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Renal > Nephrotic > Flashcards

Nephrotic Flashcards

1
Q

5 primary renal nephrotic

A

Hereditary Nephrotic Syndromes

Minimal change disease

Focal Segmental Glomerulosclerosis

Membranous nephropathy

Membranoprolifeartive GN

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2
Q

3 systemic nephrotic

A

Diabetes

Amyloid and Light Chain

SLE (membranous)

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3
Q

3 Primary renal Nephritic

A

Post Infectious
IgA
Rapid Progressive GN

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4
Q

2 systemic Nephritic

A 
Vasculitis (ANCA)
Immune Complex (SLE / HSP)
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5
Q

Nephrotic Syndrome - is BV low?

A

No - edema without low BV because primary problem is with salt excretion

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6
Q

5 SIGNS NEPHROTIC

A 
Prtoeinuria
Hypoalbuminemia 
Lipiduria (oval fat bodies)
Hyperlipidemia 
Edema
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7
Q

Complications of nephrotic

A

Hypercoagulable
Infection
Decreased VitD

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8
Q

Management nephrotic

A

ACE-I helps proteinuria (even though drops GFR a tiny bit due to efferent constriction - the drop in proteinuria is worth it)

Low Salt

Diuretics

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9
Q

Most common children

A

MCD

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10
Q

Most common adults

A

Membranous and FSGS

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11
Q

Hereditary nephrotic

presentation

A

infant / child
edema
FtoT
polyhydraminos on ultrasound

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12
Q

Hereditary nephrotic

etiology

A

mutations in nephrin / podocin

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13
Q

Minimal change disease

presentation

A

2-8y/o
edema / ascites / weight gain
normal blood pressure

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14
Q

MCD

Labs

A

renal function normal or slightly depressed

urinalsyis - 4+ protein, hyaline casts, microscopic hematuria (Rare)

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15
Q

MCD associations

A

allergy/atopy
Hodgkins
NSAIDS

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16
Q

MCD Patho

A

circulating permeability factor
leads to podocyte injury
(foot process fusion - expression of CD80 in podocytes)

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17
Q

MCD treatment

A

steroids (prednisone)

short course cytoxan if relapse

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18
Q

MCD
LM
IF
EM

A

LM - normal
IF - negative
EM - foot process fusion

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19
Q

FSGS

Labs

A

renal function normal or slightly depressed

4+ protein, hyaline casts, microscopic hematuria

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20
Q

FSGS associations

A

usually idiopathic

HIV

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21
Q

FSGS pathophsyiology

A

ciruclating factor (unknown)
Viral factor in HIV
APOL1

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22
Q

FSGS treatment

A

steroids - does not respond well to treatment

Calcineurin inhibitors / MMF

23
Q

HIV nephropathy

presents as FSGS - additional characteristics?

A

collapsed glomerular tuft
cystic tubules
tubuloreticular inclusions (reticuloendothelial)

RESPONDS to antivirals

24
Q

Membranous nephropathy

associations

A

cancer / lupus / hepB/ Hg

25
Q

membranous nephropathy

histology

A

biopsy shows BM thickening - normocellular - granular immune complex deposits that are subepithelial

26
Q

Treatment MN?

A

Steroids and cytoxin (as is immune complex mediated)

27
Q

GRANULAR DEPOSITS - SUBEPITHEIAL

A

Membranous

28
Q

what test should you do on patients with membranous?

A

cancer screen

29
Q

pathogeneis membranous?

A

Antibody to PLA2R on podocyte which is then shed and lodges in subepithelium -

30
Q

mercury linked to?

A

membranous

31
Q

HBV linked to?

A

membranous

deposits contain HBe antigen

32
Q

Membranoproliferative GN

presentation

A

HTN

Mildly reduced renal function

33
Q

MPGN Type I

associations

A

HCV
(low C3 and C4 AND + RF)
low grade infection
idiopathic

34
Q

MPGN pathology

A

GBM thickening
hypercellularity
granular immune complex deposits (SUBENDOTHELIAL)

35
Q

MPGN treatment

A

treat HCV

Steroids

36
Q

nephrotic that is HTN

A

MPGN

37
Q

MPGN type 1

complement?

A

low c3 and c4

classic pathway

38
Q

MPGN type 2

complement disorder

A

low c3 normal c4 (because activates alternate)

usually childhood

39
Q

nephrotic syndrome blood anomalies?

A

in addition to the loss of protein we see hypercholesteremia / hypokalemia / hyponatremai

40
Q

what happens to the glomerulus in nephrotic syndrome?

A

epithelial cell detachment and BM degradation - loss of polyanion

41
Q

Pathogenesis of Glomerular injury? MCD/FSGS

A 
Non-inflammatory 
circulating factors/Ig's bind GEC membranes and or GBM without fixing complement
--> loss of polyanion 
--> GEC detachment 
(MCD/FSGS)
42
Q

Pathogenesis of Glomerular injury in membranous

A

Non-inflammatory
complement fixing anti-GEC Ab’s
alternative complement pathway
may involve oxidants/proteases

43
Q 
minimal change nephropathy
clinical
morph
EM
IF
Tx/Prog
A 
nephrotic syndrome
no change
EM - foot process effacment
IF negative
steroids/good

some circulating factor that we don’t know - CD80 starts to show

44
Q

FSGS
cause
treatment

A

unknown CF
can also be due to HIV/Heroine/hyperfiltration in late stage renal disease
steroids - relapse common

45
Q

Membranous

A 
circulating immunoglobulins attack podocyte PLA2R
Subepithelial 
spikes / bm thickening
stain c3/5 - granular BM
Steroids
46
Q

Membranous 85% idio

15% other?

A

bugs
drugs
tumors
rheum

47
Q

MPGN
morph
path
treat

A

GBM thickening - double countour

chronic immune complex subendo deposition

IF - Granular GBM

STeroid / interferon

48
Q

MPGN common cause

A

hepB
sle
cryoglobin

49
Q

what % of amyloidosis cases have renal involvemnet and how does it present?

A

85%
proteinuria - histology shows amorphous pink material in glomeruli and vessels - birefrigenence green - congo red
EM - Spaghetti

50
Q

most common cause of esrd

A 
diabetes (38%)
HTN/Vascular (25%)
GN (19%)
Interstitial nephritis (4%)
PCKD (5%)
Other (9%)
51
Q

DM

kidney lesions

A

hyaline arteriolar disease
glomerulosclerosis - diffuse or nodular expansion of mesangium
BM thickening

52
Q

Kinnelsteil Wilson nodules care characteristic of

A

glomerular disease in DM

53
Q

Malignant HTN renal disease

A

vascular insult –> fibrinoid necrosis and hyperplastic arteriolitis - onion –> kidneys release renin exacerbating problem

54
Q

HTN renal disease

A

finely granular surface scarring - scarred glomeruli

hyaline depot in vessels and medial / intimal thickening

Renal (6 decks)

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