6.1 RENAL DISEASES - GLOMERULAR Flashcards

1
Q

What are the primary classifications of renal diseases based on the kidney’s affected areas?

A

Glomerular, tubular, and interstitial

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2
Q

What is the major function of the kidneys?

A

Filtration of the blood to remove waste products.

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3
Q

What is the primary cause of most glomerular disorders?

A

Immunologic disorders

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4
Q

List down all the diseases under glomerular disorders. - Glomerulonephritis

A

Acute poststreptococcal glomerulonephritis (AGN)

Rapidly progressive glomerulonephritis (RPGN)

Goodpasture syndrome

Granulomatosis with polyangiitis (GPA)

Henoch-Schönlein purpura

Membranous glomerulonephritis

Membranoproliferative glomerulonephritis (MPGN)

Immunoglobulin A Nephropathy

Chronic glomerulonephritis

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5
Q

Nephrotic Syndrome diseases

A

Focal Segmental Glomerulosclerosis
Minimal Change Disease

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6
Q

Which immunoglobulin is commonly associated with immune complex deposition in glomerular disorders?

A

Immunoglobulin A (IgA).

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7
Q

What are nonimmunologic causes of glomerular damage?

A

Exposure to chemicals/toxins,
disruption of electrical membrane charges,
deposition of amyloid material, and
thickening of the basement membrane

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8
Q

What is the hallmark urinalysis finding in acute poststreptococcal glomerulonephritis (AGN)?

A

Red blood cell (RBC) casts.

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9
Q

What laboratory test can confirm the streptococcal origin of AGN?

A

Positive anti–group A streptococcal enzyme tests (e.g., ASO and anti-DNase B).

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10
Q

What serious complication is associated with rapidly progressive glomerulonephritis (RPGN)?

A

Renal failure

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11
Q

Which autoimmune disorder produces antiglomerular basement membrane antibodies?

A

Goodpasture syndrome

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12
Q

What key antibody is identified in granulomatosis with polyangiitis (GPA)?

A

Antineutrophilic cytoplasmic antibody (ANCA).

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13
Q

What is the most serious complication of Henoch-Schönlein purpura

A

Renal involvement leading to proteinuria and hematuria

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14
Q

What urinalysis findings are common in membranous glomerulonephritis (MGN)?

A

Microscopic hematuria and elevated urine protein.

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15
Q

Which type of membranoproliferative glomerulonephritis (MPGN) is associated with dense deposits?

A

Type 2.

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16
Q

What is a common symptom of chronic glomerulonephritis (CGN)?

A

Broad casts in the urine

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17
Q

What is the most common cause of glomerulonephritis?

A

Immunoglobulin A (IgA) nephropathy (Berger disease).

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18
Q

What is the hallmark laboratory finding in nephrotic syndrome?

A

Massive proteinuria (>3.5 g/day).

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19
Q

What is the primary protein lost in nephrotic syndrome?

A

Albumin

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20
Q

What cells absorb lipid-containing proteins in nephrotic syndrome, leading to the formation of oval fat bodies?

A

Renal tubular epithelial (RTE) cells.

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21
Q

Which disorder is the most common cause of nephrotic syndrome in children

A

Minimal change disease (MCD).

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22
Q

What type of renal disease affects only certain numbers and areas of glomeruli?

A

Focal segmental glomerulosclerosis (FSGS

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23
Q

Which glomerular disorder is caused by immune complexes formed from nephrogenic group A β-hemolytic streptococcal infections?

A

Acute poststreptococcal glomerulonephritis (AGN)

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24
Q

Which glomerular disorder is a severe form characterized by crescent formations in Bowman space and a poor prognosis?

A

Rapidly progressive glomerulonephritis (RPGN)

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25
Which glomerular disorder involves antiglomerular basement membrane antibodies and often begins with respiratory symptoms?
Goodpasture syndrome
26
Which glomerular disorder is associated with granuloma-producing inflammation in small blood vessels and is diagnosed by detecting ANCA?
Granulomatosis with polyangiitis (GPA)
27
Which glomerular disorder is a systemic disorder following upper respiratory infections and is characterized by purpura and hematuria?
Henoch-Schönlein purpura
28
Which glomerular disorder is caused by thickening of the glomerular basement membrane due to IgG deposits?
Membranous glomerulonephritis
29
Which glomerular disorder involves both thickening and cellular proliferation in the glomerular basement membrane?
Membranoproliferative glomerulonephritis (MPGN)
30
Which glomerular disorder represents the advanced stage of many glomerular diseases and leads to chronic renal failure?
Chronic glomerulonephritis
31
What changes can immune system mediators cause in the glomerular membrane?
Cellular infiltration, proliferation, thickening of the glomerular basement membrane, and complement-mediated capillary damage.
32
Can glomerulonephritis progress to other disorders?
Yes, it can progress from rapidly progressive glomerulonephritis to chronic glomerulonephritis, nephrotic syndrome, and eventually renal failure.
33
What triggers acute poststreptococcal glomerulonephritis (AGN)?
Respiratory infections caused by certain strains of group A β-hemolytic streptococci with M protein in their cell wall.
34
What are the clinical symptoms of AGN?
Fever, edema (especially around the eyes), fatigue, nausea, hypertension, oliguria, proteinuria, and hematuria.
35
What are the primary urinalysis findings in AGN?
Marked hematuria, proteinuria, oliguria, RBC casts, dysmorphic RBCs, hyaline and granular casts, and WBCs.
36
What laboratory tests confirm the streptococcal origin of AGN?
Positive anti-streptococcal enzyme tests, such as antistreptolysin O (ASO) and anti-DNase B.
37
What distinguishes rapidly progressive glomerulonephritis (RPGN)?
It is a severe form of glomerular disease with a poor prognosis, often leading to renal failure.
38
What initiates RPGN?
Deposition of immune complexes in the glomerulus, often from systemic disorders like systemic lupus erythematosus (SLE).
39
What causes crescent formations in RPGN?
Damage by macrophages to capillary walls releases cells and plasma into Bowman space forming crescents of macrophages, fibroblasts, and fibrin.
40
What are key laboratory findings in RPGN as the disease progresses?
Markedly elevated protein levels, low glomerular filtration rates (GFR), increased fibrin degradation products, and cryoglobulins.
41
What triggers Goodpasture syndrome?
Cytotoxic autoantibodies against glomerular and alveolar basement membranes, often following viral respiratory infections.
42
What is the primary urinalysis finding in Goodpasture syndrome?
Proteinuria, hematuria, and RBC casts.
43
Identify the glomerular disorder characterized by granuloma formation in small blood vessels and the presence of ANCA.
Granulomatosis with Polyangiitis (GPA)
44
What are the two patterns of ANCA detected in GPA testing?
Perinuclear pattern (p-ANCA) and cytoplasmic pattern (c-ANCA).
45
What are the primary urinalysis findings in GPA?
Hematuria, proteinuria, RBC casts, and elevated serum creatinine and BUN.
46
Identify the glomerular disorder primarily affecting children and characterized by purpura and renal involvement
Henoch-Schönlein Purpura
47
What are the primary symptoms of Henoch-Schönlein purpura?
Raised red skin patches, respiratory and gastrointestinal symptoms, hematuria, and proteinuria.
48
Raised red skin patches, respiratory and gastrointestinal symptoms, hematuria, and proteinuria.
Complete recovery in over 50% of cases, though some progress to severe glomerulonephritis and renal failure.
49
Identify the glomerular disorder with pronounced thickening of the basement membrane due to IgG immune complexes.
Membranous Glomerulonephritis (MGN)
50
What disorders are associated with membranous glomerulonephritis?
Systemic lupus erythematosus (SLE), Sjögren syndrome, secondary syphilis, hepatitis B, and malignancies.
51
What are the laboratory findings in membranous glomerulonephritis?
Microscopic hematuria, elevated protein excretion, and rare RBC casts.
52
Identify the glomerular disorder with cellular proliferation in the glomerulus and capillary wall thickening.
Membranoproliferative Glomerulonephritis (MPGN)
53
What are the three types of MPGN?
Type 1: Subendothelial cellular proliferation. Type 2: Dense deposits in the basement membrane. Type 3: Combined subepithelial and subendothelial deposits.
54
What are the typical urinalysis findings in MPGN?
Hematuria, proteinuria, and decreased serum complement levels.
55
Identify the glomerular disorder characterized by progressive damage leading to end-stage renal disease.
Chronic Glomerulonephritis (CGN)
56
What are the symptoms of chronic glomerulonephritis?
Fatigue, anemia, hypertension, edema, and oliguria.
57
What are the key laboratory findings in CGN?
Hematuria, proteinuria, glucosuria, and the presence of broad casts.
58
What is another name for Minimal Change Disease (MCD)?
Lipid nephrosis or nil disease
59
What is the primary structural damage seen in Minimal Change Disease?
Damage to podocytes and the shield of negativity
60
What is the percentage of Minimal Change Disease cases in nephrotic syndrome in children versus adults?
85% to 95% in children; 10% to 15% in adults
61
What are the primary clinical symptoms of Minimal Change Disease?
Edema, heavy proteinuria, transient hematuria, normal BUN and creatinine levels
62
What factors have been associated with the etiology of Minimal Change Disease?
Allergic reactions, recent immunization, and possession of the human leukocyte antigen B12 (HLA-B12)
63
What is the proposed pathogenesis of Minimal Change Disease?
A T-cell disorder releasing cytokines that injure the glomerular epithelial foot processes
64
How does Minimal Change Disease typically respond to treatment?
Responds well to corticosteroids
65
What is the prognosis for Minimal Change Disease?
Generally good, with frequent complete remissions
66
What is the defining feature of nephrotic syndrome in terms of proteinuria?
Massive proteinuria (greater than 3.5 g/day)
67
What are the primary biochemical abnormalities associated with nephrotic syndrome?
Low serum albumin, high serum lipids, and pronounced edema
68
What circulatory disruption can lead to nephrotic syndrome?
Systemic shock decreasing blood flow and pressure to the kidneys
69
What types of damage increase glomerular permeability in nephrotic syndrome?
Damage to the shield of negativity and podocytes
70
Which protein is primarily depleted in nephrotic syndrome?
Albumin
71
What compensatory response in the liver occurs due to hypoalbuminemia in nephrotic syndrome?
Increased lipid production
72
How does hypoalbuminemia contribute to edema in nephrotic syndrome?
Decreased oncotic pressure causes fluid loss into interstitial spaces, compounded by sodium retention
73
What complications arise from immunoglobulin and coagulation factor depletion in nephrotic syndrome?
Increased risk of infection and coagulation disorders
74
What are common urinalysis findings in nephrotic syndrome?
Marked proteinuria, urinary fat droplets (lipiduria), oval fat bodies, epithelial/fatty/waxy casts, and microscopic hematuria
75
What produces oval fat bodies in nephrotic syndrome?
Absorption of lipid-containing proteins by renal tubular epithelial cells followed by cellular sloughing
76
What is a possible progression of nephrotic syndrome if untreated?
Chronic renal failure
77
What distinguishes FSGS from other glomerular diseases?
It affects only certain areas and numbers of glomeruli while others remain normal
78
It affects only certain areas and numbers of glomeruli while others remain normal
Focal Segmental Glomerulosclerosis (FSGS)
79
What are the primary causes of FSGS?
Primary (idiopathic) glomerular disease or secondary to other diseases or drug abuse
80
Which substances or conditions are commonly associated with secondary FSGS?
Heroin abuse, analgesics, HIV, and hepatitis viruses
81
What immune deposits are often found in FSGS?
Immunoglobulin M (IgM) and C3
82
What are the consistent urinalysis findings in FSGS?
Moderate to heavy proteinuria and microscopic hematuria
83
What symptoms of FSGS overlap with nephrotic syndrome and minimal change disease?
Similar symptoms due to podocyte damage