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clin med II, exam 3 > glomerulonephritis and PKD > Flashcards

glomerulonephritis and PKD Flashcards

1
Q

define glomerulonephritis

A
  • diseases that present in the nephritic spectrum and usually signifies an inflammatory process involving the glomeruli, causing renal dysfunction
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2
Q

What are the 4 main components of the glomerulus

A
  • podocytes
  • glomerular basement membrane
  • capillary endothelium
  • mesangium
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3
Q

damage to podocytes leads to

A

increased permeability and allows substances to get into the urine

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4
Q

glomerulonephritis is characterized by what two things

A
  • intraglomerular inflammatory process
  • renal dysfunction
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5
Q

List the 3 conditions in the nephritic spectrum

A
  1. asymptomatic glomerular hematuria
  2. nephritic syndrome
  3. rapidly progressive glomerulonephritis
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6
Q

“Glomerular” hematuria, dysmorphic RBCs, RBC casts and “cola-colored” urine are all consistent with what condition

A

Nephritic syndrome

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7
Q

What conditions are associated with RBC casts?

A
  • glomerulonephritis
  • vasculitis
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8
Q

Nephritic syndrome usually has how much protein in the urine

A
  • “Subnephrotic” proteinuria
    • < 3.0 g/ 24 hr
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9
Q

clinical presentation

  • cola colored urine
  • edema
    • face and eyes in am
    • feet and ankles in pm
  • HTN
  • decreased GFR
  • oliguria
A

Nephritic syndrome

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10
Q

which condition is caused from a severe injury to the glomerular wall and leads to a crescent formation (crescentic GN)

A
  • rapidly progressive glomerulonephritis (RPGN)
    • most severe and clinically urgent of nephritic spectrum
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11
Q

What is the one clinical sign that is common in all conditions in the nephritic spectrum

A

hematuria

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12
Q

distinguish extraglomerular hematuria in terms of

  • color
  • clots
  • proteinuria
  • RBC morphology
  • RBC casts
A
  • color
    • red or pink
  • clots
    • may be present
  • proteinuria
    • < 500 mg/day
  • RBC morphology
    • normal
  • RBC casts
    • absent
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13
Q

distinguish glomerular hematuria in terms of

  • color
  • clots
  • proteinuria
  • RBC morphology
  • RBC casts
A
  • color
    • red, smoky, brown or coca-cola colored
  • clots
    • absent
  • proteinuria
    • may be >500mg/day
  • RBC morphology
    • some RBCs are dysmorphic
  • RBC casts
    • may be present
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14
Q

What are the three primary disease causes of glomerulonephritis

A
  • IgA nephropathy
  • poststreptococcal GN
  • anti-GBM GN
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15
Q

What are the three secondary disease causes of glomerulonephritis

A
  • Lupus nephritis
  • Henoch-Schonlein purpura
  • Renal vascular disease
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16
Q

IgA nephropathy (Bergers disease) affects what patient populations

A
  • 2nd or 3rd decades of life
  • male
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17
Q

what causes IgA nephropathy (Bergers disease)

A
  • idiopathic
  • immune complex mediated GN
    • IgA deposition in the glomerular mesangium -> inflammatory process
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18
Q

clinical presentation

  • episode of gross hematuria
  • often follows URI
  • urine becomes cola-colored 1-2 days after illness onset
A
  • IgA nephropathy (Bergers disease)
    • can present anywhere along the nephritic spectrum
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19
Q

when should patients with IgA nephropathy (Bergers disease) be treated? what is the tx?

A
  • treat pt’s with HTN, proteinuria > 1g/d, decreased GFR
    • ACE-I or ARB
    • immunosuppressive meds
  • 1/3 have spontaneous remission
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20
Q

poststreptococcal GN affects what patient populations

A
  • bimodal
    • > 60 yo
    • children ages 5-12 yo
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21
Q

describe etiology of poststreptococcal GN

A
  • induced by group A strep infection
  • deposition of streptococcal nephritogenic antigens within the glomerulus -> triggers complement activation and inflammation
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22
Q

clinical presentation

  • varies across nephritic spectrum
  • occurs 1-3 weeks after infection
    • pharyngitis or impetigo
  • elevated antistreptolysin O titers
A

poststreptococcal GN

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23
Q

tx of poststreptococcal GN

A
  • supportive
  • children more likely to fully recover
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24
Q

Describe Anti-GBM antibody disease

A
  • autoantibodies directed against an antigen intrinsic to the glomerular basement membrane (GBM)
25
Q

Anti-GBM antibody disease usually affects what patient population

A
  • bimodal
    • M: 30s
    • M & F: 60-70s
26
Q

Anti-GBM antibody disease can present with what two conditions

A
  • glomerulonephritis alone OR
  • Goodpasture’s syndrome
27
Q

what does a patient with Goodpasture’s syndrome present with

A
  • pulmonary hemorrhage and
  • glomerulonephritis
28
Q

How do you test for anti-GBM antibodies

A
  • kidney biopsy
29
Q

treatment of anti-GBM antibody disease

A

plasmapheresis + prednisone + cyclophosphamide

30
Q

explain how SLE causes glomerulonephritis

A
  • Anti-dsDNA antibodies seen in SLE are nephritogenic
31
Q

What is Henoch-Schonlein Purpura

A
  • systemic, small vessel vasculitis
  • IgA immune complex deposition
    • skin, GI tract, kidneys
32
Q

Henoch-Schonlein Purpura usually affects what patient population

A
  • children
  • male
33
Q

Henoch-Schonlein Purpura is often preceded by what

A
  • URI often precedes by 1-3 weeks
    • i.e. streptococcal infections
34
Q

list the tetrad of clinical manifestations of Henoch-Schonlein Purpura

A
  1. palpable purpura
  2. arthritis/arthalgias
  3. abdominal pain
  4. renal disease -> glomerulonephritis
35
Q

tx of Henoch-Schonlein Purpura

A
  • supportive
  • +/- immunosuppressive medications and plasmapheresis
36
Q

Pauci-immune glomerulonephritis is caused by the following system ANCA-associated small vessel vasculitides

A
  1. Granulomatosis with polyangiitis (Wegeners)
  2. Microscopic polyangiitis
  3. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
37
Q

what are the common characteristics seen in Pauci-immune glomerulonephritis

A
  • M=F
  • > or = 55
  • Absence of immune deposits
  • frequently presents as rapid progressive GN
  • 50% have pulmonary disease
38
Q

What is the problem with ANCAs

A
  • they bind to antigens -> tissue damage
39
Q

Granulomatosis with Polyangiitis presents with what triad of symptoms

A
  1. Glomerulonephritis
  2. Upper respiratory tract involvement
  3. Lower respiratory tract involvement
40
Q

clinical presentation

  • fever, myalgia, arthralgia
  • otorrhea, purulent rhinorrhea, nasal ulcers
  • cough, hemoptysis, SOB
  • microscopic hematuria, proteinuria
A

Granulomatosis with Polyangiitis

41
Q

Microscopic polyangiitis has a similar presentation to granulomatosis with polyangiitis except

A
  • rarely have significant lung disease
  • rarely have destructive sinusitis
42
Q

patients with a hx of what are more susceptible to get Eosinophilic Granulomatosis with Polyangiitis

A
  • asthma
  • eosinophilia
43
Q

Eosinophilic Granulomatosis with Polyangiitis develops in what 3 phases

A
  1. prodromal phase
  2. eosinophilic phase
  3. vasculitic phase
44
Q

Presentation

  • segmental transmural inflammation of muscular arteries
  • middle-aged, older adult males
  • tendency to spare the lungs
  • ANCA is Negative
A

Polyarteritis Nodosa

45
Q

Polyarteritis Nodosa is caused by

A
  • idiopathic
  • triggered by HBV
46
Q

explain how transmural inflammation causes

A
  • causes luminal narrowing -> thrombosis -> ischemia/infarction
  • causes weakening of vessel wall -> microaneurysms -> hemorrhage
47
Q

clinical presentation

  • PNS and dermatolgoic symptoms
  • renal manifestations (60%)
    • renal infarctions -> proteinuria, hematuria, renal insufficiency
    • RBC casts are absent
A

Polyarteritis Nodosa

  • **this is a vasculitis, does not cause GN
48
Q

positive C-ANCA is consistent with

A

granulomatosis with polyangiitis

49
Q

Treatment for both Pauci-Immune GN and polyarteritis Nodosa

A
  • immunosuppressive
  • +/- plasmapheresis
  • steroid taper
  • immunosuppressive agents
50
Q

What is the most common form of polycystic kidney disease? what is it caused by

A
  • autosomal dominant PKD
  • mutations in PKD-1 or PKD-2 gene
51
Q

when does autosomal dominant PKD develop

A

40s or 50s

52
Q

autosomal dominant PKD causes cysts on bilat kidneys, kidney enlargement and decline in renal function. what are some extrarenal manifestations

A
  • cerebral aneurysms
  • cardiac valvular abnormalities
  • hepatic, splenic, pancreatic cysts
53
Q

clinical presentation

  • large, palpable kidneys on exam
  • HTN
  • hematuria
  • nephrolithiasis
  • UTI
  • mild proteinuria
A

autosomal dominant PKD

54
Q

how is autosomal dominant PKD diagnosed

A

US: initial test and diagnostic

55
Q

If a patient has PKD and HTN, he/she should be treated with

A

ACE-I or ARB

56
Q

autosomal recessive PKD usually affects what age group? what gene is affected

A
  • infants and children
  • mutation in PKHD1 gene
57
Q

autosomal recessive PKD usually affects what two organs

A
  • kidneys
  • biliary tract
    • see bilateral markedly enlarged kidneys and congenital hepatic fibrosis at birth
58
Q

How is autosomal recessive PKD diagnosed and treated

A
  • US
  • supportive
    • HTN management
  • dialysis, kidney transplant
  • possible liver transplant

clin med II, exam 3 (6 decks)

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