atrophy and interstital fibrosis with lymphocytes)

36
Q

Where is the kidney most commonly affected by reflux?

A

Upper and lower poles

37
Q

Chronic pyelonephritis damages the ______

A

pelvocalyceal region

38
Q

2 conditions that damage the calyces

A

chronic pyelo

analgesic nephropathy

39
Q

thyroidization describes

A

chronic pyelo morphology

40
Q

Be careful for this condition when people start chemo

A

Urate nephropathy

41
Q

bence jones proteinuria (light chains) and cast nephropathy presents in

A

Multiple myeloma

42
Q

Nephroscelrosis

A

The renal pathology associated with the sclerosis of renal arterioles and small arteries
Gross: Normal to small kidneys
Surface has fine, even granularity

43
Q

Pathogenesis of Nephrosclerosis

A
  • Medial and intimal vessel thickening is secondary to hemodynamic changes, aging, genetics, or a combination of these factors
  • Hyaline deposition in arterioles due to endothelial cell injury with extravasation of plasma proteins and increased basement membrane matrix
44
Q

High risk patients for nephrosclerosis

A

DM
Black
severe HTN

45
Q

Onion skinning

A

Malignant nephrosclerosis

46
Q

Renal artery stenosis gross appearance

A

one small kidney (the ischemic one)

47
Q

Denuded endothelium causes ______

A

blood clots

48
Q

Pentad for TTP

A 
Fever
Neuro symptoms (usually a big deal)
MAHA
Thrombocytopenia
Renal failure
49
Q

Typical patient profile for TTP?

A

middle aged women

50
Q

Obstructions increase susceptibility to _____ and ______

A

infection

stones

51
Q

Obstructions lead to ____ and _____

A

hydronephrosis

renal atrophy

52
Q

Calcium stones (%)

A

70% of all stones

radio opaque

53
Q

Struvite stones (%)

A

15%

54
Q

2 types of benign renal tumors

A

Angiomyolipoma

Oncocytoma

55
Q

What are angiomyolipomas composed of?

A

Composed of vessels, smooth muscle, fat

56
Q

What are angiomyolipomas are associated with?

A

Tuberus sclerosis (an autosomal dominant syndrome, patients develop tumors)

57
Q

Gross and micro appearance of oncocytoma

A

mahogany brown
large, eosinophilic cells with round nuclei
abundant mitochondria in cell

58
Q

Most important risk factor in Renal cell carcinoma?

A

tobacco use (smokers 2x the incidence)

59
Q

Renal cell carcinoma stats

A

3% of cancers
85% of renal cancer in adults
most common in elderly (6-7th decade)
Male predominance

60
Q

Von Hippel - Lindau syndrome

A
  • AD genetic disorder
  • Hemangioblastomas of cerebellum and retina
  • Renal cysts and carcinomas
  • VHL gene on chromosome 2p25.3
  • tumor supp. gene
61
Q

Most common type of RCC?

A

Clear cell carcinoma

62
Q

Genetic mutation in clear cell?

A

loss of chromosome 3p on (VHL gene)

63
Q

Clear cell tumor appearance?

A

Bright yellow, may have necrosis

64
Q

Papillary carcinoma?

A

10-15% of RCC
cuboidal cells with papillary growth pattern and foam cells
NO 3p loss
Trisomy 7, 17 and loss of Y

65
Q

Vegetable like cells with prominent cell membranes in this type of RCC

A

Chromophobe

66
Q

Renal cell carcinoma pattern of metastasis?

A

Renal vein
IVC
Right heart

CRAAB II (7 decks)

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