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Unit 5: Path - The Kidney > Glomerular Diseases > Flashcards

Glomerular Diseases Flashcards

1
Q

What are the characteristics of nephrotic syndrome?

A

Hypoalbuminemia, edema, hyperlipidemia, lipiduria, and SEVERE proteinuria (> 3.5 g/day)

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2
Q

What is the most common cause of secondary nephrotic syndrome in adults?

A

Diabetic glomerulosclerosis

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3
Q

What is another name for glomerulonephritis?

A

Nephritic Syndrome

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4
Q

What is Nephritic Syndrome characterized by?

A

Hematuria, Proteinuria, decreased GFR

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5
Q

What conditions does Nephrotic Syndrome lead to?

A

Elevated BUN, Elevated Serum Creat., oliguria, salt/water retention, hypertension, edema

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6
Q

What causes decreased GFR in Nephritic Syndrome?

A

Inflmmatory damage that may impair glomerular flow and filtration

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7
Q

What is the only means of definitive Dx for most glomerular diseases?

A

Renal biopsy

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8
Q

Describe the differences betwixt NephrItic and NephrOtic syndrome

A

Nephritic vs Nephrotic Syndrome Table

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9
Q

What findings are observed (uscope, IF, Electron) in minimal-change nephropathy?

A

No lesions, no ICs, no ICs

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10
Q

What findings are observed (uscope, IF, Electron) in Focal Segmental Glomerulosclerosis?

A

Focal and Segmental Glomerular Consolidation, no ICs, no ICs

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11
Q

What findings are observed (uscope, IF, Electron) in Membranous Glomerulopathy?

A

Diffuse global capillary wall thickening, diffuse capillary wall Igs, and Diffuse subepithelial dense deposits

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12
Q

What findings are observed (uscope, IF, Electron) in Membranoproliferative Glomerulonephritis?

A

Capillary wall thickening and endopaillary hypercellularity, diffuse capillary wall complement and subendothelial (type I) dense deposits; intramembranous (type II) dense deposits

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13
Q

What are the 3 major pathogenetic forms of glomerulonephritis?

A

In situ IC formation, Deposition of ICs, and ANCA

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14
Q

What is IC formation in situ glomerulonephritis?

A

Abs bind to intrinsic antigens or foreign antigens within glomeruli

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15
Q

What is circulating IC glomerulonephritis?

A

Circulating IC deposit in glomeruli and incite inflammation

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16
Q

What is the mechanism of ANCA glomerulonephritis?

A

Circulating autoAbs to antigens within neutrophil cytoplasm (myeloperoxidase or proteinase-3). This activates the neutrophils causing endothelial damage especially in glomerulus

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17
Q

What lab tests are needed to diagnose glomerular disease?

A

Light uscopy, electron uscopy, and Immunofluorescence

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18
Q

What histologic finding is associated with a rapidly progressive course?

A

Glomerular Crescent Formation

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19
Q

What is Minimal-Change Glomerulopathy characterized by?

A

Effacement of podocyte foot processes

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20
Q

A biopsy of MCG is shown below. What are characteristic light microscopic findings?

A

No changes are observed on light uscopy

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21
Q

What does electron uscopy show in a patient with MCG?

A

Podocyte foot process obliteration

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22
Q

What condition does MCG cause?

A

Nephrotic Syndrome

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23
Q

A patient Dx with MCG has azotemia. What is the likely to true Dx?

A

Focal Segmental Glomerulosclerosis

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24
Q

What parts of the glomeruli are affected in Focal Segmental Glomerulosclerosis?

A

(Focal) Some glomeruli and initially only affects the glomerular tuft (segmental)

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25
Q

A biopsy of a patient with Focal segmental glomerulosclerosis is shown below. What are the characteristic findings?

A

Periodic acid-schiff staining shows perihilar areas of segmental sclerosis and adjacent adhesions to Bowman Capsule

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26
Q

What is believed to be the general cause of FSGS?

A

Injury to or dysfunction of podocytes

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27
Q

What are agents of podocyte injury that can lead to FSGS?

A

Viruses, drugs, serum factors, congenital abnormalities

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28
Q

What are typical findings of a kidney biopsy of a patient with FSGS?

A

Segmental obliteration of capillary loops by increased matrix/cells, glassy hyalinosis (insudation of plasma proteins and lipids)

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29
Q

In patients with obesity or reduced renal mass what type of FSGS is observed?

A

Perihilar

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30
Q

In a patient with HIV, what type of FSGS is observed?

A

Collapsing sclerosis

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31
Q

T or F: Immune complexes are observed in FSGS

A

FALSE

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32
Q

What type of FSGS patient has the worst prognosis?

A

HIV and Idiopathic collapsing patients

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33
Q

What is HIV associated nephropathy?

A

Severe rapidly progressive collapsing for of focal segmental glomerulosclerosis

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34
Q

A biopsy of a patient with HIV1 associated nephropathy is shown. What are the characteristic findings of this biopsy?

A

Segmental or global collapsing pattern of focal sclerosis

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35
Q

What are typical causes of Membranous Glomerulopathy?

A

Accumulation of immune complexes in the subepithelial zone of the glomerular capillaries

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36
Q

What can membranous glomerulopathy cause?

A

Nephrotic Syndrome

37
Q

In MG, where do Immune Complexes localize?

A

Betwixt the Podocyte and the GBM in the subepithelial zone

38
Q

What are the general causes of primary membranous glomerulopathy?

A

Anti-PLA2R autoAbs, Anti-neutral endopeptidase alloantibodies

39
Q

What are some general causes of secondary membranous glomerulopathy?

A

Autoimmune disease, infectious disease, drugs, cancer

40
Q

A patient with Membranous glomerulopath is shown. What are the characteristic findings in this biopsy?

A

Slightly enlarged glomerulus, diffuse thickening of capillary walls, no hypercellularity

41
Q

A biopsy of a patient with membranous glomerulopathy is shown below. A silver stain was performed. What are the lesions observed? What stage of MG is shown?

A

Spikes in the GBM, Stage II

42
Q

A patient with membranous glomerulopathy is shown below. What markers are observed in IF testing?

A

IgG and C3

43
Q

What is the most common primary glomerular cause of nephrotic syndrome in white and Asian adults in the US?

A

Membranous glomerulopathy

44
Q

What is the most common secondary cause of nephrotic syndrome?

A

Diabetic glomerulosclerosis

45
Q

A biopsy of a patient with diabetic glomeruloscerlosis is shown below. What are typical findings observed?

A

Prominent increases in mesangial matrix, dilation of glommerular capillaries, and thickening of capillary BM. Kimmelstiel-Wilson nodules also form

46
Q

What is the leading cause of end-stage renal disease in the US?

A

Diabetic glomerulosclerosis

47
Q

From what is AA amyloid derived? What is it associated with?

A

Serum amyloid A protein (SAA); Chronic inflammatory states

48
Q

From what is AL amyloid derived? What is it associated with?

A

Either Lambda or Kappa Ig light chains, associated with multiple myeloma and B cell neoplasms

49
Q

A biopsy of a patient with amyloid nephropathy is shown. What are the characteristic findings?

A

Amorphous acellular material epands the mesangial areas and obstructs the glomerular capillaries.

50
Q

What type of stains identify amyloid?

A

Congo red stain

51
Q

What type of disease leads to monoclonal Ig deposition disease?

A

B-Cell Neoplasia

52
Q

What is the most common type of Ig that causees MIDD?

A

Kappa light chains

53
Q

What is Alport Syndrome and what causes it?

A

Hereditary Nephritis caused by abnormal glomerular basement membrane type IV collagen

54
Q

What type of inheritance is 85% of Alport Syndrome?

A

X linked and caused by a mutation in the gene for Alpha5 chain of IV collagen

55
Q

What is used to make the Dx of Hereditary Nephritis?

A

Electron Microscopy

56
Q

A biopsy of a patient with Hereditary Nephritis is shown. What are the key characteristics?

A

Lamina densa of the GBM is laminated rather than forming a single dense band

57
Q

What does Thin Glomerular Basement Membrane Nephropathy lead to?

A

Benign Hematuria

58
Q

What are the agents that typically cause Acute Postinfectious Glomerulonephritis?

A

Group A Strept (Beta Hemolytic) or Stapylococcus infection

59
Q

What is believed to be the cause of postinfectious glomerulonephritis?

A

Deposition of immune complexes of Ab plus bacterial antigens in glomeruli

60
Q

What is the general mechanism leading to postinfectious glomerulonephritis?

A

Immune complexes w/I glomeruli initiate inflamm response by activating complement and other humoral and cellular inflammatory mediators

61
Q

Shown below is the biopsy of a patient with acute poststreptococcal glomerulonephritis. What are characteristic findings?

A

Distinctive subepithelial dense deposits shaped like humps.

62
Q

A biopsy of a patient with type I membranoproliferative glomerulonephritis is shown below. What are characteristic findings?

A

Hypercellularity and capillary wall thickening, mesangialproliferation and extension into the subendothelial zone

63
Q

What was the segmentation of the glomerulus in Type I membranoproliferative glomerulonephritis called?

A

Lobular glomerulonephritis

64
Q

A renal biopsy of a patient with type II membranoproliferative glomerulonephritis is shown below. What are the typical findings?

A

Electron-dense deposits in the glomerular basement membrane

65
Q

What is the complement factor that plays a role in type II MPGN?

A

C3 nephritic factor

66
Q

What is the Dx? Type I or Type II MPGN?

A

Type II

67
Q

What is the Dx? Type I or Type II MPGN? What describes the fluorescence pattern?

A

Type I; Granular to band-like staining for C3

68
Q

Shown below is an EM of a patient with Type II MPGN. What is another name for this disease?

A

Dense deposit disease

69
Q

What is class I of SLEG? Findings?

A

Minimal mesangial lupus glomerulonephritis; No findings on light uscopy

70
Q

What is class II of SLEG? Findings?

A

Mesangial proliferative lupus glomerulonephritis; Immune complexes are confined to mesangium and cause varying degress of mesangial hypercellularity and matrix expansion

71
Q

What is class III of SLEG? Findings?

A

Focal Lupus Glomerulonephritis; ICs w/I subendothelial zone, mesangium resulting in inflamm and proliferation of mesangium and endothelium

72
Q

What is class IV of SLEG? Findings?

A

Diffuse lupus glomerulonephritis; Class III but involves > 50% of glomeruli

73
Q

What is class V of SLEG? Findings?

A

Membranous lupus glomerulonephritis; ICs primarily in the subepithelial zone

74
Q

What is class VI of SLEG? Findings?

A

Advanced sclerosing lupus glomerulonephritis

75
Q

Granular staining along tubular basement membranes and interstitial vessels is seen below. What is the Dx?

A

Diffuse proliferative lupus glomerulonephritis\

76
Q

What type of renal conditions are caused by Berger Disease?

A

IgA Nephropathy due to IgA renal complexes

77
Q

What type of IgA is most commonly deposited in Berger disease?

A

IgA1

78
Q

An IF for IgA is shown below. What is the Dx?

A

Immunoglobulin A Nephropathy

79
Q

What is anti-GBM glomerulonephritis mediated by?

A

Autoimmune response against type IV collgen in the GBM

80
Q

What symptoms are often associated with anti-GBM Glomerulonephritis? Why?

A

Pulmonary hemorrhage and hemoptysis; Target antigens are also expressed in alveolar BM

81
Q

An IF of anti-GBM glomerulonephritis is shown. What are the key characteristics?

A

Diffuse linear GBM immunostaining for IgG on basement membrane

82
Q

What other condition is observed in patients with anti-GBM glomerulonephritis?

A

Glomerular Crescents

83
Q

What is a subtype of anti-GBM glomerulonephritis that is rapidly progressive?

A

Crescentic glomerulonephritis Crescentic glomerulonephritis

84
Q

What is ANCA glomerulonephritis characterized by?

A

Glomerular necrosis and crescents

85
Q

What are ANCAs specific for in ANCA glomerulonephritis?

A

Myeloperoxidase and proteinase-3

86
Q

What condition do three quarters of those with ANCA glomerulonephritis have?

A

Systemic small vessel vasculitis

87
Q

What does ANCA glomerulonephritis and pulmonary vasculitis lead to?

A

Pulmonary-renal syndrome

88
Q

A patient with ANCA glomerulonephritis is shown. What does the silver stain reveal?

A

Focal disruption of glomerular basement membranes and crescent formation within the Bowman space

Unit 5: Path - The Kidney (11 decks)

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