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Robbins Pathology Renal (Chaptr 20,21) > Chapter 20- The Kidney > Flashcards

Chapter 20- The Kidney Flashcards

1
Q

What is the amount of blood that the kidney filters a day and into what amount of urine

A

1700L into 1 L of urine

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2
Q

In general, most damage to the glomeruli of the kidney is due to which mechanism

A

Immunologically mediated

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3
Q

In general, most damage to the tubules of the kidney is due to which mechanism

A

Toxins or infectious agents

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4
Q

In general, most damage to the interstitum of the kidney is due to which mechanism

A

Toxins or infectious agents

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5
Q

What is the meaning of azotemia

A

Elevation of the blood urea nitrogen (BUN), creatinine, and decreased GFR

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6
Q

Prerenal azotemia is usually caused by which conditions

A

Hypoperfusion of the kidneys usually do to hypotension or excessive fluid loss (shock, congestive heart failure, cirrhosis)
*Not characterized by parenchymal damage

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7
Q

What is postrenal azotemia caused by

A

Urine flow is obstructed distal to the kidney

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8
Q

What is uremia characterized by

A

Failure of the renal excretory function in addition to metabolic and endocrine alterations

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9
Q

Patients with uremia typically manifest secondary involvment of which organs

A
  • GI
  • peripheral nerves
  • Heart
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10
Q

What condition is characterized by:

  • Red cast cells
  • Hematuria
  • low GFR
  • mild to moderate proteinuria
  • Hypertension
A

Nephritic syndrome

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11
Q

What condition is characterized by:

  • Nephritic syndrome
  • Rapid decline in GFR (hours to days)
A

Rapidly progressing glomerulonephritis

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12
Q

What condition is characterized by:

  • heavy proteinuria
  • hypoalbuminemia
  • severe edema
  • hyperlipidemia and lipiduria
A

Nephrotic syndrome

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13
Q

What condition is characterized by:

  • Rapid decline in GFR
  • dysregulation of fluids and electrolytes
  • retention of metabolic waste
A

Acute kidney injury

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14
Q

What condition is characterized by:

  • diminished GFR (less than 60ml/min/1.73 for 3 months
  • persistent albuminuria
A

Chronic kidney disease

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15
Q

What condition is characterized by:

-5% of normal GFR

A

end stage renal disease (ESRD)

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16
Q

What are some of the secondary glomerular diseases

A
  • SLE
  • hypertension
  • DM
  • Fabry disease
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17
Q

What are the structural components of the glomerular basement membrane (GBM)

A

Collagen Type 4, laminin, heparin sulfate, fibronectin, entactin

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18
Q

Which aspect of GBM is crucial for structure formation

A

-NC1 domain as it allows the formation of the alpha helixes and assembly of the collagen monomers into the basement membrane

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19
Q

What is the gene coding for the alpha helix in the GMB

A

COL4A1 though COL4A6

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20
Q

What is the target for the antibodies in anti-GBM nephritis, and why is this crucial

A

NC1, which is the binding domain for many of the components in the GBM

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21
Q

What is the function of the mesangial cells

A

-Mesenchymal origin that can contract, phagocytose, proliferate, lay down matrix and collagen

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22
Q

What is the size of protein that can make it through the glomerulus

A

-less than 70 kilodaltons

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23
Q

What is the important of the Visceral epithelial cells

A

Maintenance of glomerular barrier function as its slit diaphragm, and is responsible for the synthesis of many of the GBM components

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24
Q

What is the function of nephrin

A

Transmembrane protein that extends to the neighboring foot and dimerizes, covering the filtration slit

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25
Q

What are the proteins associated with nephrin as it covers the filtration slit

A

-podocin, CD2 associated protein (CD2AP), actin skeleton

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26
Q

What are the 4 general responses to acute glomerular injury

A
  • Hypercellarity
  • Basement membrane thickening
  • Hyalinosis
  • Sclerosis
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27
Q

What are the characteristics of hypercellularity die to acute glomerular injury

A

-Infiltration of leukocytes, resulting in swelling
-Proliferation of mesangial or endothelial cells
Formation of crescents

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28
Q

What is the condition of endocapillary proliferation

A

Swelling and proliferation of mesangial cells or endothelial cells in response to acute glomerular damage

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29
Q

What is occurring in the formation of crescents

A
  • Epithelial cell proliferation following an immune injury to the capillary walls.
  • Exposure of the plasma proteins leaking into the urinary space to the procoagulants leads to fibrin deposition
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30
Q

What stain is used to see glomerular membrane thickening

A

PAS stain

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31
Q

What are the 3 forms that GBM thickening occurs by

A

1-Deposition of immune complex, followed by fibrin and amyloid
2-Increased synthesis of protein components of the BM
3-Domation of additional layers of BM

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32
Q

What condition leads to increased synthesis of BM protein components

A

Diabetic glomerulo sclerosis (also causes sclerosis of the mesangial areas)

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33
Q

What is the characteristic of the condition hyalinosis in result of acute glomerular damage

A

Accumulation of material that is homogeneous and eosinophilic by light microscopy

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34
Q

What is the characteristic of the condition sclerosis in result of acute glomerular damage

A

Deposition of extracellular collagenous matrix

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35
Q

How are many glomerulopathies classified

A

By their histology

36
Q

With regards to primary glomerulopathies, what is the meaning of diffuse

A

Involving all of the glomeruli in the kidney

37
Q

With regards to primary glomerulopathies, what is the meaning of global

A

Involving the entirety of the individual glomeruli

38
Q

With regards to primary glomerulopathies, what is the meaning of focal

A

Involving only a fraction of the glomeruli in the kidney

39
Q

With regards to primary glomerulopathies, what is the meaning of segmental

A

Affecting a part of each glomeruli

40
Q

With regards to primary glomerulopathies, what is the meaning of capillary loop or mesangial

A

Predominantly affecting the capillary or mesangial regions

41
Q

Most of the immune mediated damage to the glomerulus is via which mechanism

A

-In situ, meaning that the antibodies are attacking something in the glomerulus, rather than forming a complex and then depositing

42
Q

What are some of the fixed in situ antigens targeted

A
  • NC1 domain of Type 4 collagen
  • PLA2R antigen (membranous glomerulopathies)
  • Mesangial antigens
43
Q

In the condition primary human membranous nephropathy, what is the antigen being targeted, and where is it present

A

-Megalin aka M type phospholipase A2 receptor (PLA2R), present in the epithelial cell foot process, so is an in situ mediated damage

44
Q

What is the mechanism of destruction in primary human membranous nephropathy

A

-Antigens against PLA2R, activation of complement, deposition of complexes along the subepithelial portion of BM

45
Q

What is the characteristic of Heymann aka membranous nephropathy immune complex formation with immunofluorescence

A

Granular due to the very localized antibody antigen interaction

46
Q

What is the characteristic of circulating immune complex formation with immunofluorescence in the nephron

A

Granular, as the complex deposit unevenly

47
Q

What is the common location for “planted antigens” in the GBM

A

Mesangium

48
Q

What kidney disease can develop from cow’s milk

A

Membranous nephropathy in infants (Ab against cow albumin)

49
Q

What is the characteristic of Ab-GBM immunologic formation with immunofluorescence

A

-DIffuse linear, due to the antibodies depositing all along the membrane, and can not be mobilized to from complexes

50
Q

What organs are affected in Goodpasture syndrome

A

-Lungs and kidney

51
Q

IN the condition of anti-GBM antibodies, what commonly happens

A

Cross reacts between the lung alveoli and renal GBM, creating simultaneous lung and kidney lesions, aka Goodpastures

52
Q

What is the target of the antibodies in Goodpastures

A

NC1 in the alpha 3 chain in collagen type 4

53
Q

What is the prognosis in patients with anti-GBM antibodies

A

Poor prognosis with severe necrotizing and crescentic glomerular damage leading to rapidly progressive glomerulonephritis

54
Q

Which conditions tend to lead to chronic renal damage with regards to deposition of immune complexes

A

SLE or viral hepatitis

55
Q

What is the common location of deposition of highly cationic antigens

A

They cross the GBM and complexes reside in the subepithelial location

56
Q

What is the common location of deposition of highly anionic macromolecules

A

Cannot cross the GBM and are trapped subendothelially if even at all

57
Q

What is the common location of deposition for neutral charged immune complexes

A

Mesangium

58
Q

What is the localization of immune complex deposition in acute glomerulonephritis

A

Subepithelial humps

59
Q

What is the localization of immune complex deposition in membranous nephropathy

A

Epimembranous

60
Q

What is the localization of immune complex deposition in Heymann nephritis

A

Epimembranous

61
Q

What is the localization of immune complex deposition in lupus nephritis

A

Subendothelial

62
Q

What is the localization of immune complex deposition in membranoproliferative glomerulonephritis

A

Subendothelial

63
Q

What is the localization of immune complex deposition in IgA nephropathy

A

Mesangial

64
Q

Location of which deposits are more likely to involve an inflammatory process

A
  • Subendothelial portions of capillaries
  • Mesangial regions
  • have access to circulation
65
Q

Which deposition locations will tend to not involve an inflammatory process

A
  • Subepithelial locations

- basement membranes

66
Q

What is dense deposit disease characterized by

A

*aka membranoproliferative glomerulonephritis (MPGN type 2)

Alternative complement pathway activation

67
Q

What is the characteristic of podocytes that make it commonly a pathogenesis in kidney damage

A

-Does not replicate or repair very well

68
Q

What is the usually the process of damage and mechanism of disease with regards to podocytes

A

They are damaged, usually by toxins or antibodies, leading to effacement (flattening out) which can then lead to detachment, which allows proteins to leak

69
Q

In most forms of glomerular injury, what is the key event in the development of proteinuria

A

-Loss of normal slit diaphragms

70
Q

What is the damage amount in the kidney that will lead to a consistent progression to end stage renal failure

A

-GFR at 30 to 50% of normal

71
Q

When GFR reaches 30-50% of normal, what is the result

A

A steady progression to ESRD, regardless of the original stimulus or activity of the underlying disease

72
Q

What are the two histological characteristics of progressive renal damage in the process to ESRD

A
  • Focal segmental glomerulosclerosis (FSGS)

- Tubulointerstitial fibrosis

73
Q

What is focal segmental glomerulosclerosis (FSGS) characterized by

A

-progressive fibrosis of portions of the glomeruli after many types of renal injury, leading to proteinuria

74
Q

What is compensatory hypertrophy

A

When there are damaged glomeruli, the remaining will maintain the GFR for a short time, but then proteinuria and segmental glomerulosclerosis develops, eventually leading to total glomerular sclerosis and uremia (no urine)

75
Q

Glomerular hypertrophy is associated/caused by which conditions

A

-Hemodynamics changes, such as increases in glomerular blood flow, filtration, and transcapillary pressure, as well as hypertension

76
Q

Which cytokine plays a large role in sclerosis

A

TGF beta

77
Q

What are the common forms of treatment to prevent focal segmental glomerulosclerosis (FSGS)

A

-Inhibators of RAAS, which helps reduce the intraglomerular hypertension

78
Q

What are the mechanisms seen in causing the glomerulosclerosis

A
  • Glomerular hypertrophy and hypertension start
  • Invasion of macrophages, mesangial cell proliferation, increased accumulation of ECM
  • Sclerosis and epithelial injury occur
79
Q

What.is tubulointerstitial fibrosis characterized by

A

Tubular damage and interstitial inflammation

80
Q

What is correlation of decline in renal function with tubular damage and glomerular damage

A

Renal function decrease is more closely correlated with tubular damage

81
Q

What is the effect of proteinuria on tubular damage

A

Causes direct injury to and activation of tubular cells, which then express adhesion molecules and the start of the inflammation process

82
Q

What are the glomerular diseases under nephritic syndrome characterized by

A

-Inflammation of the glomerulus

83
Q

What condition is being described:

  • Red casts in the urgine
  • Azotemia
  • Oliguria
  • Mild to moderate hypertension
A

Nephritic syndrome

84
Q

What are the characteristics of acute proliferative glomerulonephritis

A
  • Includes poststreptococcal/postinfectious glomerulonephritis
  • Diffuse proliferation of glomerular cells wth the influx of leukocytes and lesions caused by immune complexes
85
Q

What is the typical timing in the development of poststreptococcal glomerulonephritis

A

Appears 1 to 4 weeks after a streptococcal infection of the pharynx or skin (impetigo)

86
Q

Which patients most commonly see poststreptococcal glomerulonephritis

A

Children age 6 to 10

Robbins Pathology Renal (Chaptr 20,21) (5 decks)

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