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

Chapter 20- The Kidney Flashcards

(86 cards)

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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
What are the proteins associated with nephrin as it covers the filtration slit
-podocin, CD2 associated protein (CD2AP), actin skeleton
26
What are the 4 general responses to acute glomerular injury
- Hypercellarity - Basement membrane thickening - Hyalinosis - Sclerosis
27
What are the characteristics of hypercellularity die to acute glomerular injury
-Infiltration of leukocytes, resulting in swelling -Proliferation of mesangial or endothelial cells Formation of crescents
28
What is the condition of endocapillary proliferation
Swelling and proliferation of mesangial cells or endothelial cells in response to acute glomerular damage
29
What is occurring in the formation of crescents
- 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
30
What stain is used to see glomerular membrane thickening
PAS stain
31
What are the 3 forms that GBM thickening occurs by
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
32
What condition leads to increased synthesis of BM protein components
Diabetic glomerulo sclerosis (also causes sclerosis of the mesangial areas)
33
What is the characteristic of the condition hyalinosis in result of acute glomerular damage
Accumulation of material that is homogeneous and eosinophilic by light microscopy
34
What is the characteristic of the condition sclerosis in result of acute glomerular damage
Deposition of extracellular collagenous matrix
35
How are many glomerulopathies classified
By their histology
36
With regards to primary glomerulopathies, what is the meaning of diffuse
Involving all of the glomeruli in the kidney
37
With regards to primary glomerulopathies, what is the meaning of global
Involving the entirety of the individual glomeruli
38
With regards to primary glomerulopathies, what is the meaning of focal
Involving only a fraction of the glomeruli in the kidney
39
With regards to primary glomerulopathies, what is the meaning of segmental
Affecting a part of each glomeruli
40
With regards to primary glomerulopathies, what is the meaning of capillary loop or mesangial
Predominantly affecting the capillary or mesangial regions
41
Most of the immune mediated damage to the glomerulus is via which mechanism
-In situ, meaning that the antibodies are attacking something in the glomerulus, rather than forming a complex and then depositing
42
What are some of the fixed in situ antigens targeted
- NC1 domain of Type 4 collagen - PLA2R antigen (membranous glomerulopathies) - Mesangial antigens
43
In the condition primary human membranous nephropathy, what is the antigen being targeted, and where is it present
-Megalin aka M type phospholipase A2 receptor (PLA2R), present in the epithelial cell foot process, so is an in situ mediated damage
44
What is the mechanism of destruction in primary human membranous nephropathy
-Antigens against PLA2R, activation of complement, deposition of complexes along the subepithelial portion of BM
45
What is the characteristic of Heymann aka membranous nephropathy immune complex formation with immunofluorescence
Granular due to the very localized antibody antigen interaction
46
What is the characteristic of circulating immune complex formation with immunofluorescence in the nephron
Granular, as the complex deposit unevenly
47
What is the common location for “planted antigens” in the GBM
Mesangium
48
What kidney disease can develop from cow’s milk
Membranous nephropathy in infants (Ab against cow albumin)
49
What is the characteristic of Ab-GBM immunologic formation with immunofluorescence
-DIffuse linear, due to the antibodies depositing all along the membrane, and can not be mobilized to from complexes
50
What organs are affected in Goodpasture syndrome
-Lungs and kidney
51
IN the condition of anti-GBM antibodies, what commonly happens
Cross reacts between the lung alveoli and renal GBM, creating simultaneous lung and kidney lesions, aka Goodpastures
52
What is the target of the antibodies in Goodpastures
NC1 in the alpha 3 chain in collagen type 4
53
What is the prognosis in patients with anti-GBM antibodies
Poor prognosis with severe necrotizing and crescentic glomerular damage leading to rapidly progressive glomerulonephritis
54
Which conditions tend to lead to chronic renal damage with regards to deposition of immune complexes
SLE or viral hepatitis
55
What is the common location of deposition of highly cationic antigens
They cross the GBM and complexes reside in the subepithelial location
56
What is the common location of deposition of highly anionic macromolecules
Cannot cross the GBM and are trapped subendothelially if even at all
57
What is the common location of deposition for neutral charged immune complexes
Mesangium
58
What is the localization of immune complex deposition in acute glomerulonephritis
Subepithelial humps
59
What is the localization of immune complex deposition in membranous nephropathy
Epimembranous
60
What is the localization of immune complex deposition in Heymann nephritis
Epimembranous
61
What is the localization of immune complex deposition in lupus nephritis
Subendothelial
62
What is the localization of immune complex deposition in membranoproliferative glomerulonephritis
Subendothelial
63
What is the localization of immune complex deposition in IgA nephropathy
Mesangial
64
Location of which deposits are more likely to involve an inflammatory process
- Subendothelial portions of capillaries - Mesangial regions * have access to circulation
65
Which deposition locations will tend to not involve an inflammatory process
- Subepithelial locations | - basement membranes
66
What is dense deposit disease characterized by
*aka membranoproliferative glomerulonephritis (MPGN type 2) | Alternative complement pathway activation
67
What is the characteristic of podocytes that make it commonly a pathogenesis in kidney damage
-Does not replicate or repair very well
68
What is the usually the process of damage and mechanism of disease with regards to podocytes
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
In most forms of glomerular injury, what is the key event in the development of proteinuria
-Loss of normal slit diaphragms
70
What is the damage amount in the kidney that will lead to a consistent progression to end stage renal failure
-GFR at 30 to 50% of normal
71
When GFR reaches 30-50% of normal, what is the result
A steady progression to ESRD, regardless of the original stimulus or activity of the underlying disease
72
What are the two histological characteristics of progressive renal damage in the process to ESRD
- Focal segmental glomerulosclerosis (FSGS) | - Tubulointerstitial fibrosis
73
What is focal segmental glomerulosclerosis (FSGS) characterized by
-progressive fibrosis of portions of the glomeruli after many types of renal injury, leading to proteinuria
74
What is compensatory hypertrophy
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
Glomerular hypertrophy is associated/caused by which conditions
-Hemodynamics changes, such as increases in glomerular blood flow, filtration, and transcapillary pressure, as well as hypertension
76
Which cytokine plays a large role in sclerosis
TGF beta
77
What are the common forms of treatment to prevent focal segmental glomerulosclerosis (FSGS)
-Inhibators of RAAS, which helps reduce the intraglomerular hypertension
78
What are the mechanisms seen in causing the glomerulosclerosis
- Glomerular hypertrophy and hypertension start - Invasion of macrophages, mesangial cell proliferation, increased accumulation of ECM - Sclerosis and epithelial injury occur
79
What.is tubulointerstitial fibrosis characterized by
Tubular damage and interstitial inflammation
80
What is correlation of decline in renal function with tubular damage and glomerular damage
Renal function decrease is more closely correlated with tubular damage
81
What is the effect of proteinuria on tubular damage
Causes direct injury to and activation of tubular cells, which then express adhesion molecules and the start of the inflammation process
82
What are the glomerular diseases under nephritic syndrome characterized by
-Inflammation of the glomerulus
83
What condition is being described: - Red casts in the urgine - Azotemia - Oliguria - Mild to moderate hypertension
Nephritic syndrome
84
What are the characteristics of acute proliferative glomerulonephritis
* Includes poststreptococcal/postinfectious glomerulonephritis - Diffuse proliferation of glomerular cells wth the influx of leukocytes and lesions caused by immune complexes
85
What is the typical timing in the development of poststreptococcal glomerulonephritis
Appears 1 to 4 weeks after a streptococcal infection of the pharynx or skin (impetigo)
86
Which patients most commonly see poststreptococcal glomerulonephritis
Children age 6 to 10

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

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