Glomerulonephritis. Large Group 4 -Barnes Flashcards

1
Q

What are some primary causes of nephritic syndrome? (2)

A

Acute proliferative GN (acute post-infectious)

crescentic GN

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2
Q

What are some primary causes of Nephrotic syndrome? (4)

A

Membranous GN

Minimal change disease

focal segmental glomerulosclerosis

Membranoproliferative GN

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3
Q

What can a dysmorphic RBC in the urine indicate?

A

it came from the glomerulus–> glomerular injury

can look like mickey mouse ears

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4
Q

What 3 things make up the glomerular filtration barrier?

A

endothelial cells (fenestrated)

Glomerular basement membrane (3 layers)

podocytes (with filtration slits and a diaphragm)

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5
Q

What are the major indications of nephritic syndromes?

A

hematuria (RBC casts)

HTN

azotemia

oliguria

proteinuria <3.5g/day

inflammatory glom injury

vasculitis or IC deposits

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6
Q

What are the major indications of nephrotic syndromes?

A

severe proteinuria (>3.5g/day)

hypoalbuminemia (<3g/dL)

generalized edema

hyperlipidemia

lipiduria

non-inflammatory glom injury

podocyte and basement membrane damage

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7
Q

What is the most common glomerulonephritis worldwide?

A

IgA nephropathy

“Berger’s Disease”

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8
Q

How long after URI will IgA nephropathy symptoms appear? What will be the main presenting symptom?

A

1-2 days after URI

microscopic/macroscopic hematuria

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9
Q

How is Alport’s Syndrome diagnosed?

A

biopsy kidney

thinned basement membrane with “splitting” of the lamina densa on EM

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10
Q

What are the symptoms that will appear with Alport’s syndrome?

A

sensorineural deafness and lenticonus of the lens capsule

X-linked defect in type IV collagen (mutation in C0L4A3)

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11
Q

What is the main problem in Benign Familial Hematuria? What are the symptoms? What will this look like on EM?

A

Type IV collagen genetic defect, similar to Alport’s

symptoms: hematuria, normal BP, very little proteinuria. rarely progresses to ESRD

line through the basement membrane in EM

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12
Q

What is the treatment for Alport’s?

A

ARBs and ACE Inhibitors

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13
Q

What are the different classifications of SLE? Which ones are nephritic vs nephrotic?

A

I=Minimal mesangial

II=Mesangial proliferation

III=focal proliferative

IV=diffuse proliferative

V=membranous

VI=advanced sclerotic

I and II are mild

V is nephrotic

I can progress to IV (nephritic)

and all can end at VI =RPGN

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14
Q

How long after an URI will symptoms from post-strep GN appear?

A

2-4 weeks after a URI

children infected > adults

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15
Q

What studies must be done on a sample from a kidney biopsy?

A

light microscopy

immunoflorescence

Electron microscopy

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16
Q

What blood tests are associated with SLE?

A

ANA

anti-ds DNA* specific

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17
Q

What are the presenting symptoms of SLE GN?

A
Can present as isolated Lupus Nephritis
Proteinuria
Hematuria
Hypertension
RBC casts or dysmorphic RBCs
Varying degrees of renal failure
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18
Q

What lab results are consistent with Post-strep GN?

A

+ ASO antibody

low serum complement

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19
Q

How does Post-Strep GN appear in EM?

A

Lumpy bumpy sub-epithelial deposits

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20
Q

What is causing the damage in Post-strep GN?

A

the body’s reaction to an infection (not the bacteria!!)

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21
Q

What are the typical lab and microscopic findings for Membranoproliferative GN Type I?

A

Tram tracking basement membrane (“splitting”) on PAS

low complement

lobulated light microscopy due to IC deposit between the mesangium and endothelium of BM

22
Q

What are the risk factors for Membranoproliferative GN Type I?

A

IV drug abuse

endocarditis, SLE, hepatitis B and C, cryoglouminemia

23
Q

How does Wegner’s granulomatosis present?

A
fever
recurrent sinusitis (nasal ulcers) 
hemoptysis 
micro or macroscopic hematuria 
RBC casts
24
Q

What biopsy findings are present in Wegner’s?

A

anti-PR3 Ab (c-ANCA)

small vessel vasculitis

non-caseating granulomas

25
Q

What is Churg-Strauss associated with? What antibodies are present with this?

A

asthma or allergic rhinitis (eosinophilia)

p-ANCA antibodies

26
Q

How can you differentiate between Micro-polyangitis and Churg-Strauss from Wegner’s ?

A

both Churg-Strauss and Micro-polyangitis will have p-ANCA antibodies and no granulomas.

Churg-strauss is associated with asthma and focal segmental necrotizing glomerulonephritis.

Wegner’s=c-ANCA antibodies and non-caseating granulomas

27
Q

What is the typical presentation of Goodpastures?

A
young men (20-40) 
pulmonary hemorrhage 
hemoptysis 
microscopic hematuria
RBC casts 

*poor prognosis

28
Q

What are the biopsy findings associated with Goodpastures?

A

anti-GBM

smooth, linear pattern of IgG and C3 on immunoflourescence

29
Q

What are the 3 types of RPGN? examples of each

A

Type I: anti-GBM
goodpastures

Type II: immune complex
post-infectious, SLE

Type III: pauci-immune
wegners, microscopic polyangitis

30
Q

How will the 3 types of RPGN differ in immunoflourescence?

A

I: linear

II: granular

III: nothing

31
Q

If a young African American male presents with proteinuria without hematuria, what should you suspect?

A

FSGS

32
Q

What is a fatty cast pathognomonic for?

A

Nephrotic syndrome

33
Q

What needs to be ruled out in a young patient presenting with FSGS?

A

HIV and hepatitis

34
Q

What are the 3 main risk factors for FSGS?

A

AIDS, heroin, Obesity

35
Q

What will be the biopsy findings associated with FSGS?

A

LM=global capillary collapse, sclerosis and hyalinization

EM=podocyte foot process effacement
-increased mesangial matrix in sclerotic region

36
Q

What is the typical biopsy finding in minimal change disease?

A

podocyte foot process effacement

NO immune complexes (no Ig or complement involved)

37
Q

How does Minimal Change Disease respond to steroids?

A

GREAT!

38
Q

What type of GN is associated with cancer?

A

membranous nephropathy

39
Q

What is the most common cause of nephrotic syndrome in kids? Adults?

A

Kids=minimal change disease

adults=membranous nephropathy

40
Q

What are the biopsy findings associated with membranous nephropathy?

A

LM=glomerular capillary wall thickening

silver stain BM “spikes” and domes

EM=sub-epithelial deposits and podocyte effacement

41
Q

What are the general courses of Membranous Nephropathy?

A

1/3 get spontaneous remission

1/3=continue to have relapsing nephrotic syndrome but maintain normal renal function

1/3 develop renal failure or die from complications of nephrotic syndrome

42
Q

What will the urine dipstick show in a pt with renal amyloidosis?

A

nothing

Amyloid does not show up on the dipstick, only albumin does

do a 24 hour urine protein to check for amyloidosis

43
Q

What will be the biopsy findings in renal amyloidosis?

A

LM=amyloid deposition throughout the glomerulus (smooth, bright pink)

EM=fibers deposited in BM

green bifringence on congo red stain

44
Q

What is the likely GN?

joint discomfort, facial rash, hematuria and antibodies to ds-DNA in a 25 yo woman

A

Lupus nephritis

45
Q

What is the likely GN?

Sinus infection, increasing creatinine, hematuria, hemoptysis, anti-PR3 antibodies. Crescents on renal biopsy

A

Wegner granulomatosus

46
Q

What is the likely GN?

18 yo male with DM I, normal creatinine, and nephrotic syndrome

A

diabetic nephropathy

47
Q

What is the likely GN?

50 yo with hematuria, proteinuria, increasing creatinine, hypocomplementiemia, and liver disease, secondary to Hep C

A

Type I MPGN

48
Q

What is the likely GN?

44 yo male with hemoptysis, hematuria, and increasing creatinine. crescents on biopsy and linear IF pattern

A

anti-GBM disease

goodpastures

49
Q

What is the likely GN?

40 yo male with nephrotic syndrome, inc creatinine, + HIV. podocyte effacement on EM

A

FSGS

50
Q

What is the likely GN?

14 yo female with severe edema, low serum albumin, bubbly urine. LM shows normal but diffuse podocyte effacement on EM

A

minimal change disease

51
Q

What is the likely GN?

23 yo with recurrent hematuria shortly after URIs. Creatinine is normal, no proteinuria

A

IgA nephropathy

52
Q

What is the likely GN?

19 yo male with hearing loss, non-nephrogenic range proteinuria and rising creatinine

A

Alport’s Disease