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Renal 2 > Robbins Ch. 20 - Glomerular Disease > Flashcards

Robbins Ch. 20 - Glomerular Disease Flashcards

1
Q

Selective vs. non-selective proteinuria

A

Selective = albumin ONLY

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2
Q

Multiple bands on serum protein electrophoresis (IgG and Kappa regions)

A

Multiple myeloma

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3
Q

Differential Dx for edema

A
  • Kidneys
  • Heart (perfusion)
  • Liver (protein synth)
  • GI (protein absorption)
  • Lungs (fibrosis)
  • Other
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4
Q

4 compartments of kidney

A
  • Glomeruli
  • Tubules
  • Interstitium
  • Vessels
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5
Q

See Bence-Jones proteinuria, think ____

A

Tubular pathology

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6
Q

Light chains of Ig’s deposited in proximal tubules

A

Myeloma kidney

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7
Q

Azotemia

A

Increased serum BUN and creatinine via decreased GFR

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8
Q

Prerenal azotemia

A

Hypoperfusion of kidneys (hemorrhage, shock, volume depletion, CHF) –> azotemia

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9
Q

Post-renal azotemia

A

Obstruction distal to kidney –> azotemia

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10
Q

Uremia

A

Azotemia + other clinical findings and biochemical abnormalities due to renal damage

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11
Q

Rapid decline in GFR

A

Acute kidney injury

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12
Q

See acute kidney injury (AKI), think damage to ______

A

ANY of the 4 areas

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13
Q

Definition of chronic kidney disease

A
  • Diminished GFR (
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14
Q

Severe CKD can present as?

A

Uremia

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15
Q

Definition of end stage renal disease (ESRD)

A

GFR

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16
Q

Typical presentations of glomerular disease (6)

A
  • Nephritic syndrome
  • Nephrotic syndrome
  • Asymptomatic hematuria or proteinuria
  • Chronic renal failure (CKD)
  • Acute renal failure (AKI)
  • Renal tubular defects
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17
Q

Typical presentations of tubulointerstitial disease (6)

A
  • Acute renal failure (AKI)
  • Renal tubular defects
  • UTI
  • Urinary tract obstruction
  • Renal tumors
  • Nephrolithiasis
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18
Q

Nephrotic syndrome

A 
Proteinuria (> 3.5 g/day)
Hypoalbuminemia
Severe edema
Hyperlipidemia
Lipiduria
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19
Q

Nephritic syndrome

A

Hematuria
Azotemia
Oliguria
Hypertension

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20
Q

Rapidly progressive glomerulonephritis (RPGN)

A

Nephritic syndrome
Rapid decline in GFR
Crescent formations

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21
Q

Isolated urinary abnormalities

A
  • Microscopic hematuria
    AND/OR
  • Subnephrotic proteinuria
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22
Q

Chronic renal failure (CKD)

A

Azotemia –> uremia (over several months)

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23
Q

How does the glomerulus respond to injury?

A
  • Hypercellular (proliferation)
  • Basement membrane thickening
  • Hyalinosis (protein deposition) and sclerosis (matrix)
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24
Q

Hypercellular response to glomerular injury

A
  • Mesangial/endothelial proliferation
  • Leukocyte infiltration
  • Crescent (epithelial cell) formations in urinary space (RPGN)
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25
Q

Basement membrane thickening in glomerular injury

A

Electron-dense deposits (immunologic)

  • Ag-Ab complex depositions
  • In situ reactions to Ag’s in BM
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26
Q

In situ reactive feature of BM

A

Collagen type 4

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27
Q

Most common SYSTEMIC diseases w/ glomerular involvement

A
  • SLE

- DM

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28
Q

See glomerular disease + pulmonary bleeding…

Think ______

A
  • Goodpasture syndrome (anti-BM Ab’s)

- Wegener granulomatosis

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29
Q

See nephrotic syndrome…

Think ______

A
  • Membranous glomerulopathy (adult)
  • Minimal-change disease (child)
  • FSGS (adult)
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30
Q

See IgA nephropathy…

Think ______

A
  • Recurrent hematuria or proteinuria
  • Henoch-Schonlein purpura (renal + skin + viscera)
  • Berger disease (renal IgA nephropathy)
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31
Q

See mixed nephrotic/nephritic pattern…

Think ______

A
  • Dense deposit disease (MPGN type 2)
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32
Q

HEREDITARY glomerular diseases

A
  • Alport syndrome

- Thin basement membrane disease

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33
Q

See subepithelial deposits…

Think ______

A
  • Acute glomerulonephritis
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34
Q

See epimembranous deposits…

Think ______

A
  • IN SITU complex deposition (Heymann)
  • Membranous nephropathy
  • Dense deposit disease
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35
Q

See subendothelial deposits…

Think ______

A
  • CIRCULATING complex deposition
  • Lupus nephritis
  • MPGN
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36
Q

See mesangial deposits…

Think ______

A
  • Acute proliferative glomerulonephritis (IgG, C3 deposits)

- IgA nephropathy (IgA deposits)

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37
Q

2 types of ANTIBODY-mediated glomerular injury

A
  • In-situ complex deposition

- Circulating complex deposition

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38
Q

2 types of IN-SITU complex deposition

A
  • Fixed, intrinsic antigen (glomerular BM, other)

- Planted antigen

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39
Q

2 types of CIRCULATING complex deposition

A
  • Endogenous antigens

- Exogenous antigens (drugs, organisms)

40
Q

Other 2 types of glomerular injury besides Ab-mediated

A
  • Cell-mediated

- Alternate complement-mediated

41
Q

See basement membrane deposits…

Think ______

A
  • IN-SITU complex deposition (intrinsic Ag)
  • Anti-GBM
  • Goodpasture syndrome
42
Q

Progression to ESRF presents with what 2 features?

A
  • FSGS

- Tubulointerstitial fibrosis

43
Q

Acute proliferative glomerulonephritis

Pathology presentation

A

Immune complex glomerular injury due to EXOGENOUS antigen

  • Hypercellularity (completely full glomerulus on histo)
  • Leukocyte infiltration (exudate in glomerular tuft)
  • SubEPITHELIAL deposits
  • GRANULAR IgG and C3 in mesangium
44
Q

Acute proliferative glomerulonephritis:

Patient presentation

A
  • Sick Child (6-10 y/o)
  • Previous throat or skin infection
  • Dysmorphic red cells or RBC casts
  • Periorbital edema
  • Oliguria, hematuria, mild proteinuria, mild HTN
45
Q

Typical cause of acute proliferative glomerulonephritis

A

Streptococcal (Beta-hemolytic strep) infection

46
Q

Confirm diagnosis of post-strep APGN

A

ASO titer –> SpeB

47
Q

Treatment of post-strep APGN

A

Water and salt restriction

NOT antibiotics

48
Q

See nephritic syndrome…

Think _______

A
  • Acute proliferative (post-infection) glomerulonephritis

- Rapidly progressive glomerulonephritis

49
Q

Pathologic differences between APGN and RPGN

A

RPGN = CRESCENTS, chronic glomerulosclerosis over time

50
Q

Linear deposits of IgG and C3 in the GBM

A

Type 1 RPGN

51
Q

Linear deposits of IgG and C3 in GBM

Pulmonary hemorrhage

A

Goodpasture syndrome (anti-BM Ab’s)

52
Q

Genetic predisposition to RPGN/goodpasture

A

HLA-DRB1

53
Q

Treatment for type 1 RPGN

A

Plasmapheresis (to remove circulating antibodies)

54
Q

Causes of type 2 RPGN

What type of APGN can progress to RPGN?

A
  • Acute proliferative glomerulonephritis
  • Lupus nephritis
  • IgA nephropathy
  • Henoch-Schonlein purpura

ADULTS with it, NOT kids

55
Q

Type 1 vs. type 2 RPGN

A

Type 1 = Anti-GBM antibody, LINEAR deposits

Type 2 = Immune complex deposition, GRANULAR deposits

56
Q

Treatment for type 2 RPGN

A

Treat underlying disease (NOT plasmapheresis)

57
Q

Dx of type 3 RPGN

A
  • No anti-GBM antibodies or immune complexes

- Circulating ANCAs

58
Q

Only nephrotic syndrome disease with NO hematuria

A

Minimal change disease

59
Q

Common pathologic feature of nephrotic syndrome diseases

A

FOOT PROCESS FUSION

60
Q

MOST COMMON systemic causes of nephrotic syndrome

A
  • Diabetes mellitus

- SLE

61
Q

Primary membranous glomerulopathy:

Genetic causes/factors

A
  • HLA-DQA1

- Anti-PLA2R antibodies

62
Q

Membranous glomerulopathy:

Pathology presentation

A
  • BM (or capillary wall) thickening w/in glomerulus
  • Epimembranous/subepithelial GRANULAR IgG deposits (SPIKE AND DOME)
  • Effaced/fused foot processes
63
Q

Minimal change disease:

Patient presentation

A
  • SEVERE EDEMA
  • CHILD
  • Previous viral respiratory infection or immunization
  • SELECTIVE proteinuria (albuminuria)
64
Q

Minimal change disease:

Pathology presentation

A
  • Foot process fusion

- Lipiduria

65
Q

Patients with minimal change disease can tend to also develop ______

A

Hodgkin (B-cell) lymphoma

66
Q

Treatment of minimal change disease (MCD)

A

Corticosteroids (VERY responsive)

67
Q

Pathophysiology of nephrotic syndrome

A
  • Ab’s against epithelial (podocyte) antigens
  • Injury via cytokines, etc.
  • Foot process fusion + detachment
  • Defective GBM and filtration slits –> proteinuria
68
Q

Patient presentation in FSGS vs. MCD

A
  • ADULT
  • Severe edema
  • Hematuria, reduced GFR, HTN
  • NON-SELECTIVE proteinuria
  • POOR response to corticosteroids
  • Significant progression to CKD
69
Q

HIV-infected individual with glomerular disease

A

FSGS “collapsing variant”

70
Q

MAJOR pathologic difference for FSGS

A

IgM, NOT IgG

71
Q

See nephrotic/nephritic mix…

Think ______

A

Membranoproliferative glomerulonephritis

72
Q

MPGN:

Pathology presentation

A
  • GBM thickening and splitting
  • MESANGIAL cell proliferation –> SPLITS GBM
  • Leukocyte infiltration
  • Accentuation of LOBULAR architecture
73
Q

MPGN type 1 vs. type 2:

Pathology

A

Type 1 = Subendothelial deposits, IgG + C3

Type 2 = Intra-GBM deposits, C3 ONLY

74
Q

Primary MPGN type 1:

Patient presentation

A
  • Child or young adult w/ proteinuria (nephrotic)
  • Microscopic hematuria (nephritic features)
  • Mild HTN
  • Progression to chronic renal failure (50%) over years
75
Q

Secondary MPGN type 1:

Patient presentation

A
  • Adult
  • Chronic antigenemia (infection, autoimmune, neoplasia)
  • Progression to chronic renal failure (50%) over years
76
Q

Causes of antigenemia in secondary MPGN type 1

A
  • Hep C
  • SLE endocarditis
  • CLL, lymphoma, melanoma
  • Neoplasia/cancer
77
Q

MPGN type 2:

Patient presentation

A
  • Child - PRIMARY disease
  • Hematuria (nephritic syndrome)
  • Severe renal disease
  • Poor prognosis
  • Recurrence following renal transplantation
78
Q

Deposits in MPGN type 2

A

C3NeF (“nephritic factor”) = IgG autoAb that binds C3 convertase and ACTIVATES ALTERNATIVE PATHWAY

79
Q

IgA nephropathy:

Pathology presentation

A
  • IgA deposits in mesangium

- Mesangial proliferation and matrix increase

80
Q

Child/young adult (10-30)
Male, causasian or asian
Red/purple blotches on abdomen and buttox
Recurrent hematuria (NO PROGRESSION of renal disease)
Previous URI or visceral infection

A

Henoch-Schonlein purpura (IgA nephropathy)

81
Q

Patients with HSP are known to be at risk for _____

A

Gluten enteropathy and liver disease

82
Q

Most likely glomerular diseases to progress to CGN

A
  1. Crescentic GN (RPGN)
  2. FSGS
  3. MPGN
  4. Membranous nephropathy / IgA nephropathy
  5. Acute proliferative glomerulonephritis
83
Q

Chronic glomerulonephritis

A
  • DIFFUSE, GLOBAL glomerular disease

- Commonly with NO Dx’d antecedent glomerulonephritis

84
Q

See FHx of hematuria or recurrent in childhood…

Think _____

A
  • Alport syndrome

- Thin basement membrane disease

85
Q

Alport syndrome

A
  • IRREGULAR thickened BM (“moth eaten” or “frayed”)

- Vision issues

86
Q

Thin Basement Membrane Disease

A
  • Hematuria via thinned glomerular BMs

- Mutation in collagen type 4

87
Q

Secondary renal diseases (systemic diseases) that present with NEPHROTIC syndrome/PROTEINURIA

A
  • Diabetic neuropathy
  • Hepatitic C (MPGN type 1)
  • HIV (FSGS)
88
Q

Secondary renal diseases (systemic diseases) that present with NEPHRITIC syndrome/HEMATURIA

A
  • SLE
  • Bacterial endocarditis (APGN)
  • Goodpasture (RPGN)
  • HSP (IgA nephropathy)
89
Q

What percentage of ESRD is due to diabetic nephropathy?

What percentage of DM patients progress to ESRD?

A

30%

40%

90
Q

Processes involved in formation of diabetic glomerular lesions

A
  • Metabolic defect in hyperglycemia –> thickened GBM

- Hemodynamic effects from glomerular hypertrophy –> glomerular sclerosis

91
Q

Microscopic pathology of diabetic kidney

A
  1. DIFFUSE THICKENING OF BMs (tubular and glomerular)
  2. Mesangial matrix sclerosis –> compressed capillaries
  3. Nodular glomerulosclerosis (PAS-positive)
  4. Thickened, HYALINIZED arterioles
92
Q

Nodular glomerulosclerosis

A

Diabetic glomerulosclerosis

93
Q

Kimmelstiel-Wilson Disease

A

Diabetic glomerulosclerosis

94
Q

Gross pathology of diabetic kidney

A
  • Diffuse granular, pitted surface

- Thinning of renal cortex

95
Q

Those with diabetic kidney are at risk for what?

Evidenced how?

A

Secondary infections

Irregular cortical depressions 2º to pyelonephritis

96
Q

Does diabetic nephropathy generally affect large or small vessels?

A

SMALL

97
Q

SLE nephritis

A
  • Subendothelial IgG dense deposits (“WIRE LOOPS”)

- Hyperproliferation of glomerulus

Renal 2 (11 decks)

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