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MS2 Renal > 9/23- Renal Review 1- Pathology > Flashcards

9/23- Renal Review 1- Pathology Flashcards

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
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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

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3
Q

What is seen here?

A

Chronic renal failure (Thyroid-like?)

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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
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5
Q

What are the arrows pointing at?

A

Slit diaphragms

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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)
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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
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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
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9
Q

What is seen here?

A

Normal glomerulus

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10
Q

What is seen here?

A

Hypercellular mesangium

  • Still see open cap loops branching off
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11
Q

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

A

IgA immune deposits in mesangium -> IgA Nephropathy

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12
Q

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

A

IgA nephropathy

  • Mesangial immune deposits
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13
Q

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

A

IgA nephropathy

  • Variable, mesangial hypercellularity
  • Ranging to crescents
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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

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15
Q

IgA nephropathy with skin rash is what?

A

Henoch-Schonlein purpura

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16
Q

What is seen here?

A

Leukocyte infiltration

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17
Q

What is seen here?

A

Crescent formation

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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
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19
Q

What is the #1 cause of crescentic GN?

A

ANCA (Pauci-immune) GN

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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)
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21
Q

What is seen here?

A

Increased matrix

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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
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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
Q

What disease?

A

Lupus GN

26
Q

What disease?

A

IgA nephropathy

27
Q

Where are the deposits?

A

Epi/intramembranous deposits

28
Q

Where are the deposits?

A

Subendothelial deposits

29
Q

Where are the deposits?

A

Mesangial deposits

30
Q

What is this (arrow)?

A

Subepithelial hump ?

31
Q

What disease is this?

A

Postinfectious glomerulonephritis

32
Q

What other blood tests would be ordered if suspected postinfectious GN?

A
  • Anti-streptococcal antibody (ASO) titers
  • Streptozyme
  • Complements (alternate pathway)
33
Q

What disease is this describing?

  • Young female presents with shortness of breath and rapid loss of renal function?
A
  • Crescentic glomerulonephritis!
  • Linear IgG deposits along glomerular BM (also along tubular BM, inset)
  • This is Anti-GBM disease
34
Q

How do you treat pt with anti-GBM?

A
  • Immunosuppression
  • Plasmapheresis
35
Q

What antigen is the anti-GBM antibody against?

Located where?

A

Non collagenous portion of the alpha 3 chain of collagen type IV

  • In GBM
  • In tubules
  • In pulmonary system
36
Q

What is seen here?

A

Membranoproliferative glomerulonephritis

37
Q

What are 2’ causes of Membranoproliferative GN?

A
  • Infection (Hepatitis B,C )
  • Malignancy (lymphoma, CLL)
  • Cryoglobulinemia
  • Hereditary complement deficiency
  • Alpha -1 antitrypsin deficiency
38
Q

What is seen here?

A

Type I MPGN

  • Membrane reduplication (splitting- tram track)
  • Asterisks = interposition
39
Q

What is seen here?

A

Type II MPGN

  • Ribbon like densities (worm-like darkening of GBM)
40
Q

What is seen here?

A

Global glomerulosclerosis

41
Q

What is seen here?

A

Segmental glomerulosclerosis

42
Q

What is seen here?

A

Nodular glomerulosclerosis

43
Q

What is seen here?

A

Focal Segmental Glomerulosclerosis (pattern)

44
Q

What is seen here?

A

Podocyte effacement… FSGS

45
Q

What will IF show for FSGS?

A

Typically negative

46
Q

What are the 1’ causes of FSGS? 2’?

A

Primary:

  • Inherited mutations (nephrin, podocin)

Secondary:

  • HIV
  • Heroin
  • Sickle Cell disease
  • Obesity
  • HTN
  • Reflux nephropathy
  • Single kidney
47
Q

Reflux of infected urine may cause what?

A

Pyelonephritis

48
Q

What can cause infection of tubulointerstitial compartment?

A
  • 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
Q

What is seen here?

A

AIN- Acute interstitial nephritis

  • Hypercellular
50
Q

What is seen here?

A

ATN- Acute tubular necrosis

  • Pink and dead
  • Not rich in inflammatory cells
  • “Just quietly die”
51
Q

What are vascular changes that may affect kidney?

A
  • 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
Q

Thin basement membranes present how?

A
  • Diffuse thinning of GBM
  • Present with hematuria
53
Q

What is Hereditary nephritis?

  • Presentation
  • Pathophysiology
  • Genetics
A

Hereditary nephritis

  • Hematuria
  • Deafness, ocular disorders (Alport syndrome)
  • Defective assembly of type IV collagen
  • Most are X-linked
54
Q

What is seen here?

A

“Basket weaving” appearance to GBM in Alport Syndrome (Hereditary Nephritis)

55
Q

Fibrinous vs. fibrinoid

A

Fibrinous (left) - chronic

Fibrin (right)- acute; pink coagulum of fibrin and serum proteins

MS2 Renal (25 decks)

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