Nephritis Nephrosis TBL Flashcards

1
Q

How is nephrotic syndrome defined?

A
  1. acute onset of edema
  2. proteinuria (>3.5g/d)
  3. hypoalbuminemia
  4. hyperlipidemia
  5. lipiduria
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2
Q

What is acute nephritic syndrome

A
  1. edema
  2. hypertension
  3. azotemia (sometimes oliguria)
  4. nephritic urinary sediment (RBC, WBC, cellular casts)
  5. mild proteinuria
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3
Q

What is Rapidly Progressive glomerulonephritis (RPGN). How serious is it?

A

rapid decrease of GRF associated with evidence of GN on urinary sediment
GLOMERULAR CRESENT
-emergency need fast tx

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4
Q

What are the 3 components of the glomerular epithelial barrier

A
  1. fenestrated capillary endothelium
  2. glomerular basement membrane
  3. podocytes
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5
Q

What prevents plasma proteins from leaking into the urinary space?

A

Slit diaphragms bridgeing the filtration slits between adjacent podocyte foot processes

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6
Q

What is the etiology of GN?

A

deposition of immune complexes
leukocyte infiltration
inflammation disruption of the filtration barrier

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7
Q

What is Membranous Nephropathy (MN) or Membranoproliferative glomerulonephritis (MPGN)

A

abnormal thickening of the GBM

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8
Q

What is the differential diagnosis for nephropathy?

A
  1. Focal and segmental glomerulosclerosis (FSGS)
  2. collapsing GN
  3. Minimal change disease (MCD)
  4. Membranous nephropathy (MN)
  5. Diabetic Nephropathy (DN)
  6. disorders associated with plasma cell dyscrasias (amyloidosis)
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9
Q

What are causes of MCD?

A

NSAID, Hodgkin’s lymphoma, idiopathic

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10
Q

What are causes of secondary FSGS?

A

Reduced nephron mass
Sickle cell disease
Massive obesity
inherited podocytopathy

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11
Q

What are causes of Collapsing GN?

A
HIV-associated nephropathy
Pamidronate use (breast cancer, myeloma pts)
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12
Q

What are causes of Membranous Nephropathy?

A

SLE –> antirheumatic drugs
Hep B
Solid tumors

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13
Q

What are some deposition disease associated with Nephropathy?

A

Amyloidosis

Light chain deposition disease

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14
Q

What is the management for Nephropathy? (proteinuria, edema, hyperlipidemia)

A
Proteinuria:
1. ACE inhib
2. angiotensin II receptor blocker (ARB)
Edema
1. salt restriction
2. loop diuretics
Hyperlipidemia
1. statins
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15
Q

What are the characteristics of MCD? presentation?

A
  1. normal renal biopsy findings by light/immunofluorescency microscopy
  2. primary cause of nephrotic syndrom in children
  3. presents with rapid onset of anasarca + hypoalbuminemia, hyperlipidemia, proteinuria
  4. ELECTRON MICROSCOPY: effacement of foot processes
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16
Q

Characteristics of Primary FSGS?

A
  1. leading cause of nephrosis in BLACKS
  2. most common nephrosis etiology
  3. accumulation of fibrous scar tissue
  4. associated with HYPERTENSION
  5. progress to ESRD
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17
Q

What 2 things are MCD NOT associated with?

A
  1. Hypertension

2. severely diminished renal function

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18
Q

How do you distinguish MCD and FSGS?

A

pts w MCD respond to steroids

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19
Q

How is FSGS Dx’d?

A

electromicroscopy:

diffuse effacement of foot processes, with AREAS OF SCLEROSIS

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20
Q

How are primary and secondary FSGS different?

A

Primary: immunosuppressive therapy is indicated
Secondary: more gradual onset, MINIMAL EDEMA, minimal HYPOALBUMINEMIA
—should be thought of more as renal damage (sclerosis due to compensatory effort)

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21
Q

what are the causes secondary FSGS?

A

damage/loss of glomeruli:

  1. renal agenesis
  2. Sickle cell disease
  3. vesicoureteral reflux
  4. surgical removal of kidney
    - -remaining glomeruli have higher load = hypertrophy/sclerosis
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22
Q

What is the Tx for Secondary FSGS?

A

ACEI, ARB, BP control, diuretics, statins

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23
Q

What is the etiology of Inherited FSGS?

A

podocyte protein mutations (nephrin, podocin, a-actinin-4, TRPC6)
= podocyte loss = FSGS

24
Q

What are the age ranges for the specific mutations in Inherited FSGS?

A

Nephrin - birth
Podocin - Childhood
a-actining + TRPC6 - adult

25
Q

What is the presentation of Collapsing Glomerulonephropathy

A
  1. Huge proteinuria (>10g/d)
  2. elevated creatinine
  3. rapid progression to ESRD
26
Q

What virus is Collapsing glomerulopathy associated with?

A

Parvovirus B19

27
Q

What the the lab results of Collapsing glomerulopathy?

A

US: large echogenic kidney

enormous WAXY CASTS

28
Q

What is the Tx of Collapsing glomerulopathy?

A

HAART

ACEI, ARB

29
Q

What is the cause of MN?

A

immune deposts beneath foot processes specific for podocyte protein = GBM thickening

30
Q

How is Primary and Secondary MN diagnosed?

A

primary: biopsy, phospholipase A2 receptor Ab
secondary: complement levels, ANA, Hep B Ags, presence of infection

31
Q

What is MN associated with in older people?

A

malignancy

GI, prostate, breast, lung

32
Q

What are signs of amyloidosis causes of renal dysfunction?

A
  1. older nondiabetic w/ severe albuminuria (w/ HF, hepatomegaly, peripheral neuropathy)
  2. CONGO red staining
  3. MACROGLOSSIA
  4. circulating/urinary free light chains
33
Q

What is the main cause of Nephritic syndrome?

A

inflammation within the glomerulus

34
Q

What is the lab difference between Glomerulonephritis and nephrotic disorders

A

C3, C4 is abnormal in glomerulonephritis

35
Q

What does a low C3 value with a normal C4 value indicate?

A

Poststreptococcal Glomerulonephritis or Dense Deposit disease

36
Q

What does a low C3 and low C4 value indicate?

A
  1. lupus nephritis
  2. GN associated with chronic infection (endocarditis)
  3. hep C associated MembranoProlifGN
  4. cryoglobinemia
37
Q

What type of GN is indicated by normal complement levels?

A

Small vessel vasculitis associated w/ ANCAs and anti-GBM disease

38
Q

What is the most common cause of GN? what age/race is most common

A

IgA nephropathy. whites/asians , younger men/boys

39
Q

What are the Sx of IgAN?

A
HX OF URI
asymptomatic microscopic hematuria
mild proteinuria
BROWN urine
flank pain
40
Q

What other disease is IgAN associated with?

A

RA
spondyloarthropathies
GI (celiac, chronic liver disease)
Henoch-Schonlein purpura (lesions on legs/forearms)

41
Q

what group is SLE related GN common in?

what is Dx?

A

young women - black or hispanic

check ANA titers

42
Q

what are Sx of Poststreptococcal Glomerular Nephritis (PSGN)

A
gross hematuria
proteinuria
edema
SEVERE HTN
azotemia, sometimes oliguria
43
Q

How is PSGN diagnosed

A

Hx (2-3 weeks after pharyngitis or skin infections cause group A B-hemolytic Strep)

Hypocomplementemia (low C3, normal C4)
anti-streptolysin O (ASO) titers
DNase B, hyaluronidase Abs

44
Q

What kind of pts have Endocarditis-associated glomerulonephritis

A

IV drug users

prosthetic heart valves

45
Q

What are Sx of EAGN?

A

right heart involvemnt
myalgias, arthralgias, purpura
LOW C3, LOW C4
elevated ESR, CRP

46
Q

what type of infection is associated with Acute Renal failure

A

Acute endocarditis from S. Aureus

47
Q

Where is type 1 MPGN seen most often? what are Sx?

A
adolescents/young adults
severe proteinuria
nephrotic syndrome
accompanying nephritic features
hematuria, RBC casts
Azotemia, HTN
48
Q

In adults, what is type 1 MPGN usually seen secondarily to?

A
chronic infection process
systemic autoimmune disorder
lymphoma
Hep C Virus (MOST COMMON)
mixed cryoglobulinemia
49
Q

What are the lab results of MPGN?

A

low levels of complement C3, C4

mixed nephritis-nephrotic presentation

50
Q

What are histological features of MPGN?

A

duplication of the GBM (tram tracks)

51
Q

what is the presentation of Dense deposit Disease?

A

nephrotic syndrome in childhood/adolescnece
low C3, normal C4
HTN
microscopic hematuria

52
Q

What are the prominent risk factors of Rapidly progressive glomerulonephritis?

A
  1. small-vessel vasculitis

2. auto-Abs against the GBM

53
Q

What does RPGN renal biopsy look like?

A

cresentic lesion on renal biopsy

54
Q

what causes primary FSGS?

A

idiopathic

55
Q

What is RPGN caused by?

A

Goodpasture syndrome (anti-GBM Abs) - “ribbonlike staining”
SLE
Wegemers Granulomatosis (vasculitis)
CRESCENT LESIONS