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RENAL PATHOLOGY 1 Flashcards

Covers glomerular lesions - Powerpoints of Nephrotic, Nephritic and Systemic disorders involving the kidney (58 cards)

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1
Q

4 glomerular diseases presenting as nephritic syndrome

A
  1. Acute Proliferative (Postinfectious and Infection-Associated) Glomerulonephritis
  2. Immunoglobulin A (IgA) nephropathy
  3. Lupus nephritis
  4. Crescentic (Rapidly progressive) glomerulonephritis (RPGN)
    a. Anti-GBM antibody–mediated disease
    b. Complication of any of the immune complex nephritides
    c. Pauci-immune - granulomatosis with polyangiitis, eosinophilic granulomatosis polyangiitis, microscopic polyangitis
    d. Alport syndrome
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2
Q

Pathogenesis of primary membranous nephropathy

A

Antibodies to M-type phospholipase A 2 receptor (PLA 2 R)

Note: PLA2R is a a podocyte transmembrane receptor

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3
Q

Idenitfy the finding shown in the attached image

A

Fatty casts containing cholesterol droplets which are anisotropic and exhibit maltese cross appearance under polarized light.

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4
Q

1. What is your diagnosis?

History of Hep C infection

Palpable purpura + weakness + arthralgias

Type I MPGN

2. What is the composition of the immune complex deposits?

A
  1. Mixed cryoglobulinemic vasculitis
  2. Mixed IgG and IgM complex deposition.
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5
Q

2 key hemodynamic changes assoc with diabetic nephropathy

A

Glomerular hyperfiltration

Glomerular hypertension

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6
Q

List 3 pauci immune crescentic glomerulonephritic lesions

A
  1. Granulomatosis with polyangiitis (formerly Wegener granulomatosis)
  2. Microscopic polyangiitis
  3. Eosinophilic granulomatosis with polyangiitis (formerly Churg Strauss)
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7
Q

Nephritic/ Nephrotic?

Edema, hyperlipidemia

Free fat, oval fat bodies on urinalysis

>3.5g/24 h proteinuria

A

Nephrotic Syndrome

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8
Q

Most common cause of ESRD in the United States

A

Diabetic nephropathy

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9
Q

Pathogenesis of Anti- GBM mediated disease

A

autoantibodies specific for the NC1 domain of the α3 chain of type IV collagen

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10
Q

Characteristic renal morphology assoc with ANCA assoc vasculitis

A

Pauci immune type of crescentic (rapidly progressive) glomerulonephritis

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11
Q

Renal amyloidosis presents as nephrotic or nephritic syndrome?

A

Nephrotic syndrome (60%)

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12
Q

Type of hypersensitivity assoc with Goodpasture syndrome

A

Type II - §complement, and Fc receptor mediated inflammation induces damage.

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13
Q

What is responsible for the finding seen in the image?

A

The image indicates crescent formation.

Crescents form due to proliferation of parietal epithelial cells derived from lining of Bowman’s capsule and influx of macrophages

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14
Q

What’s your diagnosis?

Chronic sinusitis

Hemoptysis

CXR: bilateral nodular and cavitary infiltrates

Hematuria, RBC casts

Renal biopsy: crescentic glomerulonephritis

A

Granulomatosis with polyangiitis (GPA)

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15
Q

Nephritic/ nephrotic?

Glomerular hematuria + RBC casts+ Dysmorphic RBCs+ variable proteinuria +renal insufficiency + hypertension.

A

Nephritic Syndrome

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16
Q

What will you see on Electron microscopy in the condition described?

58 year old male

Nephrotic range proteinuria

Seropositive for Hep B

LM shows uniform , diffuse thickening of the glomerular capillary wall

A

Diagnosis: Membranous nephropathy

EM: Subepithelial deposits, spike and dome pattern

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17
Q

What is the underlying defect associated with the condition described?

Hypertension, RBC casts, Hematuria

Bilateral sensorineural hearing loss

anterior lenticonus

A

Diagnosis: Alport Syndrome

Defect: Mutations that interfere with assembly of type IV collagen

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18
Q

Why does edema develop in nephrotic syndrome?

A

Increased permeability of glomerular capillary wall –>proteinuria–>hypoalbuminemia–>decreased intravascular colloid osmotic pressure–> edema

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19
Q

Why do patients with nephrotic syndrome develop hyperlipidemia?

A

Increased lipoprotein synthesis

Decreased lipid catabolism

Abnormal transport

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20
Q
  1. Type of amyloid assoc with hemodialysis
  2. Most common presentation of amyloidosis assoc with hemodialysis
A
  1. β 2 -microglobulin
  2. Carpal tunnel syndrome
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21
Q

Morphology of spleen in SLE

A

onion skin lesions due to concentric intimal and smooth muscle cell hyperplasia of central penicilliary arteries

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22
Q

1. What’s your diagnosis?

6-10 years, post pharyngeal/ skin infection

LM: See attached image

2. Why is there a decline in the serum concentration of C3 in this condition?

A
  1. Post streptococcal glomerulonephritis
  2. Activation of the complement system and consumption of complement components.
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23
Q

EM finding assoc with dense deposit disease

A

Intramembranous deposition of a ribbonlike, homogeneous, extremely electron-dense material of unknown composition as well as in the mesangium

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24
Q

EM finding in FSGS

Study These Flashcards
A

Effacement of foot processes

25
decreased glycosylation of O-linked glycans in the hinge region of the IgA1 molecule
IgA nephropathy (Berger disease)
26
**Which glomerular lesion of diabetic nephropathy is being described below?** **_LM:_** ovoid or spherical, PAS-positive nodules of mesangial matrix at periphery of the glomerulus
Nodular Glomerulosclerosis aka Kimmelstiel-Wilson disease
27
Most frequent cause of nephrotic syndrome in children
Minimal change disease
28
Chronic sinusitis Hemoptysis CXR: bilateral nodular and cavitary infiltrates Hematuria, RBC casts Renal biopsy: crescentic glomerulonephritis **_Antibodies assoc with this condition?_**
PR3 ANCAs | (Wegener granulomatosis)
29
List 2 important secondary causes for Membranous nephropathy
Drugs- Penicillamine, Gold Infections- Hepatitis B and C
30
List 2 antibodies specific for SLE
Anti dsDNA Anti-Smith
31
Why is nephrotic syndrome assoc with an increased risk of thrombosis?
Loss of AT III in urine
32
What do the immune complex deposits in Berger disease contain?
IgA and C3
33
Type of hypersensitivity mechanisms operational in SLE
1. Type III - caused by immune complexes 2. Type II - Autoantibodies specific for blood cells àopsonize these cells --\>phagocytosis and destruction --\> cytopenias
34
3 secondary causes for FSGS
HIV, Obesity, Sickle cell disease
35
Underlying mechanism of neonatal lupus
transplacental passage of maternal IgG autoantibodies to SSA/Ro and/or SSB/La intracellular ribonuclear proteins
36
Which malignancy may be associated with Minimal change disease?
Hodgkin Lymphoma
37
**What's your diagnosis?** Microscopic hematuria 1-2 days after an URTI Complement levels normal Proteinuria, dysmorphic RBCs, RBC casts are present. LM: See attached image
Diagnosis: IgA nephropathy LM shows mesangial widening due to accumulation of matrix+ immune complex deposits+cell proliferation.
38
earliest clinical sign of the development of diabetic kidney disease
the onset of microalbuminuria
39
4 renal complications of diabetes
1. Diabetic nephropathy 2. Type 4 (hyporeninemic, hypoaldosteronemic) metabolic acidosis with hyperkalemia 3. increased incidence of bacterial and fungal infections of the genitourinary tract 4. increased risk for pyelonephritis 5. papillary necrosis
40
Morphologic finding assoc with diffuse lupus nephritis on Light microscopy
circumferential capillary wall thickening--\> ‘wire looping' Subendothelial deposits Proliferation of epithelial cells- crescents
41
Hereditary FSGS is assoc with which mutation?
Mutations in genes that encode proteins localized to the _slit diaphragm_ – **nephrin, podocin.**
42
Most common cause of glomerulonephritis worldwide
Immunoglobulin A (IgA) nephropathy
43
1 persistent Clinical manifestation of neonatal lupus
Congenital heart block
44
Cause for hypocomplementemia in lupus nephritis
During acute flareups, increased formation of immune complexes results in complement activation, often leading to hypocomplementemia.
45
3 categories of Crescentic (Rapidly Progressive) Glomerulonephritis
I.Anti-GBM antibody mediated II.Immune complex–mediated III.Pauci-immune
46
Most common cause of nephrotic syndrome in the elderly
Membranous nephropathy
47
**What is your diagnosis?** 45 year old male History of Hepatitis C infection Hematuria, periorbital and pedal edema, hypertension LM: Duplication of the basement membrane and hypercellular glomeruli EM: discrete subendothelial deposits IF: IgG and C3 in granular pattern
Type I MPGN
48
**What will you see on EM?** 4 year old child 5g/24h proteinuria that follows a respiratory tract infection
**EM:** effacement of foot processes in visceral epithelial cells
49
What's your diagnosis? asthma, allergic rhinitis, lung infiltrates, peripheral hypereosinophilia, extravascular necrotizing granulomata Increased serum IgE level Renal biopsy: crescentic glomerulonephritis MPO ANCA present
Eosinophilic granulomatosis with polyangiitis
50
IF pattern in Anti-GBM mediated disease
Linear deposits of IgG
51
How does hyperglycemia lead to formation of excess basement membrane material ?
1. Advanced glycation end products (AGEs) bind to RAGE on Tcells and macrophages--\> TGF-beta---\> excess BM material 2. Advanced glycation end products (AGEs) bind to RAGE on vascular smooth muscle cells--\> synthesis of ECM 3. Advanced glycation end products (AGEs) directly cross link ECM proteins--\> resiatnt to digestion--\> accumulate
52
**What's your diagnosis?** Palpable purpura on buttocks and lower extremities Arthritis colicky abdominal pain Renal biopsy: mesangial deposits of IgA
Henoch Schonlein Purpura (IgA vasculitis)
53
Pathogenesis of Dense Deposit Disease (Type II MPGN)
Presence of a circulating autoantibody called C3 nephritic factor
54
Most common cause of idiopathic nephrotic syndrome in adults especially Hispanic and African-American polulation
Focal Segmental Glomerulosclerosis
55
**What's your diagnosis?** 6-10 year old child, post pharyngeal/ skin infection LM: enlarged, hypercellular glomeruli IF: Granular deposits of IgG and C3 **What's the location of deposits on EM?**
Post streptococcal glomerulonephritis _subepithelial_ deposits, forming “humps”
56
Morphologic finding assoc with renal amyloidosis
eosinophilic acellular confluent masses or interlacing broad ribbons in the glomeruli
57
3 hallmark glomerular lesions assoc with diabetic nephropathy
1. Capillary basement membrane thickening 2. Diffuse mesangial sclerosis 3. Nodular glomerulosclerosis
58
Morphology of HIV assoc nephropathy
FSGS+ focal tubular segment dilation filled with proteinaceous material

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