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Renal/Respiratory > Glomerular Disease 1 > Flashcards

Glomerular Disease 1 Flashcards

1
Q

what are the possible mechanisms of glomerular disease? (three)

A

• Immunocomplex deposition
– Circulate then deposit in glomerulus
• eg DNA-anti-DNA complexes in Lupus
– activates complement resulting in neutrophil chemotaxis

  • Antibodies against GBM or glomerular antigens
  • Cytokine production by inflammatory cells
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2
Q

circulating cause of glomerular disease

A

immune complex deposition

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3
Q

in situ cause of glomerular disease

A

anti-gbm, membranous: antibody against glomerular antigen

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4
Q

nomenclature of glomerular disease: possible types

A

diffuse, focal, global, segmental

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5
Q

how does glomerular disease present?

A
  • loss of time (temporal change)
  • hematuria (quality)
  • proteinuria (quantity)
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6
Q

nephrotic syndrome characteristics

A 
• Proteinuria > 3.5 g/day
• Hypoalbuminemia
• Edema
     – Loss of plasma oncotic pressure vs Na/H20 retention
• Hyperlipidemia
     – increased hepatic protein
production
• Lipiduria
• Hypercoagulability
     – loss of Proteins C & S
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7
Q

characteristics of nephritic syndrome

A 
• Mild proteinuria
• Hematuria
     – RBCs, RBC casts, dysmorphic
RBCs
• Hypertension
• Edema
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8
Q

common characteristic for both nephrotic and nephritic syndromes

A

both may have varying degrees of renal dysfunction

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9
Q

causes of acute glomerularnephritis

A 
– IgA nephropathy
– Post-infectious GN
– Anti-GBM disease/Goodpasture’s – Small vessel vasculitis
– Lupus nephritis
– Membranoproliferative GN
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10
Q

IgA nephropathy prevelance and age of onset

A
  • Most common GN worldwide

* Most patients between age 10-50

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11
Q

features of IgA nephropathy

A

• Hematuria is most prominent feature
– 50-60% episodic gross hematuria
– 30% persistent microhematuria
– 10% acute GN or nephrotic syndrome
• Proteinuria, if present, is generally mild
• Many cases are subclinical

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12
Q

symptoms of IgA nephropathy

A
  • Dysuria and loin pain may accompany hematuria
  • Hematuria frequently occurs in conjunction with an upper respiratory infection (“synpharyngitic hematuria”)
  • HTN may be present in patients with more advanced disease
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13
Q

IgA nephropathy histology features on LM

A

• LM: Variable mesangial hypercellularity (mesangial proliferation)
– May see segmental proliferation, segmental sclerosis and necrosis with crescents

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14
Q

IgA nephropathy histology features on IF

A

• IF: Mesangial IgA deposition (KEY/bolded)

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15
Q

IgA nephropathy histology features on EM

A

• EM: Mesangial electron dense deposits (“paramesangial”)

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16
Q

IgA nephropathy prognosis

A

• Prognosis based on serum creatinine, BP, and degree of proteinuria
– 40% of patients will slowly develop chronic kidney disease

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17
Q

IgA nephropathy treatment

A
  • Fish oil may slow progression of disease
  • ACE-inhibitors used to control blood pressure
  • Corticosteroids, other immunosuppressants also may be used in progressive disease
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18
Q

Henoch-Schönlein Purpura cause

A

• Systemic disorder characterized by IgA deposition in multiple organs

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19
Q

Henoch-Schönlein Purpura manifestations

A

– skin–characteristic non-blanching purpura on legs and buttocks
– joints–transient arthralgias
– GI tract–abdominal pain, vomiting, melena, hematochezia
– kidney–hematuria, proteinuria; rarely progressive renal failure

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20
Q

post-infectious GN classic example and characteristics

A
  • Post-streptococcal GN– classic example
  • Follows infection in nephritogenic strain of group A beta-hemolytic streptococcus
  • Occurs 7-14 days after pharyngitis; 14-28 days after skin infection
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21
Q

post-strep GN clinical features

A

• Sudden onset hypertension, azotemia, oliguria, edema (periorbital) and cola- or tea-colored urine

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22
Q

post-strep lab findings

A

– low C3 complement level
– Anti-streptolysin O (ASO) can be elevated (high anti-DNase B titers)
– Urinalysis: red blood cell casts, mild proteinuria

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23
Q

post-strep histology features on LM

A

• LM: Enlarged, hypercellular glomeruli. Diffuse mesangial and endocapillary proliferation with neutrophils. May see crescents.

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24
Q

post-strep histology features on IF

A

• IF: Granular capillary wall and mesangial IgG and C3

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25
Q

post-strep histology features on EM

A

• EM: Mesangial and large subepithelial “hump-like” deposits (KEY/bolded)

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26
Q

post-strep GN prognosis

A

• 95% of children will recover with conservative management
~1% progress to renal failure
• 60% of adults will recover promptly

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27
Q

rapidly progressive GN features

A
  • Classic nephritic syndrome with rapid progression (days to weeks) to renal failure
  • Sometimes referred to as “crescentic GN”
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28
Q

causes of rapidly progressive GN

A 
– Anti-GBM/Goodpasture’s 
– Immune complex GN
     • Lupus nephritis
     • Post-infectious
     • Cryoglobulinemia
– ANCA associated GN (Pauci immune)
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29
Q

rapidly progressive GN histology findings

A
  • segmental necrosis (early)

- segmental necrosis and cellular crescent

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30
Q

Anti-GBM/Goodpasture’s Syndrome clinical findings

A 
• Males > Females
• May present as a pulmonary-renal syndrome:
     – Hemoptysis
     – Pulmonary infiltrates
     – Glomerulonephritis
• GN alone in anti-GBM disease
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31
Q

Anti-GBM/Goodpasture’s Syndrome cause

A

• Due to circulating anti-GBM antibody

– Antigen is α3-chain of type IV collagen

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32
Q

Anti-GBM/Goodpasture’s Syndrome diagnosis

A

– + anti-GBM antibody in blood

– Linear IgG and C3 on kidney biopsy IF

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33
Q

Anti-GBM/Goodpasture’s Syndrome treatment

A

– Plasmapheresis
– Prednisone
– Cytoxan

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34
Q

Pauci-immune GN characteristics

A

• Crescenteric GN with little deposition of immune reactants
– “Pauci-immune”

– As opposed to:
• Anti-GBM disease
• IgA nephropathy
• Lupus nephritis

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35
Q

Pauci-immune GN causes

A

• Idiopathic or associated with antineutrophil cytoplasmic antibody (ANCA) vasculitis

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36
Q

Small vessel vasculitis diseases (3)

A

• Microscopic polyangiitits (MPO-ANCA/p-ANCA)
– No granulomatous inflammation and no asthma

• Wegener’s granulomatosis (PR3-ANCA/c-ANCA)
– Necrotizing granulomatous inflammation; no asthma

• Churg-Strauss syndrome
– Necrotizing granulomatous inflammation, asthma, eosinophilia

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37
Q

vasculitis focal necrotizing lesion locations

A
  • glomerular capillaries
  • alveolar capillaries
  • epineural
  • dermal venules
38
Q

Wegener’s Granulomatosis characteristics

A

• Granulomatous vasculitis of medium to small arterioles

39
Q

Wegener’s Granulomatosis findings

A

• c-ANCA + in 80%

40
Q

Wegener’s Granulomatosis presentation

A 
• Presentation:
     – Upper resp tract symptoms (sinusitis, nasal lesions, hemoptysis)
     – Mononeuritis multiplex 
     – Pupura
     – Nephritis
41
Q

Wegener’s Granulomatosis finding on renal biopsy

A

cresenteric GN without immune deposits

42
Q

RPGN Summary for Anti-GBM disease (clinical, light microscopy, and IF microscopy)

A
  • clinical: + anti-GBM antibody in blood
  • light microscopy: Crescenteric GN
  • IF microscopy: Linear IgG an C3
43
Q

RPGN Summary for Immune-complex (clinical, light microscopy, and IF microscopy)

A
  • clinical- Lupus Post-strep
  • light microscopy-Crescenteric GN
  • IF microscopy- Variable deposition of IC and complement
44
Q

RPGN Summary for Pauci-immune (clinical, light microscopy, and IF microscopy)

A
  • clinical-ANCA+
  • light microscopy-Crescenteric GN
  • IF microscopy-Negative
45
Q

nephrotic syndrome-primary renal diseases

A

• Primary renal disease
– membranous nephropathy
– focal segmental glomerulosclerosis (FSGS)
– minimal change disease*
– *In children ~80% will have minimal change disease

46
Q

secondary causes of nephrotic syndrome

A

– systemic diseases: Diabetes mellitus, SLE, amyloidosis
– infections: HIV, Hepatitis B, Hepatitis C, syphilis
– drugs: classical examples include NSAIDs, gold, penicillamine

47
Q

nephrotic syndrome lab studies/tests to help with a diagnosis

A

• Helpful laboratory studies for secondary causes:
– ANA, anti-dsDNA, complement levels (lupus)
– serum & urine protein electrophoreses (amylodosis)
– HBV & HCV serologies
– cryoglobulins
– syphilis serology

• Renal biopsy generally indicated

48
Q

nephrotic syndrome treatments

A

– ACE-inhibitor or angiotensin-II receptor blocker to lower intraglomerular pressure and reduce proteinuria
– lipid-lowering therapy (“statins”)
– diuretics, salt restriction to improve edema

49
Q

minimal change disease characteristics

A

• Most common cause of nephrotic syndrome in children

 - peak incidence ages 2-6
 - 5% progress to end-stage renal disease
50
Q

minimal change disease treatment and prognosis

A
  • spontaneous remissions can occur
    • treatment with steroids often induces remission although relapses occur in about 75%
    • fewer relapses after puberty
51
Q

minimal change disease causes

A

• In adults, can be idiopathic or associated with:
– drugs: NSAIDs (bolded)
– neoplasms: Hodgkin’s lymphoma (bolded), pancreatic, prostate, lung, colon, & renal cell carcinomas, mesothelioma, oncocytoma
– infections: syphilis, HIV

52
Q

minimal change disease histologic features on LM

A
  • LM: Glomeruli, interstitium and tubules appear normal (KEY/bolded)
  • (lipid may been seen in PCT cells-Pathoma/First Aid)
53
Q

minimal change disease histologic features on IF

A

• IF: Negative or mesangial IgM

54
Q

minimal change disease histologic features on EM

A

• EM: Podocyte foot process effacement (fusion) (KEY/bolded)

55
Q

minimal change disease treatment

A

• Children respond well to corticosteroids
• The majority of adults with minimal change disease respond to steroids
– usually takes longer than in children
– partial remissions may occur

56
Q

membranous nephropathy prevalence

A
  • Most common cause of nephrotic syndrome in Caucasian adults
  • Secondary causes account for ~15- 20% of cases
57
Q

secondary causes of membranous nephropathy

A

– Infections: HBV (bolded)
– Connective tissue diseases: SLE (bolded)
– Neoplasms: carcinoma of lung, colon, stomach, breast; non-Hodgkin’s lymphoma (bolded)
• Consider age appropriate cancer screening
– Drugs: gold, penicillamine, mercury, NSAIDs, captopril

58
Q

membranous nephropathy clinical findings

A

• Onset is generally insidious
• Patients usually present with heavy proteinuria & nephrotic syndrome
– HTN & azotemia occur later
– Occult malignancies and infections may become evident later
– Renal vein thrombosis occurs in ~ 20%

59
Q

membranous nephropathy histologic findings on LM

A

• LM: diffuse thickening of GBM, GBM “spikes” on silver stain (KEY/bolded)

60
Q

membranous nephropathy histologic findings on IF

A

• IF: granular GBM deposits of IgG

61
Q

membranous nephropathy histologic findings on EM

A

• EM: Subepithelial deposits (with “spike and dome” appearance)

62
Q

key membranous nephropathy finding

A

immune deposits form on sub epithelial aspect of glomerular basement membrane; podocyte with effaced foot processes

63
Q

membranous nephropathy outcomes

A

“Rule of thirds”:
– 1/3 spontaneous remission
– 1/3 partial remissions with stable function
– 1/3 slowly progressive loss of renal function

64
Q

membranous mephropathy treatment

A
  • Patients without poor prognostic factors might be managed conservatively with ACE-I and/or ARB and followed closely
  • Otherwise, steroids +/- other immunosuppressive drugs are used
65
Q

Focal segmental glomerulosclerosis (FSGS) characteristics/who it effects

A

• Most common cause of idiopathic nephrotic syndrome in African-Americans

66
Q

Focal segmental glomerulosclerosis (FSGS) clinical features

A

• More aggressive than minimal change disease:
– Hypertension, hematuria more common
– renal dysfunction is commonly progressive – ESRD occurs 5-20 years after presentation

67
Q

primary FSGS

A

• Primary FSGS–usually presents with acute onset of nephrotic syndrome

68
Q

secondary FSGS

A

• Secondary FSGS–usually manifests with slowly increasing renal insufficiency and proteinuria

69
Q

hereditary FSGS

A

• Hereditary FSGS–mutations in proteins that make up the glomerular slit diaphragm

70
Q

Causes of secondary FSGS

A 
– Drugs: NSAIDs, heroin
– Infections: HIV (bolded)
– Massive obesity
– Healed previous glomerular injury
– Loss of functioning renal mass: unilateral agenesis, reflux nephropathy, etc.
71
Q

FSGS histologic findings on LM

A
  • LM: Focal and segmental glomerular sclerosis with capillary collapse, hyaline and lipid deposition and adhesion to Bowman’s capsule (KEY/bolded)
  • (hyalinosis-Pathoma/First Aid)
72
Q

FSGS histologic findings on IF

A

• IF: Negative or IgM and C3 in mesangium or in segmental scars

73
Q

FSGS histologic findings on EM

A

• EM: Podocyte foot process effacement; may see segmental sclerosis

74
Q

FSGS prognosis

A
  • Prognosis correlates with degree of proteinuria–ACE inhibitors decrease proteinuria
  • Corticosteroids can induce remission in some patients
75
Q

FSGS treatment

A

• Treatment for steroid-resistant patients and patients who relapse is problematic
– Immunosuppressives
• Progression to ESRD in 50% at 10 years

76
Q

glomerular diseases with nephrotic and nephritic features

A
  • Membranoproliferative Glomerulo-nephritis (MPGN)

- Systemic Lupus Erythematosus (SLE); Lupus Nephritis

77
Q

Membranoproliferative Glomerulo-nephritis (MPGN) characteristics

A
  • Proteinuria & hematuria commonly coexist • Hypertension occurs in 1/3
  • Low C3 complement is a prominent feature
78
Q

Membranoproliferative Glomerulo-nephritis (MPGN) clinical features

A

• Variable clinical presentation
– 50% nephrotic syndrome
– 30% asymptomatic proteinuria ± hematuria
– 20% acute GN

79
Q

causes of secondary MPGN

A

– Connective tissue diseases: SLE
– Cryoglobulinemia
– Infections: Hepatitis C virus (bolded), HBV, endocarditis, abscesses
– Neoplasms

80
Q

MPGN histologic features of LM

A

• LM: hypercellular glomeruli, endocapillary cell proliferation, lobular appearing glomeruli

81
Q

MPGN histologic features of IF

A

• IF: granular C3 deposition

82
Q

MPGN histologic features of EM

A

• EM: Subendothelial deposits

83
Q

Type I MPGN causes

A

HBV, HCV, may also be idiopathic

84
Q

Type II MPGN causes

A

associated with C3 nephritic factor (stabilizes C3 convertase –> decreased serum C3 levels)

85
Q

Systemic Lupus Erythematosus (SLE) characterization

A

• A multi-system auto-immune disorder
– abnormal autoantibody production
– immune complex deposition
– inflammatory cell infiltration

86
Q

Lupus Nephritis causes what?

A
  • Common cause of diffuse proliferative GN

* Many of the different clinical syndromes of renal disease can be occur in the setting of SLE

87
Q

lupus nephritis clinical findings

A

• 40% of patients develop overt nephritis
– follow U/A in SLE patients
– HTN suggests the presence of renal disease

88
Q

lupus nephritis diagnostic tests

A

• Renal biopsy is important in order to classify the lesion in SLE

89
Q

lupus nephritis classifications

A

Class I-VI

90
Q

lupus nephritis treatment

A

• General principles of management of any class of lupus nephritis:
– aggressive BP control
– control of lipid levels
– appropriate treatment of extrarenal involvement

• Classes III-V: usually treated with corticosteroids + cytotoxic therapy
– Class IV: renal failure rate 25% by 5-10 years

91
Q

key points to know from this lecture:

A

You should know:
• the difference between nephrotic and nephritic (GN) syndromes
• which glomerular diseases cause nephrotic syndrome vs glomerulonephritis
• the clinical and histopathologic features of IgA nephropathy, post-infectious GN, and the RPGNs (these are GNs)
• the clinical and histopathologic features of minimal change disease, membranous nephropathy, and FSGS (these are nephrotic diseases)
• that SLE can cause a number of different glomerular diseases

Renal/Respiratory (8 decks)

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