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CVPR > Renal Week 1 - Nephrotic/nephritic > Flashcards

Renal Week 1 - Nephrotic/nephritic Flashcards

1
Q

2 protein components of podocyte slit diaphragm

A

Nephrin

Podocin

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2
Q

Classic and common mechanisms of pitting edema in nephrotic syndrome

A

Classic (low V, low P): low serum albumin -> low oncotic pressure -> fluid leaks out -> increased ADH/Na retention -> more fluid out
Common (high V, high P): primary defect in Na excretion -> retention

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3
Q

Complications of nephrotic syndrome

A 
Hypercoagulable state: protein deficiency, increased ATIII production and renal vein thrombosis
Infection (loss of Ig and complement)
Decreased vitamin D
Hypercholesterolemia
HypoNa/K
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4
Q

Management of nephrotic syndrome

A 
Low salt diet
Diuretics
BP control
Decrease GFR (ACEI)
Replace Vit D binding proteins
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5
Q

Hereditary Nephrotic Syndrome

A

Mostly kids
Mutation in nephrin or podocin
Foot process fusion on EM

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6
Q

Minimal change dz: age, UA, cell markers/pathogenesis

A 
2-8 years old
UA: 4+ protein, hyaline casts
CD-80 expression on podocytes (usually on APCs)
Foot process fusion on EM
Circulating factor damaging podocyte
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7
Q

Associations of minimal change dz

A

Allergy
Hodgkin’s Lymphoma
NSAIDs

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8
Q

Treatment of minimal change dz

A

Steroids

Course of oral cytoxan for frequent relapsers

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9
Q

FSGS: age, UA, pathogenesis

A

20-40 years
UA: 4+ protein, hyaline casts, micro hem
Viral factor: HIV infecting podocyte
Genetic factor: APOL1 polymorphism (AA, sleeping sickness protection)

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10
Q

FSGS associations

A 
Idiopathic
HIV associated
Sickle cell
Obesity
Heroin nephropathy
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11
Q

FSGS treatment

A

Steroids
Calcineurin inhibitors or other immunosuppresion
Anti-viral for HIV

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12
Q

HIV Nephropathy

A

FSGS
Tubular dilation
Reticulo-endothelial inclusions

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13
Q

Membranous nephropathy associations

A 
Idiopathic
CA (Lung esp)
Lupus
Hep B (tx interferon)
Heavy metals
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14
Q

Membranous nephropathy: age, pathogenesis

A 
Adults
Immune complex disease
Thickened BM
Subepithelial deposits on podocyte side of BM (granular deposits on IF)
Ab binding to PL A2 podocyte receptor
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15
Q

Membranoproliferative GN type I associations

A

Hep C (autoimmune, palpable purpura)
Low grade systemic infection
Neoplasm
CT disease (lupus)

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16
Q

MPGN type I presentation, pathogenesis

A

Endothelial deposits (WBC)
Complement is low due to activation (C3 and C4)
GBM thickening and hypercellularity

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17
Q

MPGN type II

A

Same presentation at type I

Low C3, nml C4 -> alternative pathway activation

18
Q

Nephrotic syndromes: primary renal dz

A 
Hereditary
MCD
FSGS
MN
MPGN (I and II)
19
Q

Nephrotic syndromes: systemic

A

Diabetes
Amyloid and Light chain dz
SLE (membranous)

20
Q

Nephritic syndromes: primary renal

A

Post strep GN
IgA nephropathy
RPGN (anti-GBM, idiopathic)

21
Q

Nephritic syndromes: systemic

A 
Vasculitis (ANCA associated)
Immune complex (SLE, HSP)
22
Q

Nephrotic syndrome: overall theme and major criteria

A

Increased glomerular permeability

  1. Albuminuria
  2. Hypoalbuminemia
  3. Edema
  4. Hyperlipidemia
23
Q

Nephrotic mechanisms of injury

A

Non-inflammatory
Podocyte injury and retraction: loss of size selectivity and loss of polyanion
Injury to clathrin pit, absorbed and secreted as deposit
Progress into CRF

24
Q

Renal amyloidosis: types, path, stain

A 
Kidney involved in 85%
Different LC types: AA/AL
Fluffy pink in glomeruli and vessels
Red congo stain/polarized light/granny apple green
Spilled uncooked spaghetti
25
Q

Causes of chronic renal failure

A

Most common: diabetes

Next: vascular/HTN dz

26
Q

DM in CRF

A

Hyaline arteriolar disease (increased thickness)

Diabetic GS: hypercellularity, diffuse/nodular mesangial expansion, BM thickening

27
Q

Uremia definition

A

Group of manifestations with severe loss of all renal functions

28
Q

Nephritic syndrome: major criteria

A

Hematuria (RBC and casts)

29
Q

Signs of aggressive disease and usual association

A

RPGN (2x Scr or 50%

30
Q

Treatment of nephritic syndrome

A

Treat symptoms
Immunosuppression
Plasma exchange

31
Q

4 examples of glomerulonephritis

A

IgA nephropathy (HSP = systemic,

32
Q

IgA nephropathy: deposition, prognosis, type

A

Mesangial immune complex deposition
Focal
30% regress, 30% to ESRD, 40% chronic renal dz
Nephritic or nephrotic

33
Q

Lupus nephritis: deposition, presentation, type, pathoneumonic finding

A

Mesangial (hematuria)
Subendothelial (hematuria, nephritic syndrome)
Subepithelial (proteinuria)
>90% scarring -> nephritic and progressive failure
Nephritic or nephrotic or both
Pathoneumonic = tubuloreticular body

34
Q

Anti-GBM disease: deposition, presentation

A

Antibody to glomerular antigen (linear)
Usually bad: pulmonary-renal, crescents, RPGN
Big treatment

35
Q

ANCA associated vasculitis: deposition, presentation, unique treatment

A

ANCA but few immune complexes seen
Usually bad: pulmonary-renal, RPGN
Normal treatment + B cell targeted therapy

36
Q

ANCA vasculitis examples

A

Granulomatosis with polyangiitis (C-ANCA, PR3)
Microscopic polyangiitis (P-ANCA, MPO)
Eosinophilc granulomatosis (Churg-Strauss)(more P-ANCA)
Renal limited vasculitis (usually P-ANCA)

37
Q

Two diseases that mimic nephritic dz

A

Benign Familial Hemauria (thin BM dz)
Alport’s dz (nephritis, deaf, ocular lesions)
Collagen IV mutation, basket-weave pattern on microscopy

38
Q

Proliferative glomerulonephritis: types and consequences

A

Endocapillary: occlusion of capillary loops
Mesangial: >3 nuclei in space
Epithelial: crescents, fill Bowman’s space

39
Q

Post-infectious GN: etiology, morphology, stain, tx

A

Post strep, acute nephritic
Diffuse proliferative
Starry sky on IF
Supportive therapy

40
Q

IF Staining and diseases

A

Linear: Goodpasture’s, Anti-GBM
Granular: IgA, SLE, endocarditis, idiopathic
None: vasculitis, idiopathic

41
Q

Renal lupus WHO classes

A 
I = no change
II = mesagnial glomerulitis
III = Focal, segmental
IV = Diffuse (>55%)
V = membranous

CVPR (5 decks)

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