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Renal Pathology > Glomerular Diseases > Flashcards

Glomerular Diseases Flashcards

1
Q

Renal disease is divided into diseases of?

A
  1. glomeruli
  2. tubules
  3. interstitium
  4. vessels
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2
Q

Glomerular diseases are caused mainly by?

A

immunologically mediated

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3
Q

Tubular and interstitial disorders are often due to?

A

toxins or infections

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4
Q

How do glomerular and tubular diseases affect each other?

A
  1. glomerular disease impairs the tubular blood supply and increases tubular toxins
  2. tubular disease causes increased intraglomerular pressure
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5
Q

Describe how vascular disorders affect glomerular function?

A

decreases the amount of filtrate

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6
Q

What is Azotemia?

A

Increased serum BUN (blood urea nitrogen) and creatinine, due to reduced glomerular filtration rate
- causes are pre-renal, renal and post-renal

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7
Q

What is uremia?

A

Azotemia plus clinical signs/symptoms
- gastroenteritis, peripheral neuropathy,
fibrinous pericarditis

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8
Q

What is acute renal failure?

A

Abrupt anuria or oliguria with rapidly progressive azotemia identified by increase in BUN or ammonia
- urine output < 400 ml/24 hr

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9
Q

What are the causes of acute renal failure?

A
  1. Vascular obstruction (polyarteritis nodosa, malignant hypertension, hemolytic-uremic syndrome)
  2. Rapidly progressive glomerulonephritis
  3. Acute tubular necrosis
  4. Acute tubulointerstitial nephritis
  5. Pyelonephritis with papillary necrosis
  6. DIC
  7. Urinary obstruction
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10
Q

What is chronic renal failure?

A

Azotemia progressing to uremia over a period of years

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11
Q

What are the stages of chronic renal failure?

A
  1. diminished renal reserve (GFR 50% normal) with normal BUN/Cr,
  2. renal insufficiency - azotemia, anemia, hypertension, polyuria, nocturia,
  3. renal failure: GFR < 20% normal, kidneys cannot regulate volume or solutes and patients develop edema, metabolic acidosis and hypocalcemia,
  4. end stage renal disease: GFR <5% normal, represents the end stage of various renal diseases
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12
Q

What is nephrotic syndrome?

A

Proteinuria > 3.5 g/day

  • hypoalbuminemia (serum level <3 g/dl)
  • hyperlipidemia
  • lipiduria
  • severe edema (anasarca)
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13
Q

What is the pathophysiology of nephrotic syndrome?

A
  1. Increased permeability to plasma proteins cause massive proteinuria, hypoalbuminemia and generalized edema (pitting, periorbital & dependent edema)
  2. Hyperlipidemia due to increased lipoprotein synthesis and decreased catabolism
  3. Lipiduria due to leakage of lipoproteins with albumin
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14
Q

What is nephritic syndrome?

A

Grossly visible hematuria, hypertension, variable proteinuria, azotemia, oliguria, edema, RBC casts

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15
Q

Name categories under Primary Diseases?

A
  1. Diseases associated with Nephrotic syndrome

2. Diseases associated with Nephritic syndrome

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16
Q

Name the diseases associated with nephrotic syndrome?

A
  1. Minimal change disease
  2. Focal segmental glomerulonephritis
  3. Membraneous glomerulonephritis
  4. Systemic disease (SLE, diabetes,
    amyloidosis)
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17
Q

Name the disease associated with Nephritic syndrome?

A
  1. Acute diffuse proliferative glomerulonephritis (post-streptococcal or not)
  2. Rapidly progressive (crescentic) glomerulonephritis
  3. Membranoproliferative glomerulonephritis
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18
Q

Name secondary renal diseases?

A

Systemic lupus erythematosus (SLE), diabetes, amyloidosis, polyarteritis nodosa, Goodpasture syndrome, Wegener granulomatosis, Henoch-Schonlein purpura, bacterial endocarditis

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19
Q

Name hereditary glomerular diseases?

A

Alport syndrome, thin membrane disease, Fabry disease

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20
Q

What are the microscopic manifestations of kidney disease?

A
  1. hypercellularity
  2. basement membrane thickening
  3. hyalinization and sclerosis of glomeruli
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21
Q

Describe hypercellularity?

A
  • cellular proliferation
  • white blood cells (acute and chronic),
  • crescents (white blood cells and epithelial cells)
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22
Q

Describe basement membrane thickening?

A
  1. highlighted by PAS stain and electron microscopy;

2. EM also shows electron-dense deposits (usually immune complexes) in or adjacent to basement membrane

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23
Q

What is hyalinization and sclerosis of glomeruli?

A 
end result of glomerular damage
Changes can be:  
 - diffuse (all glomeruli) or focal;
 - global (entire glomerulus)
 - segmental (part of glomerulus) or mesangial
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24
Q

Describe the pathogenesis of glomerular injury?

A

Usually immune mediated via antibody deposition , or cell mediated injury
- Antibodies deposited are either to insitu
antigens or circulating immune complexes

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25
Q

Insitu antigens are?

A
  1. Intrinsic (part of the basement membrane)
  2. Planted antigens - deposited in basement membrane
    • may be exogenous (drugs, infectious
      agents) or endogenous (DNA,
      immunoglobulin, immune complexes)
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26
Q

Circulating immune complexes are?

A
  1. endogenous (DNA, tumors)
  2. exogenous (infectious products)
    • deposits are usually mesangial or
      subendothelial, resolve by macrophage
      phagocytosis
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27
Q

Minimal change disease is also known as?

A

lipoid necrosis, nil disease, foot process disease

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28
Q

What is minimal change disease?

A

disorder where there is damage to the glomeruli

- the damage can not be seen under a regular microscope but only an electron microscope

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29
Q

Describe the epidemiology of minimal change disease?

A

Causes 80% of cases of nephrotic syndrome in children (usually ages 2-6) and 20% in adults

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30
Q

What are the causes of minimal change disease?

A

Associated with respiratory infections, immunizations, allergies, NSAID usage, acute interstitial nephritis, Hodgkin lymphoma

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31
Q

Describe the clinical presentation of minimal change disease?

A

nephrotic syndrome, selective for albumin, often with severe edema or proteinuria, but with minimal microscopic glomerular alterations and usually no hypertension, no hematuria, no azotemia

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32
Q

Describe the micro morphology of minimal change diseases?

A
  1. normal glomeruli

2. tubules have lipid droplets due to reabsorption of lipoproteins that leak from glomeruli (“lipoid nephrosis”)

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33
Q

What is seen under immunofluorescence of minimal change disease?

A

negative

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34
Q

What is seen under the electron microscope of minimal change disease?

A

Extensive foot process fusion; microvillous transformation of epithelial cells

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35
Q

Describe the treatment of minimal change disease?

A

90% of children respond to steriods initially (foot processes return to normal), some children become steroid dependent/resistant, but this usually resolves at puberty
- Older adults with hypertension and severe proteinuria have a higher risk of reversible renal failure

36
Q

What is focal segmental glomerulosclerosis?

A

A histologic pattern of glomerulosclerosis (some glomeruli, part of capillary tuft) associated with heavy proteinuria

37
Q

What is the clinical settings for FSGS?

A

HIV, IgA nephropathy, hypertension, sickle cell disease, morbid obesity, obstruction, reflux, congenital or idiopathic

38
Q

Describe the epidemiology of FSGS?

A

Children have better prognosis than adults

39
Q

What are the causes of FSGS?

A

May be a continuum with minimal change disease

40
Q

Describe the micro morphology of FSGS?

A
  1. Segmental sclerosis, hyaline deposits and foam cells or lipoid droplets in focal glomeruli
  2. focal tubular atrophy with interstitial fibrosis, hyaline thickening of afferent arterioles
41
Q

What is seen in the immunofluorescence of FSGS?

A

IgM and C3 in sclerotic segments

42
Q

Describe the prevalence of HIV associated nephropathy?

A

10+%

- up to half or more renal biopsies show it

43
Q

When is HIV associated nephropathy seen?

A

before AIDS

44
Q

What causes HIV associated nephropathy?

A

anti-HIV Abs

45
Q

What is the microscopic morphology seen in HIV associated nephropathy?

A

typical lesion is focal segmental glomerulosclerosis (FSGS)

– accompanied by characteristic collapse of capillaries

46
Q

Describe the clinical presentation of HIV Associated nephropathy?

A

usually proteinuria, maybe severe enough to cause nephrotic syndrome

47
Q

Describe the prognosis of HIV associated nephropathy?

A

worse in adults

- patients with HIV can have a variety of other renal problems

48
Q

What is membranous glomerulonephritis?

A

when the small blood vessels in the glomeruli which filter wastes in the blood become damaged and thickened
- Most common cause of nephrotic syndrome in adults due to in situ immune complexes in GBM

49
Q

What are the causes of membranous glomerulonephritis?

A

85% are idiopathic autoimmune disease

50
Q

Secondary cases of membranous glomerulonephritis are associated with?

A
  1. cancer ( lung, colon, melanoma)
  2. hepatitis B/C, malaria
  3. schistosomiasis
  4. drugs
  5. SLE
  6. diabetes
  7. thyroiditis
    - it causes 40% of cases in adults, 5% in
    children
50
Q

What is seen microscopically in membranous glomerulonephritis?

A
  • uniform diffuse capillary wall thickening without hypercellularity and without mesangial sclerosis - narrow capillary lumina
  • glomerular spikes
  • Proximal convoluted tubules contain hyaline droplets, reflecting protein re-absorption
50
Q

What is seen in the immunofluoresence of membranous glomerulonephritis?

A

granular diffuse peripheral deposits

- IgG and C3

51
Q

Describe the clinical course of membranous glomerulonephritis?

A

insidious onset of nephrotic syndrome

- must rule out secondary causes

52
Q

What is post-streptococcal glomerulonephritis?

A

Deposition of immune complexes from antibodies against organisms
- Aka post-infectious or acute glomerulonephritis

53
Q

Post-streptococcal glomerulonephritis is associated with what conditions?

A
  1. nephritogenic strains of Streptococcus pyogenes (beta hemolytic Strep group A)
  2. endemic malaria, toxoplasmosis, hepatitis B/C, HIV, varicella, spirochetes
54
Q

Describe post-streptococcal glomerulonephritis in children age 6-10?

A
  1. abrupt onset of hematuria, oliguria, fever, malaise and nausea 1-4 weeks after strep infection of pharynx or skin (impetigo)
  2. RBC casts, proteinuria, periorbital edema, hypertension
  3. 95% recover and 1% develop RPGN - poor prognosis
55
Q

Describe PSG in sdults?

A
  1. May have atypical presentation with sudden hypertension, edema, elevated BUN;
  2. 60% recover, others develop rapidly progressive glomerulonephritis
56
Q

What is seen in laboratory tests for PSG?

A
  1. anti-streptococcal antibody titers

2. low C3 (due to consumption)

57
Q

What is seen microscopically in PSG?

A

glomeruli - globally and diffusely enlarged and hypercellular due to neutrophils and macrophages

58
Q

What is seen in immunofluoresence of PSG?

A
  1. lumpy-bumpy (granular) deposition of IgG

2. IgM and C3 in peripheral glomerular loops

59
Q

What is seen under the electron microscope of PSG?

A

Subepithelial humps (immune complex deposits)

60
Q

What is membranoproliferative glomerulonephritis?

A
  1. Alterations in basement membrane and proliferation of mesangial cells
  2. Presents with nephritic and nephrotic syndrome and hypertension
    - intermittent remissions
    - Aka lobular or mesangio-capillary glomerulonephritis
61
Q

Describe the epidemiology of membranoproliferative glomerulonephritis?

A

5% of cases of GN affecting children and young adults

62
Q

What is seen microscopically in membranoproliferative glomerulonephritis?

A
  • irregular thickening of glomerular basement membrane by interposition of mesangial cells between endothelium and basement membrane
  • causing tram track/double contour appearance
  • large glomeruli, lobules are accentuated; neutrophils often present
63
Q

What is seen under an electron microscope for membranoproliferative glomerulonephritis?

A

dense deposits in endothelium and mesangium cause large glomeruli with lobular accentuation

64
Q

What is rapidly progressive (crescentic) glomerulonephritis?

A

Crescents are end result of damage to glomerular basement membrane or Bowman’s capsule

  • due to deposition of fibrin and inflammatory cells
  • Crescents affect 50% of glomerular circumference, 70% of glomeruli
65
Q

What causes Rapidly progressive (crescentic) glomerulonephritis?

A

Rapid, usually irreversible loss of renal function associated with severe oliguria, unresponsive to steroids
- Symptoms of nephritic syndrome, nephrotic syndrome and renal failure

66
Q

What is the gross anatomy of crescent glomerulonephritis?

A

enlarged, pale kidneys with cortical petechial hemorrhages

67
Q

Describe the micro anatomy of crescent glomerulonephritis?

A

Crescents in glomeruli are proliferation of parietal epithelium of Bowman capsule with macrophages, neutrophils, lymphocytes, fibrin, collagen

68
Q

What is seen under an electron microscope of crescent glomerulonephritis?

A

wrinkling and focal disruptions in glomerular basement membrane

69
Q

What is IgA nephropathy?

A
70
Q

Describe the epidemiology of IgA nephropathy?

A
  1. Most common glomerular disease worldwide

2. Common in children and young adults, who present with hematuria after respiratory infection

71
Q

Describe the characteristics of IgAnephropathy?

A
  1. Slowly progressive: 25%-50% have renal
    failure at 20 years
  2. high serum IgA
72
Q

Name the secondary diseases IgA nephropathy is associated with?

A
  1. gluten enteropathy

2. liver disease

73
Q

State the poor prognostic features of IgA nephropathy?

A

prominent arteriolar hyalinization, older age, heavy proteinuria, hypertension

74
Q

Describe the micro anatomy of IgA nephropathy?

A

normal or hypercellular glomeruli

75
Q

What is seen under the immunofluorescence of IgA nephropathy?

A

IgA and C3 in mesangium

76
Q

What is seen under the electron microscope of IgA nephropathy?

A

electron-dense deposits in mesangium

77
Q

What is diabetic nephropathy?

A

kidney damage that results from having diabetes

- End stage renal disease in 30% of type I

78
Q

What causes diabetic nephropathy?

A

glomerular disease, arteriolar sclerosis, pyelonephritis & papillary necrosis
- causes 20% of deaths in those younger than age 40

79
Q

Describe characteristics of diabetic nephropathy?

A
  • Proteinuria occurs in 50%
  • Early increased GFR and microalbuminemia are predictive of future diabetic nephropathy
  • Tight diabetic control reduced renal disease
80
Q

Describe the microscopic anatomy of diabetic nephropathy?

A
  1. Basement membrane thickening and increased mesangial matrix, in ALL patients.
  2. Diffuse glomerulosclerosis - increase in mesangial matrix, basement membrane thickening and obliteration of capillary loops
  3. Nodular lesions – aka Kimmelstiel-Wilson nodules; - ovoid, spherical, laminated hyaline masses in peripheral of glomerulus - eventually obliterate glomerular tuft
  4. Hyalinization of afferent arterioles (hyaline arteriolosclerosis) - specific for diabetes
81
Q

Describe the microscopic anatomy of diabetic nephropathy?

A
  1. Basement membrane thickening and increased mesangial matrix, in ALL patients.
  2. Diffuse glomerulosclerosis - increase in mesangial matrix, basement membrane thickening and obliteration of capillary loops
  3. Nodular lesions – aka Kimmelstiel-Wilson nodules; - ovoid, spherical, laminated hyaline masses in peripheral of glomerulus - eventually obliterate glomerular tuft
  4. Hyalinization of afferent arterioles (hyaline arteriolosclerosis) - specific for diabetes
82
Q

What is chronic glomerulonephritis?

A

end stage disease due to progression of various types of glomerulonephritis,

  • occasionally there is no prior history of kidney disease
  • Paradoxically, nephrotic syndrome decreases as glomeruli disappear
83
Q

Name the kidney diseases that lead to chronic glomerulonephritis?

A
  1. rapidly progressive (90%)
  2. focal segmental glomerulosclerosis (50-80%)
  3. membranous GN (50%),
  4. membranoproliferative (50%)
  5. IgA nephropathy (30-50%) (slow)
  6. Poststreptococcal
  7. others
84
Q

Describe the gross anatomy of chronic glomerulonephritis?

A

symmetrically small kidneys with thin granular cortex and increased peripelvic fat

85
Q

Describe the micro anatomy of chronic glomerulonephritis?

A

glomerulosclerosis, arterial and arteriolar sclerosis, tubular atrophy & interstitial fibrosis (thyroidisation of tubules), lymphocytes

Renal Pathology (3 decks)

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