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Renal > 05.05 - Glomerular Structure, Injury (Nichols, Handorf) - Based on word doc > Flashcards

05.05 - Glomerular Structure, Injury (Nichols, Handorf) - Based on word doc Flashcards

1
Q

Hyaline Sclerosis in HTN vs DM

A

In HTN, just afferent arteriole; In DM, both

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1
Q

Anti-GBM disease is associated with

A

Smoking, being male

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1
Q

Location of In situ immune complex formation and deposition

A

Subepithelial

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1
Q

What does Trichrome stain highlight

A

Collagen

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2
Q

Treatment of Anti-GBM Ab disease

A

Removing them with Plasmapharesis

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2
Q

IgA Nephropathy is due to

A

Production of Abnormal IgA that self-aggregates and binds IgG –> immune complex formation –> Mesangial cell activation –> Complement-mediated injurious inflammation

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2
Q

What stain highlights the GBM

A

Jones silver stain

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2
Q

What is becoming the most common type of Crescentic Glomerulonephritis

A

Pauci-immune

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3
Q

3 most common types of glomerular disease

A

(1) HTN, (2) Diabetic, (3) Immune-mediated

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3
Q

Most common cause of glomerular disease

A

Hypertension

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3
Q

Platelet mechanisms of glomerular injury in immune-mediated disease

A

Release AA metabolites

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3
Q

In situ immune complex formation with Ab’s against podocyte cell membrane antigens causes great majority of

A

Membranous Glomerulonephritis

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4
Q

Calcium binding properties

A

Features of Entactin

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4
Q

What does Global Glomerular Disease refer to

A

Involves all of a single glomerulus

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5
Q

Feedback loop with hypertensive kidney disease

A

Glomerular Disease causes HTN, and HTN causes glomerular disease

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5
Q

What happens to GBM in DM

A

Glycosylated plasma proteins get trapped –> GBM gets thickened

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5
Q

What does Diffuse Mesangial Sclerosis mean

A

Sclerosis of all the mesangium in one glomerulus

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6
Q

What causes Crescentic Glomerulonephritis

A

Leakage of Plasma Proteins into urinary space (particularly when mixed with Ab’s, Immune Complexes, Inflammatory Cytokines, Inflammaotry cells, and ROS)

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6
Q

Location of immune complex deposition in Post-Strep Glomerulonephritis

A

Subepithelial

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8
Q

Important Concept: ____ is a major mechanisms of glomerular injury

A

Antibody deposition

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9
Q

Mutations in what result in congenital nephrotic syndromes?

A

Nephrin and Podocin

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10
Q

Urine in Malignant HTN

A

Marked Proteinuria, Microscopic Hematuria

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11
Q

Features of Perlecan

A

Strong negative charge - prevents Albumin from entering

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12
Q

Crescent Glomerulonephritis is associated with

A

Rapid Progression of Disease

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12
What activates the Complement pathway in IgA Nephropathy
Mesangial cells are activated in response to binding and phagocytosing immune complexes --\> Proliferate and increase production of ECM proteins and cytokines
13
Features of Laminin
Binds to other components
14
Features of Entactin
Calcium binding properties
14
Form of Glomerulonephritis w/ localization of immune complexes in the mesangium
IgA Nephropathy
14
Subepithelial Humps
Pattern of immune complex deposits in Post-Strep Glomerulonephritis EM
15
Leukocyte mechanisms of glomerular injury and malfunction
Leakage of lysosomal proteases and ROS, Production of AA metabolites that reduce GFR
17
What is the Non-Collagenous Domain
Non-helical globular domain
19
Infectious diseases involve what parts of nephron
Tubules and Interstitium far more often than glomeruli
20
What are Thrombotic Microangiopathies
Loss of normal endothelial function needed to prevent thrombosis
20
Result of Foot Process Effacement
Retraction and loss of SPD; Detachment from GBM and degradation of GBM --\> Plasma protein linkage
20
What mediates the accelerated aging in DM
Advanced Glycation end-products (AGE)
21
What is Arterio-Nephro-Sclerosis
(1) Narrowing of lumen from plasma leakage; (2) Gradual ischemic atrophy of glomerulus; (3) End result is global sclerosis of glomeruli
23
In whom is malignant HTN more common
Black males around 40
24
What tends to have a Linear pattern on immunofluorescence and be invisible on EM
Anti-GBM Ab deposition
26
2 diseases associated leading to Arterionephrosclerosis
HTN, DM
27
Wire Loops
Extensive confluent subendothelial deposits thickening the capillary walls
29
Nephrin and its associated protein are crucial to
Maintaining selective permeability of glomerular filtration barrier
31
Gross appearance of kidney in malignant HTN
Flea-Bitten
31
Crescent-shaped area of inflammation w/ proliferation of parietal epithelial cells
Crescentic Glomerulonephritis
32
2 diseases associated with ApoL1 mutation
Arterionephrosclerosis, Focal Segmental Glomerulosclerosis
33
Strong negative charge - prevents Albumin from entering
Features of Perlecan
35
What happens to arterioles in Malignant HTN
Fibrinoid Necrosis of Arterioles
36
What is Crescentic Glomerulonephritis
Crescent-shaped area of inflammation w/ proliferation of parietal epithelial cells
37
Diseases caused by Ab's against epitope in the NC1 domain of alpha3 chain cause
Glomerulonephritis w/ Hematuria
38
Effects if DM on nephron
Mesangial cell hypertrophy and hyperplasia; Diffuse mesangial matrix production; Podocyte injury and apoptosis; Thickening of tubular BM's
39
Most common glomerular disease
Vascular, Hypertensive Nephropathy
40
What causes the damage in IgA Nephropathy
Complement activation generates the injurious inflammation
42
In whom is end-stage renal disease due to HTN more common
8x more common in blacks
43
What can cause Crescentic Glomerulonephritis
Leakage of plasma proteins into urinary space (particularly when mixed with Ab's, Immune Complexes, Inflammatory Cells, and ROS)
44
Renal neoplasms arise from
Tubular Epithelium
46
Result of injury to glomerular capillary endothelium
Loss of normal endothelial function needed to prevent thrombosis
47
Pattern of immune complex deposition in immunofluorescence
Clumps, granular pattern
48
Goodpasture Syndrome
Glomerulonephritis w Hematuria, along w/ Pulmonary Hemorrhage and Hemoptysis
48
What does PAS stain highlight
Cellular cytoplasmic inclusions
50
Effect of supra-normal glomerular capillary pressure on glomerulus
GBM thickening, Mesangial Hypertrophy and Hyperplasia, Mesangial Matrix production
52
When proliferating parietal epithelial cells and infiltrating macrophages and inflammatory exudate and leaked plasma create a visible crescent of inflammation around glomerular tuft of cpaillaries
Crescentic Glomerulonephritis
54
Slit Pore Diaphragm proteins that serve to bind adjacent pediceles
Cadherin, FAT
56
Glomerular diseases that involve the capillary endothelium or subendotheial portion of glomeruli tend to cause
Hematuria
57
Site of Ab deposition in SLE
Subendothelial
58
Compensation for nephron loss requires
Increased filtration per glomerulus and increased glomerular transcapillary pressure
59
In conditions causing severe loss of protein thru slit pore diaphragms, EM frequently shows
Fusion of Foot Processes = Effacement
61
Ab against NC1 domain + Ab's against lung basement membrane
Goodpasture Syndrome
62
Second most common glomerular disease
DM
63
Mesenchymal cells w/ phagocytic and contractile properites
Mesangial Cells
64
With what is C-ANCA associated
Granulomatosis with Polyangiitis
65
Vascular clotting disorders such as HUS, TTP, and DIC involve what part of nephron
Glomerulus
65
Anti-GBM Ab deposition tends to have what pattern
Linear pattern on immunofluorescence and be invisible on EM
67
End result of many glomerular diseases
Fibrous replacement of glomerulus = Glomerulosclerosis
69
What is hypothesized to happen in Post-Strep Glomerulonephritis
Antigens and Ab's arrive in glomerulus separately and form complexes in situ
70
Features of Fibronectin
Connection and adhesion of components
71
Extensive confluent subendothelial deposits thickening the capillary walls
Wire Loops
72
Connection and adhesion of components
Fibronectin
73
Glomerular diseases that involve which side of glomerulus are worse
Capillary side
75
What causes the great majority of Membranous Glomerulonephritis
In situ immune complex formation with Ab's against podocyte cell membrane antigens
76
Glomerular diseases that involve only the podocytes, slit diaphragm, or subepithelial portion of the glomeruli tend to cause
Proteinuria
78
Presentation of Malignant HTN
Symptoms of increased intracranial pressure: Headache, Scotomas, Vomitting
80
What happens to surviving nephrons after nephron loss
Hypertrophy, with hyperplasia of glomerular and tubular cells, longer tubules
81
Hyperplastic Arteriosclerosis + Arterial Fibrinoid Necrosis
Malignant HTN
82
What causes Flea-Bitten Kidney
Small arteries/arterioles damaged by malignant HTN rupture all over kidney
83
Toxic diseases tend to involve what part of nephron
Tubules more than Glomeruli
85
(1) Narrowing of lumen from plasma leakage; (2) Gradual ischemic atrophy of glomerulus; (3) End result is global sclerosis of glomeruli
What is Arterio-Nephro-Sclerosis
86
Glomerulonephritis w Hematuria, along w/ Pulmonary Hemorrhage and Hemoptysis
Goodpasture Syndrome
87
Histopathologic correlate of the clinical syndrome of rapidly progressive glomerulonephritis
Crescentic Glomerulonephritis
88
What does Segmental Glomerular Disease mean
Involves only part of glomerulus
89
Membranous glomerulopathy is characterized by
Increased glomerular basement membrane, w/out an increase in cells
90
What percent of glomerular disease in children is primary? In adults?
95%; 60%
91
With what is P-ANCA associated
Microscopic Polyangiitis, Churg-Strauss
92
Cell binding of basement membrane is mediated mostly by
Integrins
93
Slit Pore Diaphragm proteins that play role in filtration
Nephrin, Podocin
94
Effect of AA metabolites on glomerulus
Reduce GFR
95
AI diseases highly favor what part of nephron
Glomeruli

Renal (31 decks)

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