9/23- Renal Review 1- Pathology Flashcards

(55 cards)

1
Q

What are characteristics of Acute renal failure?

A
  • Oliguria or anuria
  • Increased BUN and creatinine
  • Decreased GFR
  • Injury of any compartment of the kidney can result in ARF
  • Glomeruli
  • Tubules/Interstitium
  • Vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are characteristics of Chronic renal failure?

A

Prolonged course

  • Diminished reserve, GFR 50%
  • Renal insufficiency, GFR 20-50%
  • Chronic renal failure, GFR <20%
  • End stage, GFR 5%

Systemic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is seen here?

A

Chronic renal failure (Thyroid-like?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What glomerular properties account for the very low urinary protein content or normal urine?

A

Charge barrier

  • GBM negatively charged (Heparan sulphate)
  • Podocyte and endothelium negatively charged (Sialoproteins)

Size barrier

  • Porous GBM
  • Slit diaphragm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the arrows pointing at?

A

Slit diaphragms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the issues at play in nephrotic syndrome (mechanistic)?

A

Charge issues

  • Increased matrix of GBM (with diabetes or electron dense deposits with membranous glomerulopathy)

Podocyte changes

  • Effaced foot processes (minimal change disease, focal segmental glomerulosclerosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the issues at play in nephritic syndrome (mechanistic)?

A

Disruption of capillary loops with spillage of protein and red cells

  • Active urinary sediment Spilled proteins may incite crescent formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are histologic alterations of glomerular injury?

A

Hypercellularity

  • Mesangial cells
  • Endothelial cells
  • Leukocyte infiltrates
  • Crescents

Basement membrane thickening

  • Immune complex deposition
  • Membrane reduplication
  • Increased matrix

Hyalinosis and Sclerosis

  • Extracellular insudated plasma proteins
  • Sclerosis contains collagen
  • FSGS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is seen here?

A

Normal glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is seen here?

A

Hypercellular mesangium

  • Still see open cap loops branching off
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is seen here (what disease does it indicate)?

A

IgA immune deposits in mesangium -> IgA Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is seen here (what disease does it indicate)?

A

IgA nephropathy

  • Mesangial immune deposits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is seen here (what disease does it indicate)?

A

IgA nephropathy

  • Variable, mesangial hypercellularity
  • Ranging to crescents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is seen here?

A

Endocapillary and mesangial proliferation

  • Can’t see cap loops
  • Mesangium all blurred together
  • Looks like catcher’s mitt

Membranoproliferative GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IgA nephropathy with skin rash is what?

A

Henoch-Schonlein purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is seen here?

A

Leukocyte infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is seen here?

A

Crescent formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Crescent Glomerulonephritis/RPGN?

A
  • Variant of acute nephritis
  • Three groups:

1. Immune complex GN

  • SLE
  • Post-infectious
  • IgA/HSP

2. Anti-GBM GN

3. Pauci-immune (ANCA)

  • IF/EM will distinguish
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the #1 cause of crescentic GN?

A

ANCA (Pauci-immune) GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Pauci-immune GN?

A

(ANCA GN)

  • No 1 cause of crescentic GN
  • May be renal limited or systemic (Wegener’s, Churg-Strauss, Microscopic polyangiitis)
  • 80% of pts have circulating ANCA
  • ANCA is pathogenic (mouse studies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is seen here?

A

Increased matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is seen here? Where are deposits?

What diseases are indicated?

A

Left: granular/globular epimembranous distribution (?)

  • Seen in Membranous GN (or lupus or 2’…)

Right: linear epimembranous distribution (?)

  • Seen in Anti-GBM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are possible locations for deposits?

A
  1. Subepithelial (humps)
  2. Epimembranous
  3. Subendothelial
  4. Mesangial
  5. Intramembranous
24
Q

What disease?

A

Membranous GN

25
What disease?
Lupus GN
26
What disease?
IgA nephropathy
27
Where are the deposits?
Epi/intramembranous deposits
28
Where are the deposits?
Subendothelial deposits
29
Where are the deposits?
Mesangial deposits
30
What is this (arrow)?
Subepithelial hump ?
31
What disease is this?
Postinfectious glomerulonephritis
32
What other blood tests would be ordered if suspected postinfectious GN?
- Anti-streptococcal antibody (ASO) titers - Streptozyme - Complements (alternate pathway)
33
What disease is this describing? - Young female presents with shortness of breath and rapid loss of renal function?
- Crescentic glomerulonephritis! - Linear IgG deposits along glomerular BM (also along tubular BM, inset) - This is Anti-GBM disease
34
How do you treat pt with anti-GBM?
- Immunosuppression - Plasmapheresis
35
What antigen is the anti-GBM antibody against? Located where?
Non collagenous portion of the alpha 3 chain of collagen type IV - In GBM - In tubules - In pulmonary system
36
What is seen here?
Membranoproliferative glomerulonephritis
37
What are 2' causes of Membranoproliferative GN?
- Infection (Hepatitis B,C ) - Malignancy (lymphoma, CLL) - Cryoglobulinemia - Hereditary complement deficiency - Alpha -1 antitrypsin deficiency
38
What is seen here?
Type I MPGN - Membrane reduplication (splitting- tram track) - Asterisks = interposition
39
What is seen here?
Type II MPGN - Ribbon like densities (worm-like darkening of GBM)
40
What is seen here?
Global glomerulosclerosis
41
What is seen here?
Segmental glomerulosclerosis
42
What is seen here?
Nodular glomerulosclerosis
43
What is seen here?
Focal Segmental Glomerulosclerosis (pattern)
44
What is seen here?
Podocyte effacement... FSGS
45
What will IF show for FSGS?
Typically negative
46
What are the 1' causes of FSGS? 2'?
_Primary:_ - Inherited mutations (nephrin, podocin) _Secondary:_ - HIV - Heroin - Sickle Cell disease - Obesity - HTN - Reflux nephropathy - Single kidney
47
Reflux of infected urine may cause what?
Pyelonephritis
48
What can cause infection of tubulointerstitial compartment?
- Reflux of infected urine -\> pyelonehpritis - Toxins -\> damage tubular epithelium as urine is concentrated - Allergic reactions from excreted substances - Ischemic injury -\> tubule damage due to their high metabolic demands Degree of tubulointerstitial damage correlates with decline in renal function
49
What is seen here?
AIN- Acute interstitial nephritis - Hypercellular
50
What is seen here?
ATN- Acute tubular necrosis - Pink and dead - Not rich in inflammatory cells - "Just quietly die"
51
What are vascular changes that may affect kidney?
- Flow related changes (e.g. hypertensive changes) - Inflammatory (such as vasculitis) * Remember that the capillary loops of the glomerulus are small vessels and can be inflamed and damaged in vasculitis settings (such as ANCA vasculitis). - Embolic disease * Cholesterol emboli * Septic emboli
52
Thin basement membranes present how?
- Diffuse thinning of GBM - Present with hematuria
53
What is Hereditary nephritis? - Presentation - Pathophysiology - Genetics
Hereditary nephritis - **Hematuria** - **Deafness, ocular** disorders (**Alport** syndrome) - Defective assembly of **type IV collagen** - Most are **X-linked**
54
What is seen here?
"Basket weaving" appearance to GBM in Alport Syndrome (Hereditary Nephritis)
55
Fibrinous vs. fibrinoid
**Fibrinous** (left) - chronic **Fibrin** (right)- acute; pink coagulum of fibrin and serum proteins