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Flashcards in Renal Deck (115)
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31

What is the response to Tx of membranous nephropathy?

poor response to steroids causing chronic renal failure

32

How does membranoproliferative glomerulonephritis present on H&E? EM? IF?

HE: thick glomerular BM often w/ "tram-track" appearance
EM: 2 types based on location of deposits (sub endothelial or intramembranous)
IF: IC deposition = granular IF

33

What is the response to Tx of membranoproliferative GN?

poor response to steroids leads to chronic renal failure

34

Describe the pathophys of renal disease in diabetes mellitus

high glucose leads to NEG of vascular BM causing HYALINE ARTERIOSCLEROSIS (thick wall damages lumen) =>
glomerular EFFERENT arteriole constriction leads to hyperfiltration causing microalbuminuria =>
nephrotic syndrome w/ sclerosis of mesangium => formation of Kimmelstiel Wilson nodules (dense sclerosis)

35

What is the response to Tx of diabetic nephrotic syndrome? why?

ACE like hyaline arteriosclerosis causes efferent constriction so ACE inhibitors slow dz progression

36

How does amyloidosis affect the kidney? How can it be proven to be the cause?

MC systemic organ in systemic amyloidosis=>
amyloid deposits in mesangium causing nephrotic syndrome

Apple-green birefringence under polarized light after Congo red stain

37

If minimal change disease does not respond to steroids, what is the progression?

FSGS

38

Based on the location of any IC deposition, differentiate the the types of nephrotic syndrome

Membranous = sub epithelial deposits (S&D)

Type I MPGN = subendothelial

Type II MPGN = dense deposits in intramembranous portion of glomerulus

39

Type I MPGN is assoc with what?

HBV & HCV

40

Differentiate how HBV & HCV can cause nephrotic syndrome

Membranous nephropathy has sub epithelial deposits w/ spike & dome

type I MPGN has subendothelial deposits

41

Type II MPGN is assoc w/ what? Describe how it gets its appearance on EM

assoc w/ C3 nephritic factor => autoAb stabilizes C3 convertase leading to over activation of complement, inflammation, & LOW circulating C3

binds to intramembranous portion of BM in kidney causing tram-track appearance

42

Define nephritic syndrome

glomerular inflammation & bleeding =>
limited proteinuria (<3.5g/day);
oliguria & azotemia;
salt retention w/ periorbital edema progressing to HTN;
RBC casts & dysmorphic RBC in urine

43

If nephritic syndrome is suspected, how can it be confirmed?

Bx showing hyper cellular & inflamed glomeruli

44

What causes the damage in nephritic syndrome?

IC deposition activates complement leading to C5a attracting neutrophils which cause the damage

45

Differentiate the 2 types of nephritic syndrome that occurs after infections

both occur after infection

post-strept GN arises after GAS of skin or pharynx but can be occur after nonstrept organism as well

IgA nephropathy (Berger dz) occurs after mucosal infection such as gastroenteritis

46

What is the virulence factor that must be present in organism to cause PSGN?

nephritogenic strains must carry M protein virulence factor

47

When & how will patient w/ PSGN present?

2-3wks after infxn w/ hematuria (cola colored), oliguria, HTN & periorbital edema

usually kids but can be in adults

48

What is the appearance of PSGN on HE? EM? IF?

HE: hypercellular, inflamed glomeruli
EM: subepithelial humps
IF: granular = IC deposits

49

What is the Tx for PSGN?

supportive only bc progression is self limited w/ only 1% of kids going to renal failure
but
25% of adults develop rapidly progressive GN (RPGN)

50

What is the timeline for RPGN?

nephritic syndrome to renal failure in wks to months

51

How does RPGN appear on HE? IF?

HE: crescents in Bowman space
IF is variable depending on underlying cause

52

What does a linear pattern on IF assoc w/ RPGN mean? How will it present? why? who is most likely to have this dz?

Goodpasture syndrome => anti-BM Ab

Ab against collagen in glomerular (hematuria) & alveolar (hemoptysis) BM

classically is young, adult males

53

What does a granular pattern on IF in presentation of RPGN?

PSGN or diffuse proliferative GN

54

What is significant about diffuse proliferative GN?

antigen-Ab complex deposition usually sub endothelial

MC type of renal disease in SLE

55

differentiate the types of renal dz seen in SLE. What is significant about renal dz in SLE?

MC COD in SLE

membranous nephropathy is nephrotic w/ granular IF but SUBEPITHELIAL deposits (S&D)

DPGN is nephritic w/ granular IF w/ antigen-Ab complexes but are SUBENDOTHELIAL deposits

56

If a pt presents w/ crescents in Bowman space & negative IF w/ hematuria & slight proteinuria, what should the next test be? What is the Ddx?

C-ANCA => Wegener granulomatosis

P-ANCA => microscopic polyangiitis & Churg Strauss

57

What differentiates the P-ANCA assoc nephritic syndromes?

Churg Strauss has 3 things:
Granulomatous inflammation;
eosinophilia;
asthma

58

What is the MC nephropathy worldwide? present on IF? profession

IgA nephropathy

IgA IC deposits in mesangium of glomeruli

may slowly progress to renal failure

59

How does the IgA nephropathy present typically?

kid w/ episodic gross or microscopic hematuria w/ RBC casts following mucosal infection (gastroenteritis) causing IgA to increase then deposit in mesangium

60

What is an inherited nephritic syndrome? Where is the defect? how does it present?

XLR defect in type IV collagen causing thinning & splitting of glomerular BM

presents w/ isolated hematuria, sensory hearing loss, ocular disturbances