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Nephrology > Glomerulonephropathies > Flashcards

Glomerulonephropathies Flashcards

1
Q

Nephritic 3 VS Nephrotic 3

What would you find in the urine?

A

Nephritic Characteristics:

  1. +red cells - white blood cells
  2. red cell or mixed cellular casts
  3. variable degrees of proteinuria

Nephrotic Characteristics

  1. proteinuria > 3.5 g/day
  2. lipiduria
  3. fatty casts
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2
Q

Nephritic Causes

9

A
  1. Postinfectious glomerulonephritis
  2. IgA nephropathy
  3. Henoch-Schönlein purpura (HSP also termed IgA vasculitis [IgAV])
  4. Mesangial proliferative glomerulonephritis
  5. Lupus nephritis
  6. Thin basement membrane disease
  7. Hereditary nephritis
  8. Membranoproliferative glomerulonephritis
  9. Rapidly progressive (crescentic) glomerulonephritis
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3
Q

Nephrotic Causes

4

A
  1. Systemic…Diabetic nephropathy, amyloidosis, systemic lupus
  2. Minimal change disease (children)
  3. Focal segmental glomerulosclerosis (FSGS)
  4. Membranous nephropathy
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4
Q

What are the two patterns of nephritic disease? 2

A
  1. Focal nephritic

2. Diffuse nephritic

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5
Q
  1. What is a focal nephritic pattern?
  2. What does the UA show? 3
  3. Example? 1
A
  1. Inflammatory lesions in less than ½ of glomeruli
  2. UA shows
    - RBCs,
    - occasional RBC casts,
    - mild proteinuria
  3. Example: IgA nephropathy
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6
Q
  1. What is a diffuse nephritic pattern?
  2. What does the UA show? 4
  3. Example? 1
A
  1. Affects > ½ of the glomeruli
  2. UA similar to focal,
    - but w/ more proteinuria,
    - also edema,
    - HTN, and/or
    - renal insufficiency

Example: post-streptococcal glomerulonephritis (PSGN)

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7
Q
  1. Nephrotic syndrome affects how much of the glomeruli?
  2. What is it lacking? 2
  3. What will it cause? 3
  4. Example?
A
  1. Affects many of the glomeruli
  2. Without obvious
    - inflammation or
    - immune complex deposition
    • edema,
    • hyperlipidemia,
    • hypoalbuminemia
  4. Example: diabetic nephropathy
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8
Q
  1. Poststreptococcal glomerular nephritis (PSGN) is the most common cause of what?
  2. Primarily occurs where?
  3. What age are at greatest risk?
A
  1. Most common cause of acute nephritis worldwide
  2. It primarily occurs in the developing world.
  3. The risk of PSGN is greatest in children between 5-12 years of age.
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9
Q

Poststreptococcal glomerular nephritis (PSGN)

  1. Occurs after what? 2
  2. What does not necessariliy protect pts from this?
A
    • Usually occurs 1-3 weeks post strep throat
    • 3-6 weeks post skin infection with group A beta-hemolytic strep (GABS)
  2. Antibiotic treatment does not always prevent glomerular disease
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10
Q

Poststreptococcal glomerular nephritis (PSGN)
Pathophysiology:

  1. Caused by?
  2. Can be associated with? 2
  3. What does the resulting glomerular immune complex disease trigger? 2
A
  1. Caused by glomerular immune complex disease induced by specific nephritogenic strains of group A beta-hemolytic streptococcus (GABS). ALMOST ALWAYS!
  2. Can also be be associated with various
    - viral illnesses and
    - parasitic infections
    • complement activation and
    • inflammation.
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11
Q

Poststreptococcal glomerular nephritis (PSGN):
Clinical Signs/Symptoms
9

A
  1. Often asymptomatic
  2. Microscopic hematuria leading to Gross hematuria
  3. Proteinuria (can reach nephrotic range)
  4. Edema
  5. Hypertension
  6. Increased serum creatinine
  7. Variable decline in GFR
  8. Hypocomplementemia (C3, C4)
  9. Acute Renal Failure and need for dialysis is uncommon
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12
Q

Poststreptococcal glomerular nephritis (PSGN):

What lab test should we do if we suspect this?

A

Serology… for elevated titers of antibodies to extracellular streptococcal products is evidence of a recent GABS infection.

The streptozyme test!!!!

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13
Q

Poststreptococcal glomerular nephritis (PSGN):
The streptozyme test measures 5 streptococcal antibodies, & is positive in 95% of patients due to pharyngitis and about 80% of those with skin infections
What are the 5 antibodies?

A
  1. Anti-streptolysin (ASO)*****
    - many people will just order this
  2. Anti-hyaluronidase (AHase)
  3. Anti-streptokinase (ASKase)
  4. Anti-nicotinamide-adenine dinucleotidase (anti-NAD)
  5. Anti-DNAse B antibodies
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14
Q

Poststreptococcal glomerular nephritis (PSGN). When is a renal biopsy perfomred?
2

A
  1. other glomerular disorders are being considered because they deviate from the natural course of the PSGN
  2. presents late without a clear history of prior streptococcal infection
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15
Q
  1. Persistently low C3 levels beyond 6 weeks are suggestive of a diagnosis of what?
  2. Recurrent episodes of hematuria are suggestive of what?
A
  1. membranoproliferative glomerulonephritis.

2. IgA nephropathy and are rare in PSGN.

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16
Q

Poststreptococcal glomerular nephritis (PSGN) treatment?

3

A

Management is supportive and focused upon treating the volume overload

  1. sodium and water restriction
  2. diuretic therapy Lasix (furosemide) - will also treat what- HTN
  3. In patients with acute renal failure, dialysis may be required
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17
Q

Poststreptococcal glomerular nephritis (PSGN) prognosis?

2 paths

A
  1. Most patients, particularly children, have complete clinical recovery, and resolution of their disease process begins within the first 2 weeks.
  2. A small subset of patients have late renal complications (hypertension, increasing proteinuria, and renal insufficiency
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18
Q
  1. IgA Nephropathy aka Berger’s Disease most common lesion to cause what?
  2. Commonly in what races? 2
  3. Gender?
  4. Commonly in what age?
A
  1. to cause primary GN in the developed world
  2. Higher frequency in Asians and Caucasians—relatively rare in blacks
  3. Male to Female ratio of 2:1
  4. Age—80% are between 15-35YO at diagnosis
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19
Q

IgA Nephropathy/Berger’s Disease

  1. Etiology?
  2. What is the initiating event?
  3. Dysregulated synthesis and metabolism of IgA results in ?
  4. Environmental factors that drive the generation of pathogenic IgA? 2
A
  1. The etiology of primary IgA nephropathy is generally unknown.
  2. The initiating event is the mesangial deposition of IgA.
  3. IgA immune complexes with characteristics that favor mesangial deposition and accumulation.
    • dietary antigens and
    • mucosal infections
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20
Q

IgA Nephropathy Presentation
Typically presents in one of three ways: First way?
3

A

50% present with:

  1. Gross hematuria*****
    - May be recurrent
    - Usually after URI “synpharyngitic hematuria.”
  2. Flank Pain
  3. Fever
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21
Q

IgA Nephropathy Presentation
Typically presents in one of three ways: Second way?
2

A

30% present with:

  1. Microscopic hematuria
    - -May eventually lead to gross hematuria
  2. Mild proteinuria
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22
Q

IgA Nephropathy Presentation
Typically presents in one of three ways: Third way?
5

A

10% present with:
1. Nephrotic syndrome (proteinuria, lipiduria, fatty casts)- Which looks like=

  1. Edema
  2. Renal insufficiency
  3. Hypertension
    - -Rare malignant hypertension
  4. Hematuria
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23
Q

IgA Nephropathy Diagnosis
2

What else may mesangial IgA be seen with? 3

IgA nephropathy may rarely be seen with other glomerular diseases such as? 2

A
  1. Suspicion based on clinical history, and urinalysis
  2. Confirmation is by kidney biopsy
  3. Mesangial IgA deposition may also be seen with
    - cirrhosis,
    - celiac disease and
    - HIV infection
    • minimal change disease and
    • granulomatosis with polyangiitis (Wegener’s)
24
Q

IgA Nephropathy Diagnosis.

Confirmation is by kidney biopsy. What will we see? 2

A
  1. Prominent IgA deposits in the mesangium and along glomerular capillary walls
  2. C3 and IgG are also deposited
25
Q

Treatment of IgA Nephropathy
General intervention?
2

A
  1. Blood pressure control (all)

2. ACEIs and/or ARBs

26
Q

In which IgA nephropathy pts should we make sure are on an ACE and ARB? 3

Pts with severe or progressive disease need to be on what? 2

A

For patients w/

  1. persistent proteinuria,
  2. slightly reduced GFR and
  3. mild/mod changes on biopsy

Look for reduction in protein excretion

  1. Corticosteroids and/or
  2. immunosuppressants
27
Q

IgA Nephropathy Prognosis

  1. What happens to most pts?
  2. Some have persistant, low grade what? 2
  3. Slow progression to what occurs in 50% of individuals?
  4. Clinical predictors of progression include? 3
  5. What pts are at low risk for progressive kidney disease?
A
  1. Most patients enter a sustained clinical remission
  2. hematuria and/or proteinuria
  3. end-stage renal disease
  4. Clinical predictors of progression include:
    - elevated serum creatinine
    - hypertension
    - persistent protein excretion above 1000 mg/day.
  5. Patients who have recurrent episodes of gross hematuria without proteinuria
28
Q

Henoch-Scholein Purpura (HSP)/ IgA Vasculitis‏ is characterized by what?

Usually occurs in what ages?

A

Systemic vasculitis characterized by the tissue deposition of IgA-containing immune complexes

HSP usually occurs between ages of 3-15

29
Q

The underlying cause of HSP is unknown, but the main theory is?

A

HSP represents an immune-mediated vasculitis that may be triggered by a variety of antigens

30
Q

Henoch-Scholein Purpura (HSP)/ IgA Vasculitis‏
Tetrad of clinical manifestations?

What is present?

Can develop over what time?

A
  1. Palpable purpura without thrombocytopenia or coagulopathy
  2. Arthritis/arthralgias
  3. Abdominal pain

Renal disease (GN)

Can develop over days to weeks and manifestations can vary in order of presentation

31
Q

HSP Nephritis
1. Pathogenesis is similar to what?

  1. What is the range of clinical presentation?
  2. How does the prognosis differ in children and then adults?
A
  1. The pathogenesis is similar to that of IgA nephropathy, with identical histologic findings
    • Can have mild (asymptomatic hematuria) to
  • varying degrees of proteinuria, to
  • severe presentation with nephrotic syndrome and even renal failure
    3. Generally mild in children, while adults are more likely to develop moderate to severe disease.
32
Q

HSP nephritis diagnosis is confirmed by? But what is t reserved for?

Whats an easier marker? 2

A
  1. The diagnosis is confirmed by kidney biopsy:
    - -A kidney biopsy is reserved for when diagnosis is uncertain or severe renal involvement
  2. marked proteinuria and/or
  3. impaired renal function during the acute episode
33
Q

HSP Nephritis
1. Prognosis?

  1. A minority of pts develop what? 2
  2. For pts with crescentic glomerulonephritis how should we treat? 2
  3. What about for pts who progress to end stage renal failure? 2
A
  1. Renal disease in HSP is favorable in most patients, but recurrence of HSP is common.

2.

  • persistent renal manifestations or
  • end-stage renal disease
    • pulse IV methylprednisolone, followed by
    • oral prednisone may be effective.
  2. Dialysis and renal transplantation can be performed in those patients who progress to end-stage renal disease.
34
Q
  1. Rapidly Progressive Glomerulonephritis (RPGN) is marked by how?
  2. What will our urine look like?
  3. Onset and progression of this disease?
  4. Characterized morphologically by what?
  5. Clinically by what?
A

Clinical syndrome:
1. Acute glomerulonephritis marked by a rapid progression to end-stage renal failure

  1. Features of glomerular disease in urine (coca cola urine)
  2. Progressive loss of renal function over short period of time (days, weeks, months)
  3. extensive crescent formation!!!
  4. clinically by progression to end-stage renal disease
35
Q

What does the cresentic GN refer to?

A

Crescent formation nonspecific response to severe injury to glomerular capillary wall

36
Q

Cresentic GN:
1. Initially what does it begin as?

  1. This results in? 3
A
  1. active inflammation of the capillary wall
    • the movement of plasma products, including fibrinogen, into Bowman’s space with subsequent fibrin formation,
  • the influx of macrophages and T cells, and
  • the release of proinflammatory cytokines.
37
Q

What finally develops to cause the crescents?

What stage of the disease does this represent?

A

Followed by the development of fibrocellular and fibrous crescents,

which represent a stage of the disease that is not likely to respond to immunosuppressive therapy

38
Q

What are the different types of RPGN?

3

A
  1. Anti-glomerular basement membrane
  2. Immune complex RPGN
  3. Pauci-immune RPGN
39
Q

Describe the following:

  1. Anti-glomerular basement membrane (GBM/Goodpasture’s syndrome)
  2. Immune complex RPGN 3
  3. Pauci-immune RPGN 2
A
  1. antibody disease of lungs and glomerulus caused by anti-GBM antibodies.
  2. deposition of immune complexes in the glomeruli
    - IgA nephropathy
    - Postinfectious glomerulonephritis
    - Lupus nephritis
  3. a necrotizing glomerulonephritis and vasculitis
    - ANCA positive
    - Systemic symptoms of a vasculitis
40
Q

RPGN:
1. Insideous Onset will present how? 2

  1. More acute onset will present how? 4
  2. If GBM type it will present how? 4
A

Insidious onset:

  1. Fatigue
  2. Edema

More acute onset:

  1. Macroscopic hematuria
  2. Oliguria
  3. Edema
  4. Renal insufficiency

If GBM type:

  1. pulmonary hemorrhage
  2. Hemoptysis
  3. pulmonary infiltrates
  4. dyspnea
41
Q

RPGN Evaluation

4

A
  1. Urinalysis
  2. High BUN and Creatinine
  3. Renal biopsy
  4. Serologic assays to determine type and cause
42
Q

RPGN Evaluation

What will we see on the urinalysis? 3

A
  1. hematuria
  2. red cell casts and other casts
  3. proteinuria
43
Q

RPGN Evaluation

What will we see on the serological assays? 3

A
  1. ANCA
  2. anti-GBM antibodies
  3. antinuclear antibodies
44
Q

RPGN Treatment

  1. What is essential to minimize the degree of irreversible renal injury? 3
  2. Empiric therapy with severe disease while awaiting biopsy results? 3
  3. How does the biopsy help us?
A
  1. Early diagnosis with
    - renal biopsy and
    - serologic testing and
    - early treatment
    • Pulse methylprednisolone
    • Oral or IV cyclophosphamide
    • Sometimes plasmapheresis
  3. Treatment more specific after biopsy results
45
Q
  1. What is Acute interstitial nephritis (AIN)?
  2. What is it characterized by?
  3. Pathologically how does interstitial nephritis occur?
A
  1. is a renal lesion that causes a decline in creatinine clearance
  2. characterized by an inflammatory infiltrate in the kidney interstitium.
  3. Interstitial inflammatory response with edema and possible tubular cell damage
46
Q

Interstitial Nephritis etiologies?

3

A
  1. Drugs account for 70% of cases
  2. Infectious diseases
  3. Immunologic entities:
47
Q

Drugs that cause interstitial nephritis?

8

A
  1. Penicillin
  2. Cephalosporins
  3. Sulfanamides
  4. Sulfanamide containing diuretics
  5. NSAIDs
  6. Rifampin
  7. Dilantin
  8. Allopurinol
48
Q

Infectious etiologies of interstitial nephritis?

5

A
  1. Streptococcal infections
  2. Leptospirosis
  3. Cytomegalovirus
  4. Histoplasmosis
  5. Rocky Mountain spotted fever
49
Q

Immunologic etiologies of interstitial nephritis?

4

A
  1. Lupus
  2. Sjogren’s syndrome
  3. Sarcoidosis
  4. Cryoglobulinemia
50
Q

Interstitial Nephritis presentation?

8

A
  1. Fever (>80%)
  2. Rash (25-50%)
  3. Arthalgias
  4. Peripheral blood eosinophilia (80%)
  5. Red cells in urine (95%)
  6. White cells and white cell casts in urine
  7. Oliguria
  8. Azotemia
51
Q

Interstitial Nephritis
evaluation:
Urinalysis shows?
3

A
  1. RBCs in urine (95%)
  2. White cells and white cell casts in urine
  3. Proteinuria commonly found in NSAID related interstitial nephritis**
52
Q

Treatment for interstitial nephritis? 2

Prognosis? 3

If renal failure persists what should we treat with? 2

A
  1. Supportive measure
  2. Removal of inciting agent
  3. Carries a good prognosis
  4. Rarely progresses to End Stage Renal Disease
  5. Recovery usually over weeks to months

If renal failure persists:

  1. Short course of corticosteroids
  2. High dose Methylprednisolone or Prednisone for 1-2 weeks, then taper
53
Q

Nephrotic Syndrome 5 VS Glomerulonephritis 5?

A

Nephrotic Syndrome

  1. Edema
  2. Proteinuria
  3. Hypoproteinemia
  4. Elevated LDL
  5. Hypercoagulability (↑fibrinogen, factor V)

Glomerulonephritis

  1. R = Red urine (hematuria)
  2. O = Oliguria
  3. P = Proteinuria
  4. E = Elevated BP, BUN
  5. Low C3
54
Q

What could a low C3 be due to?

3

A
  1. Post-Strep
  2. Membranoproliferative
  3. SLE
55
Q

Treatment of Acute GN in General:
1. Whats the most common type of GN?

  1. When would we admit someone with GN? 3
  2. What do we need to monitor?
  3. What do we want to treat to avoid sequelae and with what? 3
A
  1. Most common type of Acute GN
  2. Admit if
    - HTN,
    - edema, or
    - signs of renal failure
  3. Monitor/correct electrolyte anomalies
  4. Treat HTN to avoid sequelae
    - Diuresis → loop diuretics like Lasix
    - Fluid and salt restriction
    - Anti-hypertensives
56
Q

Treatment Specific to PSGN?

A

Antibiotics

57
Q

PSGN:

  1. HTN resolves in how long?
  2. C3 levels return to normal in how many weeks?
  3. Gross hematuria resolves in how long?
  4. Microscopic hematuria resolves in how long?
  5. Proteinuria resolves in how long?

Progression to renal dysfunction RARE

A
  1. ~ 1-2 weeks
  2. ~ 6 weeks
  3. ~ 6 weeks
  4. ~ 1 year
  5. ~ 6 months

Nephrology (15 decks)

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