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CPR III > Renal Pathology 3: Glomerular Disease (Dobson) > Flashcards

Renal Pathology 3: Glomerular Disease (Dobson) Flashcards

1
Q

Renal visceral epithelial cells in the corpuscle

A

Podocytes - part of the renal corpuscle that prevents large negatively charged proteins (ex albumin) from being filtered

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2
Q

What are the components of the glomerular basement membrane (GBM)

A

predominantly collagen type IV; laminin, and other proteins

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3
Q

Hyalinosis

A

accumulation of material that is homogenous and eosinophilic by LM; typically this is the end result of various forms of glomerular damage

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4
Q

Sclerosis

A

characterized by the deposition of ECM (type IV) collagen; stains with trichrome stain; typical builds up in mesangial areas (diabetic glomerulosclerosis)

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5
Q

Glomerulosclerosis

A

sclerosis in the mesangial areas (seen in diabetic glomerulosclerosis)

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6
Q

Nephritic Syndromes clinical features

A

Usually sicker;
Hematuria
Proteinuria +/- edema (periorbital)
Azotemia
HTN

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7
Q

Post-streptococcal glomerulonephritis

A

Nephritic syndrome; symptoms occur 1- 3 weeks following a group A strep (strep pyogenes) infection (strep throat - pharyngitis or impetigo - skin infection); deposits are seen in both subendothelium AND subepithelium (“sub epithelium hump”); coca cola hematuria

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8
Q

Goodpature syndrome

A

both kidney and lung involvment; anti-GBM against collagen type IV; IF shows linear pattern; causes RPGN

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9
Q

SLE

A

causes nephritic syndrome (if nephrotic think membranous nephropathy); diffuse proliferative glomerulonephritis is the most common presentation of lupus nephritis; DNA anti-DNA IC deposition; steroid tx

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10
Q

“wire loop” structures on light microscopy

A

DNA anti-DNA IC deposition seen in lupus nephritis that caused diffuse proliferative glomerulonephritis seen in nephritic syndrome

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11
Q

Henoch-Schonlein Purpura (HSP)

A

Nephritic syndrome; causes renal disease similar to IgA nephropathy; IgA vasculitis syndrome characterized by rash, abdominal pain, arthritis and nephritis; characteristic LE palpable purpura;

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12
Q

IgA nephropathy

A

Nephritic syndrome; Berger disease or IgAN; affects children and young adults; IC deposits in the mesangium; upper respiratory or GI infection and then hematuria 1-2 days later; episodic gross hematuria

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13
Q

ANCA disorders

A

Wegener’s granulomatosis (c-ANCA)
Microscopic polyangiitis (p-ANCA)
both can cause RPGN Type III

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14
Q

Nephrotic syndrome clinical features

A

Massive proteinuria ( > 3.5g)
Hypoalbuminemia
Generalized edema
Hyperlipidemia and lipiduria

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15
Q

Membranous Nephropathy

A

most common nephrotic syndrome in white adults; usually idiopathic; antibody binding to PLA2R; can be associated with Hep. B or C, lupus, or drugs. Thick glomerular membranes on H&E (usually thin), due to immune complex deposition; granular IF, “spike and dome” appearance on EM

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16
Q

Minimal Change Disease

A

most common cause of nephrotic syndrome in children; usually idiopathic; may be associated with Hodgkin lymphoma; cytokines mediate damage to the podocytes.

Hallmark: normal glomeruli on H&E stain (barely see any change “minimal”) but may see effacement of the foot processes on EM

Treatment: excellent response to STEROIDS b/c damage is mediated by cytokines

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17
Q

Focal Segmental Glomerulosclerosis (FSGS)

A

most common nephrotic syndrome in Hispanics and African Americans; usually idiopathic; may be associated with HIV, heroin use, and sickle cell disease*.

focal and segmental sclerosis on H&E; effacement of foot processes on EM; does NOT respond to steroids (unlike with minimal change disease); progresses to chronic renal failure

Treated with Renin-Angiotensin System inhibitors

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18
Q

Collapsing variant of FSGS

A

AKA HIV associated nephropathy

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19
Q

Kimmelstiel-Wilson nodules

A

nodular glomerulosclerosis AKA Kimmelstiel-Wilson nodules seen in diabetic nephropathy; basically pink round deposits of laminated mesangial matrix

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20
Q

Membranoproliferative Glomerulonephritis (MPGN)

A

Nephrotic syndrome (mixed) - thick capillary membranes on H&E with a “tram track” or “double-contour” appearance due to immune complex deposition (granular IF); can progress to ESRD

Type 1: HBV/HCV and more often associated with tram track appearance (Nephrotic)
Type 2: C3NeF found in patients. (Nephritic) AKA as dense-deposit disease

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21
Q

“tram track” or “double-contour” appearance on H&E

A

Membranoproliferative Glomerulonephritis (MPGN) type 1 - seen in Nephrotic Syndrome

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22
Q

C3 Nephritic factor

A

C3NeF is associated with type 2 Membranoproliferative Glomerulonephritis (MPGN) in nephritic syndrome AKA dense deposit disease

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23
Q

Alport syndrome

A

X linked inherited defect in type IV collagen (del COL4A5); thinning and splitting of the GBM; “basket-weave” appearance; presents as isolated hematuria, sensory hearing loss and ocular disturbances

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24
Q

Diabetic nephropathy

A

Nephrotic syndrome; nodular glomerulosclerosis by Kimmelstiel-Wilson nodules on LM; leading cause of end-stage renal disease (ESRD)

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25
Q

Treatment for minimal change disease

A

Treatment: excellent response to STERIODS b/c damage is mediated by cytokines; only nephrotic syndrome where you get an excellent response to treatment

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26
Q

Patient with HIV that develops nephrotic syndrome; what is on your differential diagnosis?

A

Focal Segmental Glomerulosclerosis; the most common nephrotic syndrome in Hispanics and African Americans; usually idiopathic; may be associated with HIV*, heroin use, and sickle cell disease.

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27
Q

“spike and dome” appearance on EM

A

Membranous Nephropathy - nephrotic syndrome

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28
Q

Systemic Amyloidosis

A

Amyloid deposits in mesangium resulting in nephrotic syndrome; characterized by apple-green birefringence under polarized light.

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29
Q

In what disorders are subepithelial deposits seen?

A

Membranous glomerulopathy
Minimal change disease (MCD)
Focal segmental glomerulosclerosis (FSGS)

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30
Q

What adaptive changes do you see in acute kidney injury?

A

Hypercellularity; proliferation of mesangial or endothelial cells; and formation of crescents* = RPGN (very quick onset)

31
Q

What adaptive changes do you see in chronic kidney injury?

A

LM: thickening of the capillary walls as seen with PAS staining
EM (better diagnostic tool with chronic injury): deposition of electron-dense material and
-focal nodular glomerulosclerosis with diffuse glomerulosclerosis (diabetes)

32
Q

What differential should come to mind when there is focal nodular glomerulosclerosis with diffuse glomerulosclerosis on EM?

A

Diabetes nephropathy

33
Q

Explain pathophysiology of nephrotic syndrome to L varicocele.

A

decrease of antithrombin III, leads to a hypercoagubule state, renal vein thrombosis (RVT), if L renal vein is involved, can lead to blockage of the L testicular v and can then lead to L varicocele

34
Q

Clinical presentation of Minimal Change Disease

A

10 year old kid who experienced flu-like symptoms about two weeks ago now presents with generalized edema. Check urine and there is proteinuria. Check blood and there is hypoalbuminemia.

35
Q

What would the LM show in the case of Focal Segmental Glomerulosclerosis (FSGS)

A

obliterated capillaries with hyaline deposition; urine test would show non-selective proteinuria.

36
Q
A
37
Q
A
38
Q

the term “diffuse”

A

involving all of the glomeruli in the kidney

39
Q

the term “global”

A

involving the entirety of individual glomeruli

40
Q

the term “focal”

A

involving only a fraction of the glomeruli in the kidney

41
Q

the term “segmental”

A

affecting a part of each glomerulus

42
Q

the term “capillary loop or mesangial”

A

affecting predominantly capillary or mesangial regions

43
Q
A

IF microscopy of classic anti-GBM disease

44
Q

In what disorders are subendothelial deposits seen?

A

lupus nephritis and membranoproliferative glomerulonephritis (MPGN)

45
Q

In what disorders are mesangial deposits seen?

A

IgA nephropathy

46
Q

Podocytopathy is a feature in what types of glomerular injury?

A

Podocytopathy = epithelial cell injury = loss of podocytes
seen in FSGS, HIV, and Diabetic nephropathy

47
Q

the term “granular” on IF should make you think of what?

A

immune complex deposition

48
Q

Where is IgA usually secreted

A

IgA is normally secreted by mucus membranes (think upper respiratory or GI infection)

49
Q

What is a huge characteristic of Henoch-Schonlein Purpura (HSP)?

A

Lower extremity palpable purpura

50
Q

Focal or diffuse mesangial proliferation on microscopy?

A

IgA nephropathy; post-strep GN, membranoproliferative glomerulonephritis (MPGN), dense deposit disease

51
Q

Treatment for IgA

A

Glucocorticoids (steroids)

52
Q

Deposits in both subendothelium AND subepithelium (“sub epithelium hump”) should make you think of what?

A

Post streptococcal glomerulonephritis

53
Q

What test should you order if you suspect Post streptococcal glomerulonephritis?

A

serum anti-STREPtolysin-O (ASO) and anti-DNase B titers (elevated after group A strep infection)

54
Q

What is the most common pattern seen in lupus nephritis?

A

diffuse proliferative glomerulonephritis seen in nephritic syndrome

55
Q

DNA anti-DNA immune complex deposition in the subendothelial space should make you think of what?

A

lupus nephritis that caused diffuse proliferative glomerulonephritis seen in nephritic syndrome

56
Q

LM shows mesangial hypercellularity and enlarged lobular glomeruli should make you think what?

A

Membranoproliferative Glomerulonephritis (MPGN)

57
Q

Dense-deposit disease

A

Membranoproliferative Glomerulonephritis (MPGN) type II; deposition of unknown material in the basement membrane (causes thickening); EM would look like a thick black line

58
Q

Rapidly Progressive Glomerulonephritis (RPGN) on LM

A

segmental necrosis and breaks in the glomerular basement membrane

59
Q

Fibrin deposits and crescent formation should make you think what?

A

Rapidly Progressive Glomerulonephritis (RPGN)

60
Q
A

sub-epithelial hump seen in Post-Streptococcal Glomerulonephritis in Nephritic syndrome; deposits are seen in both subendothelium AND subepithelium

61
Q
A

H&E of crescent-shaped mass, seen in Rapidly Progressive Glomerulonephritis (RPGN) AKA Crescentic glomerulonephritis

62
Q

RPGN Type I

A

Anti-GBM antibody mediated; Goodpasture syndrome; involves kidney and lung; IF linear pattern

63
Q

RPGN Type II

A

Immune complex deposition mediated; think SLE (anti-dsDNA antibodies) or Henoch-Schonlein Purpura (HSP)

64
Q
A

wire loop pattern on LM; SLE (anti-dsDNA); causes RPGN Type II

65
Q
A

IF of IgA deposits in the mesganium; seen IgA nephropathy in nephritic syndrome (Berger Disease)

66
Q

RPGN Type III

A

Glomerular lesions associated with systemic disease; think ANCA disorders; Wegener’s granulomatosis (c-ANCA) and Microscopic polyangiitis (p-ANCA); both will have a negative IF (unlike type I and type II)

67
Q
A

“spike and dome” appearance on EM; membranous nephropathy seen in nephrotic syndrome

68
Q
A

H&E of Focal Segmental Glomerulosclerosis (FSGS) seen in nephrotic syndrome

69
Q
A

Kimmelstiel-Wilson nodules seen in diabetic nephropathy in nephrotic syndrome

70
Q
A

H&E with a “tram track” or “double-contour” appearance due to immune complex deposition; seen in type I MPGN (nephrotic)

71
Q
A

EM of ribbon-like, homogenous, extremely electron-dense material of unknown composition seen in type II MPGN (nephritic) AKA dense deposit disease

72
Q

Isolated hematuria, sensory hearing loss and ocular disturbances in a family should make you think of what?

A

Alport Syndrome; X linked; will see thinning and splitting of the GBM “basket-weave” appearance

73
Q
A

“basket-weave” appearance; thinning and splitting of the GBM as seen in Alport syndrome

CPR III (20 decks)

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