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PATHPROS > RENAL PATHOLOGY 1 > Flashcards

RENAL PATHOLOGY 1 Flashcards

Covers glomerular lesions - Powerpoints of Nephrotic, Nephritic and Systemic disorders involving the kidney

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
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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

A

Effacement of foot processes

25
Q

decreased glycosylation of O-linked glycans in the hinge region of the IgA1 molecule

A

IgA nephropathy (Berger disease)

26
Q

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

A

Nodular Glomerulosclerosis aka Kimmelstiel-Wilson disease

27
Q

Most frequent cause of nephrotic syndrome in children

A

Minimal change disease

28
Q

Chronic sinusitis

Hemoptysis

CXR: bilateral nodular and cavitary infiltrates

Hematuria, RBC casts

Renal biopsy: crescentic glomerulonephritis

Antibodies assoc with this condition?

A

PR3 ANCAs

(Wegener granulomatosis)

29
Q

List 2 important secondary causes for Membranous nephropathy

A

Drugs- Penicillamine, Gold

Infections- Hepatitis B and C

30
Q

List 2 antibodies specific for SLE

A

Anti dsDNA

Anti-Smith

31
Q

Why is nephrotic syndrome assoc with an increased risk of thrombosis?

A

Loss of AT III in urine

32
Q

What do the immune complex deposits in Berger disease contain?

A

IgA and C3

33
Q

Type of hypersensitivity mechanisms operational in SLE

A
  1. Type III - caused by immune complexes
  2. Type II - Autoantibodies specific for blood cells àopsonize these cells –>phagocytosis and destruction –> cytopenias
34
Q

3 secondary causes for FSGS

A

HIV, Obesity, Sickle cell disease

35
Q

Underlying mechanism of neonatal lupus

A

transplacental passage of maternal IgG autoantibodies to SSA/Ro and/or SSB/La intracellular ribonuclear proteins

36
Q

Which malignancy may be associated with Minimal change disease?

A

Hodgkin Lymphoma

37
Q

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

A

Diagnosis: IgA nephropathy

LM shows mesangial widening due to accumulation of amtrix+ immune complex deposits+cell proliferation.

38
Q

earliest clinical sign of the development of diabetic kidney disease

A

the onset of microalbuminuria

39
Q

4 renal complications of diabetes

A
  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
Q

Morphologic finding assoc with diffuse lupus nephritis on Light microscopy

A

circumferential capillary wall thickening–> ‘wire looping’

Subendothelial deposits

Proliferation of epithelial cells- crescents

41
Q

Hereditary FSGS is assoc with which mutation?

A

Mutations in genes that encode proteins localized to the slit diaphragm – nephrin, podocin.

42
Q

Most common cause of glomerulonephritis worldwide

A

Immunoglobulin A (IgA) nephropathy

43
Q

1 persistent Clinical manifestation of neonatal lupus

A

Congenital heart block

44
Q

Cause for hypocomplementemia in lupus nephritis

A

During acute flareups, increased formation of immune complexes results in complement activation, often leading to hypocomplementemia.

45
Q

3 categories of Crescentic (Rapidly Progressive) Glomerulonephritis

A

I.Anti-GBM antibody mediated

II.Immune complex–mediated

III.Pauci-immune

46
Q

Most common cause of nephrotic syndrome in the elderly

A

Membranous nephropathy

47
Q

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

A

Type I MPGN

48
Q

What will you see on EM?

4 year old child

5g/24h proteinuria that follows a respiratory tract infection

A

EM: effacement of foot processes in visceral epithelial cells

49
Q

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

A

Eosinophilic granulomatosis with polyangiitis

50
Q

IF pattern in Anti-GBM mediated disease

A

Linear deposits of IgG

51
Q

How does hyperglycemia lead to formation of excess basement membrane material ?

A
  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
Q

What’s your diagnosis?

Palpable purpura on buttocks and lower extremities

Arthritis

colicky abdominal pain

Renal biopsy: mesangial deposits of IgA

A

Henoch Schonlein Purpura (IgA vasculitis)

53
Q

Pathogenesis of Dense Deposit Disease (Type II MPGN)

A

Presence of a circulating autoantibody called C3 nephritic factor

54
Q

Most common cause of idiopathic nephrotic syndrome in adults especially Hispanic and African-American polulation

A

Focal Segmental Glomerulosclerosis

55
Q

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?

A

Post streptococcal glomerulonephritis

subepithelial deposits, forming “humps”

56
Q

Morphologic finding assoc with renal amyloidosis

A

eosinophilic acellular confluent masses or interlacing broad ribbons in the glomeruli

57
Q

3 hallmark glomerular lesions assoc with diabetic nephropathy

A
  1. Capillary basement membrane thickening
  2. Diffuse mesangial sclerosis
  3. Nodular glomerulosclerosis
58
Q

Morphology of HIV assoc nephropathy

A

FSGS+ focal tubular segment dilation filled with proteinaceous material

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