Renal: Glomerulonephritis Flashcards

1
Q

Nephritic or Nephrotic?

AKI w/ proteinuria 1-3 g/d

Hematuria (coca cola)

RBC Casts

Edema

HTN

decreased GFR

Oliguria

A

nephritic

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2
Q

Nephritic or Nephrotic?

Proteinuria > 3 g/d

Hypoalbuminemia

edema

hyperlipidemia

oval fat bodies

A

Nephrotic

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3
Q

Glomerulonephritis presents in nephritic or nephrotic spectrum?

A

nephritic

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4
Q

Focal or diffuse?

< 50% of glomeruli involved…

A

focal

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5
Q

What condition is described below?

nephritic disease

inflammatory process w/ renal dysfunction

often caused by immune complex deposition

A

glomerulonephritis

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6
Q

Which type of glomerulonephritis?

  • most severe/clinically urgen
  • progressive loss of renal fxn over short period of time
  • crescent formation
A

rapidly progressive glomerulonephritis

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7
Q

Glomerular or extraglomerular hematuria?

red/pink

+ clots

(-) proteinuria

normal RBCs

no RBC casts

A

extraglomerular

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8
Q

Glomerular or extraglomerular hematuria?

cola colored

(-) clots

+ proteinuria

dysmorphic RBCs

+ RBC casts

A

glomerular

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9
Q

Serologic tests in addition to UA and microscopy in glomerulonephritis…

A
Cr
ANA
anti-DS DNA ab
ANCAs
anti-GBM Abs
ASO
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10
Q

Tx of glomerulonephritis (4)

A

tx underly cause and complications (HTN, volume status)

ACE/ARB

Nephrology referral

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11
Q

Which GN?

MC primary GN

peak 2nd and 3rd decade of life

IgA deposition –> inflammatory/glomerular injury

A

IgA Nephropathy

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12
Q

Pt. presents w/ the following, concerning for…

gross, recurrent hematuria

URI w/in 1-2 days

Nephritic presentation

A

IgA Nephropathy

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13
Q

What confirms IgA nephropathy?

A

kidney biopsy

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14
Q

Tx of IgA nephropathy w/ persistent proteinuria > 1 g/d, elevated Cr, reduced GFR or HTN

A

ACE/ARB

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15
Q

slow progression to ESRD occurs in wht percentage of IgA nephropathy patients?

A

50%

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16
Q

This condition occurs after GAS infection like pharyngitis or impetigo.

more common in males

A

Post Strep GN

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17
Q

A patient presents with sxs in the nephritic spectrum 1-3 weeks after ST onset.

A

PSGN

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18
Q

Low complement
documented GAS infx

and elevated _____ or positive _____ can indicate PSG

A

elevated ASO

(+) throat/skin culture

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19
Q

Resolution of PSGN generally occurs within…

A

2 weeks

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20
Q

how common are recurrent episodes of PSGN?

A

rare

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21
Q

prognosis of PSGN depends on…

A

age and severity of sxs

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22
Q

This was previously called HSP…

A

IgA vasculitis

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23
Q

this disease:

  • deposition of IgA immune complexes
  • renal issue occurs 1 month post-URI/systemic sxs

Tetrad:

palpable purpura
arthralgia
abd. pain
renal dz

A

IgA Vasculitis

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24
Q

IgA nephropathy or vasculitis?

  • Nephritic MC, but can be nephrotic
  • favorable prognosis
  • supportive care
A

IgA Vasculitis

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25
Q

This is a rare autoimmune disorder where Abs are directed against the glomerular basement membrane…

A

Anti-GBM disease

26
Q

Anti-GBM with GN + Pulmonary hemorrhage =

A

goodpasture syndrome

27
Q

describe the 2 peaks of anti-GBM disease in the lifecycle

A

3rd decade and 6/7 decade

28
Q

Which peak of anti-GBM is more likely to present with the full constellation of goodpasture syndrome?

A

3rd decade

29
Q

GN + pulmonary hemorrhage + anti-GBM Abs =

A

goodpasture disease

30
Q

Onset of RPGN, cough, dyspnea is concerning for…

A

anti-gbm disease (goodpasture)

31
Q

What two methods confirm anti-gbm disease?

A

anti-GBM Abs in serum or biopsy

can be double positive with (+) ANCA

32
Q

How is anti-GBM treated?

A

plasmapheresis + prednisone/cyclophosphamide

33
Q

This is a complex-mediated glomerular disease directed by Anti-ds DNA Abs.

Suspicion via abn. UA and/or elevated Cr and nephritic presentation.

confirmed with renal bx

A

lupus nephritis

34
Q

Who do you refer to with lupus nephritis?

A

nephro, rheum

35
Q

Pauci-immune GN is associated with what lab which produce tissue and vascular damage?

A

ANCA

36
Q

Which three diseases are pauci-immune GN?

A

GPA
MPA
EGPA

37
Q

pauci-immune GN is characterized by what in renal histology?

A

absence of immune deposits in kidney

38
Q

Which pauci-immune GN?

  • ANCA associated, small-medium vessels
  • Necrotizing granulomatous inflammation
  • Crescentic necrotizing GN and RPGN
  • Nasal/Oral inflammation
  • Saddle nose deformity
A

Granulomatosis w/ Polyangiitis (GPA)

39
Q

What differentiates microscopic polyangiitis from GPA?

A

no granuloma

spares upper respiratory tract

40
Q

Which pauci-immune GN?

-Associated w/ asthma and eosinophilia

A

eosinophilic granulomatosis with polyangiitis

41
Q

What are the three phases of EGPA?

A

Prodrome: atopy, allergic rhinitis, asthma

eosinophilic infiltrative

Vasculitic: systemic, small medium vessels

42
Q

Absence of treatment in Pauci-Immune GN renders a poor prognosis. What two drugs can be used and what type of approach to managing the disease?

A

multi-disciplinary approach (nephro, neuro, rheum, pulm, cards, GI)

CS and cytotoxic agents

43
Q

Which Pauci-immune GN?

(+) C-ANCA

Upper respiratory sx
Lower respiratory sx
GN

A

GPA

44
Q

Which Pauci-immune GN?

(+) P-ANCA

No granuloma

spares upper respiratory tract

A

MPA

45
Q

Which Pauci-immune GN?

(+) P-ANCA

Asthma
Eosinophilia

A

EGPA

46
Q

Most renal masses (65-70%) are…

A

simple renal cysts

47
Q

On US, you see a round, sharply demarcated mass with smooth walls.

The mass is anechoic, there is no enhancement with contrast

A

Simple renal cyst

48
Q

Polycystic Kidney Disease causes an irreversible decline in kidney function. what is the etiology?

A

inherited, autosomal

49
Q

Which type of PKD?

(+) FHx

  • PKD1 or PKD2 gene
  • most common genetic cause of CKD
A

autosomal dominant PKD

50
Q

Which type of PKD?

  • massive bilateral kidney enlargement
  • Progressive decline in GFR
  • deterioration in 4th decade
  • 50% will have ESRD by 60 yo
A

ADPKD

51
Q

As cysts accumulate fluid, enlarge and compress what structures, which leads to decreased renal fxn?

A

parenchyma

52
Q

Describe the kidney function timeline from age 15 to age 60 in ADPKD…

A

15: normal
30: hyperfiltration
40: impairment
60: failure

53
Q

In addition to hepatic cysts, what are three manifestations of ADPKD?

A

HTN
Abd./Flank Pain
Hematuria
Hx UTI/nephrolithiasis

54
Q

What is the initial modality for ADPKD and what can be used when that isn’t conclusive?

A

US initial

CT/MRI if inconclusive

55
Q

What confers definitive dx of ADPKD?

A

genetic testing

56
Q

What is the definitive treatment of ADPKD?

A

transplant

57
Q

What are 4 components to managing ADPKD prior to transplant?

A

BP/salt control

Supportive tx/tx of complications

Tolvaptan

Dialysis

58
Q

Autosomal recessive PKD is primarily a disease of what population?

A

infants and children

59
Q

What two organ systems are affected by ARPKD

A

kidneys

hepatobiliary tract

60
Q

In addition to bilaterally enlarged kidneys, what else can be found with ARPKD?

A

congenital hepatic fibrosis

+/- ESRD or respiratory distress

61
Q

US can detect ARCKD after what week?

A

24 weeks