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Pathology Block C > Disease of Kidneys I - Nephrotic & Others > Flashcards

Disease of Kidneys I - Nephrotic & Others Flashcards

1
Q

What’s the main difference between nephritic and nephrotic syndromes?

A

nephritic = cellular proliferations

nephrotic = GBM damages (thickened with immune-complex infiltrates

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2
Q

What’s another name for minimal change disease?

A

liponephrosis or Mill disease

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3
Q

What population is at risk for minimal change disease?

A

pediatrics! (#1 cause of nephrotic disease in these patients)

minimal change for the mini people

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4
Q

What can effectively stop proteinuria in minimal change disease? (what’s treatment?)

A

steroids extremely effective - stops within 24hours

can use this as a test and avoid invasive biopsy (tapering off the steroids will not have recurrent proteinuria)

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5
Q

What is minimal change disease associated with?

A

atopic disorders (eczema, rhinitis) and respiratory infections and immunization

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6
Q

Is minimal change disease immune-complex mediated?

A

NO!

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7
Q

What is seen on EM of minimal change disease?

A

effacement of foot processes (looks like the epithelial cell cytoplasm is flattened out)

BM continuous

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8
Q

What is seen in H&E of minimal change disease?

A

looks normal!

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9
Q

What is seen in fluorescence in minimal change disease?

A

NORMAL bc no immune complexes

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10
Q

Why is it called minimal change disease?

A

bc minimal changes! (duh) - only change at ultrastructural level - no immune complexes; no hypercellularity

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11
Q

What’s prognosis for minimal change disease?

A

good

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12
Q

What are some unique characteristics of focal segmental glomerusclerosis?

A

only SOME glomeruli affected - of this, only PARTS/SEGMENTS (patchy)

involves sclerotic/hyalinized lesion (NOT proliferation/cellularity)

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13
Q

Who is normally affected with focal segmental glomerusclerosis?

A

older children, young adults

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14
Q

What disease was focal segmental glomerusclerosis mistakenly subtyped as?

A

minimal change disease

shared characteristic: foot process fusion

differential: it posses focal, sclerotic lesions; recurs when taken off steroids (steroid-dependent); non-selective proteinuria (minimal change is selective - no immunoglobinemia)

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15
Q

What are some other characteristics of focal segmental glomerusclerosis?

A

idiopathic or associated with HIV or other forms of focal glomerulonephritis

may have some nephritic features

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16
Q

What’s seen in H&E of focal segmental glomerulosclerosis?

A

looks okay but have patchy foamy looking sclerosis - sclerotic/hyalinized lesions (not cellular)

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17
Q

What is shown here?

A

FSGS

have adhesions called synechiae- focal lesions on top (in purple) but the rest looks okay

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18
Q

What is seen in fluorescences of focal segmental glomerulosclerosis?

A

NOT immune mediated

but you do see entrapped proteins in sclerotic lesions - LOCALIZED

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19
Q

What is seen in EM of FSGS?

A

similar to minimal change in non-sclerotic segments!

effaced foot process of epithelial cells

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20
Q

What’s the treatmet for FSGS?

A

steroids, supportive

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21
Q

What’s the prognosis for FSGS?

A

poor - recurrence in transplants

tend to progress to global (lesions being fusing together) and chronic

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22
Q

What are the characteristics od mebranous nephrotic disease?

A

most common nephrotic syndrome in adults

idiopathic or secondary (drugs, malignancy, SLE, chronic infections [TB, HBV, HCV, parasites], metabolic disorders [thyroiditis], tumors)

secondary causes chronic antigenmia (Abs form immune complexes that deposits in microvasculature)

subepithelial immune complex deposits

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23
Q

What is seen in H&E of membranous nephrotic disease?

A

no hypercelluarity/prolferation (not nephritic)

looks like normal

24
Q

What’s seen in FM of membranous nephrotic disease?

A

“lighting up like Christmas trees”

diffuse - every glomerulus have granular pattern

25
Q

What’s seen in EM of membranous nephoritic disease?

A

numerous subepithelial immune complex deposits

26
Q

What’s the treatment for membranous nephrotic disease?

A

if secondary, treat underlying disease (try to get Ag complexes cleared); otherwise, supportive

try steroids if idiopathic

27
Q

What’s the prognosis for membranous nephrotic disease?

A

very variable - can be progressive or stabilize - need patient follow-up

28
Q

What’s characteristic of Membranoproliferative GN?

A

have both nephritic and nephrotic features (proliferation and GBM changes)

UA have both RBC and proteins

can be idiopathic or secondary (SLE)

29
Q

What is Type I membranoproliferative GN?

A

66% of the cases - subendothelial deposits on capillary lumen side of BM

30
Q

What is Type II membranoproliferative GN?

A

33% of cases - intramembranous deposits on lamina densa (not really epithelial or endothelial)

31
Q

What is shared between the two types of membranoproliferative GN?

A

clinically indistinguishable - patients present the same, are managed the same and have same prognosis

low complement - both are complement consuming entities (can be consumed in the formation of immune complexes - just like post infectious)

32
Q

What is seen in H&E of MPGN?

A

hypercellularity (lots of black dots)

basket weave BM (split, splintered, duplicated)

membrane damages and proliferation!

endothelial crescents and mesangial cell proliferation

33
Q

What is particularly distinct about MPGN H&E stain?

A

BM duplication! “train track”

34
Q

What is seen in FM of MGPN?

A

lights up everywhere bc there are immune complexes (highly positive immune complex)

can be confused with “pure membranous”​ - so have to look at other diagnostic tests

35
Q

What’s seen on EM for MPGN?

A

expansion of mesangial matrix, duplication of BM

grossly distorted ultrastructure - can’t see foot processes

36
Q

What’s the treatment for MPGN?

A

steroids, immunosuppression, not effective

37
Q

What’s the prognosis for MPGN?

A

poor; progressive (may progress to RPGN clinical pattern); can recur in transplants

38
Q

What’s a major cause of renal morbidity and mortality?

A

diabetes mellitus

39
Q

What is seen secondarily in Diabetes Mellitus?

A

1) nodular glomerulosclerosis (hallmark)
2) arteriolosclerosis
3) papillary necrosis
4) uniformly thickened GBM
5) no immune deposits

40
Q

What is seen in H&E for DM Nephropathy?

A

“basketballs” nodular, rounded hyalinized balls- nodular glomerular necrosis - aka Kimmelstiel-Wilson syndrome (key diagnostic feature of diabetes)

41
Q

What is shown here?

A

diffuse thickening of BM and beginning mesangial expansion before nodules develop (loops around the periphery of hyalinized lesions)

42
Q

What’s seen on EM of DM Nephropathy?

A

thickened BM (about 5-8x thicker than foot) - no dense deposits

43
Q

What is seen in FM of DM Nephropathy?

A

no immune complexes (may have faint staining from passive absorption of Ig in nodules/BM - don’t be mislead!)

44
Q

What are the characteristics of Amyloidosis?

A

deposition of extracellular protein in glomeruli, vessel walls, interstitium

heterogenous composition (non-uniform consistency - there are multiple subtypes)

can be systemic

idiopathic and secondary

nephrotic syndrome

45
Q

What stain is used to visualize amyloidosis?

A

congo red stain

46
Q

What is seen histologically that’s unique to amyloidosis?

A

unique EM structure - nonbranching fibrils

47
Q

What is seen in H&E stain for amyloidosis?

A

diffuse and irregular pink sclerotic/hyaline deposits (not basketball like diabetes)

deposits not confined to glomeruli

48
Q

What’s seen in FM of amyloidosis?

A

light changes may give + immunofluorescence

49
Q

What are the key characteristics of SLE?

A

can mimic ANY form of GN

immune-complex mediated

progressive

significant morbidity and mortality

“the wandering one” - patients manifest differeny symptoms at different times bc different organs are infected at a time

50
Q

How is SLE diagnosed?

A

clinical features NOT renal biopsy

51
Q

What’s the hallmark of SLE?

A

anti-nuclear antibodies (ANA)- explains why disease is multi-systemic (bc it can influenceANY cell that has a nucleus - chromosomal fragments bind to ANA forming complexes that get settled in the various organs)

52
Q

What is seen in H&E of SLE?

A

membranoproliferative pattern (proliferative nephritic) - NON DIAGNOSTIC

sometimes can have crescents (<50%)

53
Q

What’s seen in FM of SLE?

A

membranoproliferative - NON DIAGNOSTIC

54
Q

What is shown here?

A

SLE - indicating that the deposits occur EVERYWHERE subepithelial and subendothelial - nondiagnostic

55
Q

What is shown here?

A

EM of SLE - showing that complexes can be subepithelial

56
Q

What is shown here?

A

EM of SLE - here showing it can be sub-endothelial

57
Q

What is seen in chronic glomerular disease?

A

end stage disease!

diffuse global GN

diffuse tubular atrophy and interstitial fibrosis

etiology may be hard to determine (must look carefully for residual clues)

Pathology Block C (7 decks)

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