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CS4: Exam 1 > 14/15: Renal Pathology - Fang > Flashcards

14/15: Renal Pathology - Fang Flashcards

1
Q

kidneys fail to differentiate

A

agenesis

incompatible with life if bilateral
adrenal glands will expand if the kidney is not there

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2
Q

failure of kidneys to develop to a normal size

A

hypoplasia

commonly unilateral

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3
Q

ectopic (pelvic) kidney complications

A

normal size, but kinking or tortuosity of the ureters may occur causing obstruction and predisposing to infection

may see pts with repeated history of stones or infections

horseshoe kidneys have lower risks than ectopic

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4
Q

Autosomal Dominant cystic diseases affect….

autosomal recessive cystic disease affect…

A

ADults

children

acquired cystic disease is dialysis associated

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5
Q

4 leading cause of ESRD

describe autosomal dominant polycystic kidney disease AKPKD

A
  • hereditary (genes PKD1 and 2)

multiple expanding cysts in both kidneys that eventually destroy with renal failure in 50s (renal functional decline is related to increase in kidney size (30 cm and dark in color) and cystic volume)

associated with hepatic cysts and berry aneurysms** (fatal subarachnoid hemorrhage - 10%)

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6
Q

normal size kidney

A

12 cm length
6 cm width
3 cm depth

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7
Q

describe autosomal recessive polycycstic kidney disease ARPKD

A

childhood

huge, white, smooth-surfaced kidneys at birth

small cysts develop from collecting ducts

associated with congenital hepatic fibrossis

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8
Q

retention aka acquired aka…

A

simple cysts - cortical

very common - not generally clinically significant

only when too big (5cm) do they become issue

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9
Q

3 studies done with renal bx

A

light microscopy LM
immunofluorescence microscopy IF
electron microscopy EM

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10
Q

podocytes aka

A

visceral epithelium

ENDOthelium - fenestrated capillary

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11
Q

focal v. diffuse

global v segmental

primary v. secondary v. idiopathic

A

WHOLE KIDNEY
less than 50%
greater than 50%

whole glomerulus
portion of glomerulus

renal disease
systemic disease
etiology unknown

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12
Q

3 patterns of IF staining in glomerulus

A

linear capillary loop pattern
ex: Anti-GBM disease

granular capillary loop pattern
ex: membranous nephropathy, lupus nephritis

mesangial pattern
ex: lupus nephritis, IgA nephropahty

renal biopsy stains G, A, and M and complements *excludes ED

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13
Q

describe three main clinical renal syndromes

acute renal failure

nephrotic syndrome

nephritic syndrome

A

oliguria - tubule injury

proteinuria - glomerulus injury

hematuria - glomerulus injury

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14
Q

nephritic syndrome

A 
HTN
oliguria
proteinuria
azotemia
hematuria
RBC casts
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15
Q

nephrotic syndrome

A 
proteinuria greater than 3.5 g/ 24 h
pitting edema and ascities due to hypoalbuminemia
hypercoagulable state
hypercholesterolemia
hypogammaglobulinemia
fatty casts
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16
Q

due to breaks in the glomerular capillary loops

due to glomerular capillary filtration defects

A

nephritic

nephrotic

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17
Q

effacement is associated with …

A

proteinuria and nephrotic syndrome

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18
Q

due to tubular injury in most cases

A

acute renal failure

19
Q

pathology of chronic renal failure

A

GROSS
Kidneys are small
Cortex thinned
Increase pelvic fat

MICRO
Glomerular sclerosis
Interstitial fibrosis
Tubular atrophy

20
Q

LM findings in chronic renal failure **

A

1- glomerular sclerosis
2 - interstitial fibrosis
3 - tubular atrophy

21
Q

primary and secondary causes of nephrotic syndrome

A

primary

  • minimal change
  • focal segmental glomerulosclerosis
  • membranous nephropathy

Secondary
- diabetic nephropathy

22
Q

minimal change disease looks like ..

A

children
puffy eyes

most common cause of nephrotic syndrome in children

23
Q

pathological appearance of minimal change

A

normal glomeruli on LM an dIF

EFFACEMENT OF FOOT PROCESSES ON EM***

lipid in tubular cells (why aka lipoid nephrosis)

usually respond to steroids

24
Q

diffuse epithelial foot process effacement =

A

minimal change disease

25
Q

proteinuria with progressive glomerular scarring

A

focal segmental glomerulosclerosis FSGS

early in the disease course, glomerulosclerosis is focal and segmental. With progression, more diffuse and global glomerulosclerosis develops

80% idiopathic primary
- can be HIV or heroin induced as well

26
Q 
nephrotic syndrome
HTN
common in african american
variable degree of decreasing renal function
microscopic hematuria
A

FSGS focal segmental glomerulosclerosis

27
Q

FSGS

LM =
IF =
EM =

A

segmental sclerosis

mild IgM and C3 or negative

diffuse epithelial cell injury

28
Q

how is FSGS different than minimal change

A

FSGS response to steroids is variable (thus differs from minimal change disease in prognosis)

29
Q

deposition of Ag-Ab complexes

A

membranous glomerulopathy

30
Q

membranous glomerulopathy

LM

IF

EM

A

LM: thickened capillary walls; “spikes” on silver stain

IF: granular IgG and C3 along the GBM

EM: subepithelial deposits

31
Q

Membranoproliferative Glomerulonephritis (MPGN)

A

usually nephrotic syndrome with a nephritic component (hematuria)

    • slowly progressive course
    • steroids and immunosuppressive agents NOT effective
    • 50% –> chronic renal failure within 10 yrs
32
Q

mesangial hypercullularity and capillary wall remodeling iwth the formation of double contours =

A

mesangiocapillary glomerulonephritis

aka MPGN

33
Q

type I v. type II MPGN

A

Subendothelial deposits –Type I

or

Intramembranous deposits– Type II
Predominant MESANGIAL involvement

34
Q

LM: “tram tracks” *** (on silver stain)
IF: granular C3 (and often with IgG)
EM: subendothelial and mesangial deposits
– mesangial interpositioning between endothelial cells and GBM

A

MPGN Type I

Granular deposition of IgG and C3 in type I (C3 alone in type II)

Type II — 70% have C3 nephritic factor (C3NeF; an autoantibody which stabilizes C3 convertase, protecting it from enzymatic degradation)
therefore, persistent C3 activation and consumption, causing hypocomplementemia
low serum C3 !!!

35
Q

LM: “tram track” (on silver stain)

IF: C3 only

EM: Intramembrane deposit.
— lamina densa - electron dense material (“dense deposit”)

A

MPGN type II

also see low serum C3

36
Q
  • dark colored urine

- RBC in urine

A

nephritic syndrome

pt may also have renal filure (increased serum creatinine and BUN - acute nephritic syndrome)

37
Q

2 conditions that cause acute nephritic syndrome

A

Diffuse proliferative glomerulonephritis ( Acute post-strep GN )

Crescentic glomerulonepritis
( 1 Goodpasture’s disease
2 Lupus nephritis
3 ANCA-associated diseases)

38
Q

hematuria, azotemia, oliguria, low C3 in children after a latent period of 1-3 weeks following a strep infection

A

ACUTE GLOMERULONEPHRITIS

POST-STREPTOCOCCAL = old term
POST-INFECTIOUS = new term

95% full recovery

39
Q

LM: diffuse proliferative GN with neutrophils

IF: scattered granular (“starry sky”) IgG, IgM, and C3 along GBM and in the mesangium

EM: subepithelial “humps” ***
– IgG, IgM, C3 along GBM FOCALLY

A

Post-strep GN

Enlarged, hypercelluar glomeruli with endothelial and mesangial cell proliferation

40
Q

crescentic

  • antic GBM Ab
  • IC
  • Anti- PMN Ab
A

crescentic GN

components of crescent: Fibrin forms and there is then proliferation of epithelial cells from the parietal wall of Bowman’s capsule, as well as influx of monocytes/macrophages, resulting in crescent formation.

41
Q

linear “cigarette smoke”

capillary loops outlined by linear anti-BM antibody

A 
type I crescentric 
goodpasture disease (antibodies against collagen IV)
42
Q

granular “lumpy-bumpy”

capillary loops outlined by granular immune complex deposits

A

type II crescentic

SLE

43
Q

rapidly progressive glomerulonephritis is most often associated with..

A

crescentic GN

CS4: Exam 1 (12 decks)

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