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Clinical Medicine 2 > Exam 3: Glomerulonephritis > Flashcards

Exam 3: Glomerulonephritis Flashcards

1
Q

What is the basic filtering unit of the kidney?

A

Glomerulus

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2
Q

What is glomerular disease?

A

Damage to the major components of the glomerulus (the podocytes, glomerular basement membrane, capillary endothelium, and mesangium

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3
Q

What are the two classifications of glomerular disease?

A

Nephritic and nephrotic

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4
Q

What is primary glomerular disease?

A

Glomerular injury that is limited to the kidney

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5
Q

What is secondary glomerular disease?

A

Renal abnormalities that result from systemic disease

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6
Q

What is the etiology of glomerulonephritis?

A

Most commonly the cause is related to the deposition of immune complexes in the glomerulus

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7
Q

What are the clinical findings of nephritic syndrome?

A

Dysmorphic RBCs with RBC casts, Smokey or cola colored urine, proteinuria, elevated creatinine, oliguria, edema, and HTN

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8
Q

What is rapidly progressive (or crescentic) glomerulonephritis?

A

The most severe and clinically urgent end of the nephritis spectrum, causes rapid loss of renal function over a comparatively short period of time

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9
Q

What is rapidly progressive glomerulonephritis commonly characterized by?

A

Extensive crescent formation

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10
Q

What are the 3 diseases in the nephritic spectrum?

A

Asymptomatic glomerular hematuria, nephritic syndrome, and rapidly progressive glomerulonephritis

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11
Q

What symptom is common with nephritic diseases?

A

Hematuria

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12
Q

What are the major causes of hematuria?

A

Transient and unexplained, UTI, kidney stones, cancer, and BPH

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13
Q

Patient presents with red or pink hematuria with clots present. There is no proteinuria and RBC morphology is normal. Is this extraglomerular or glomerular hematuria?

A

Extraglomerular

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14
Q

Patient presents with cola-colored hematuria without clots. There is some proteinuria present and RBCs are dysmorphic with RBC casts. Is this extraglomerular or glomerular hematuria?

A

Glomerular

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15
Q

What level of proteinuria is typically seen with nephritic syndrome?

A

Typically subnephrotic <3.0 g/day

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16
Q

What kind of treatment do patients with acute nephritic syndrome or RPGN need?

A

Consider immediate hospitalization

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17
Q

What is the most common cause of primary GN in the world?

A

IgA nephropathy

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18
Q

What diseases is IgA nephropathy commonly associated with?

A

Cirrhosis, celiac disease, and other infections such as HIV and EBV

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19
Q

What are the essential tests needs for GM?

A

Urine dipstick and urine microscopy

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20
Q

What serum tests should you order for GM?

A

-Creatinine/GFR. ANA, ANCA, anti-GBM, and antistreptolysin O

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21
Q

If there is evidence of proteinuria with GM, what should you consider prescribing?

A

ACE or ARB

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22
Q

When in life is IgA nephropathy likely to occur?

A

2nd and 3rd decades of life

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23
Q

What is the pathogenesis of IgA nephropathy?

A

IgA deposition in the glomerular mesangium resulting in inflammation and glomerular injury

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24
Q

Patient presents with gross hematuria 1-2 days following a URI. What are you suspicious of?

A

IgA nephropathy

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25
Q

How is IgA nephropathy diagnosed?

A
  • clinical suspicion and labs

- Confirmed ONLY by kidney biopsy

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26
Q

What are the two typical disease courses for IgA nephropathy?

A

1) Slow progression to ESRD in 50%

2) the rest may have sustained clinical remission or persistent low -grade hematuria

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27
Q

What is poststreptococcal GN (PSGN)?

A

immune complex mediated sequela of a pharyngitis or skin infection

** glomerular immune complex disease that triggers complement activation and inflammation

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28
Q

What most commonly causes PSGN?

A

Group A B-hemolytic strep

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29
Q

How soon does PSGN occur after a strep infection?

A

1-3 weeks

  • good way to distinguish from IgA since IgA occurs a few days after illness
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30
Q

How is PSGN diagnosed?

A
  • Clinical presentation and history
  • Low complement
  • Recent GAS infection
31
Q

What patients has a risk of progression to ESRD in IgA nephropathy?

A

If there is persistent proteinuria >1 g/d, evaluated serum Cr/reduced GFR, or HTN

32
Q

What is IgA vasculitis?

A

AKA henoch-schonlein purpura, an immune mediated vasculitis characterized by deposition of IgA containing immune complexes

33
Q

What is the classic tetrad with IgA vasculitis?

A

Palpable purpura, arthralgias, abdominal pain, and renal disease

34
Q

What is the treatment for IgAV nephritis?

A

Supportive care, symptomatic therapy, and targeted therapy to decreased complications

35
Q

When do renal symptoms occur in IgAV nephritis?

A

Typically a few days to one month after onset of systemic symptoms, may present with nephritic or nephrotic syndrome, and favorable prognosis in most

36
Q

What is anti-GBM disease?

A

AKA goodpasture disease, an autoimmune disorder in which circulating antibodies are directed against an antigen intrinsic to the glomerular basement membrane an the alveolar basement membrane

37
Q

What is goodpasture syndrome?

A

When patient has syndrome of GN and pulmonary hemorrhage

38
Q

When in life are patients more susceptible to developing anti-GBM disease?

A
  • first peak: third decade of life (more males)

- Second peak: 6th and 7th decade (more females)

39
Q

What is the difference between goodpasture disease and goodpasture syndrome?

A

Syndrome: describes the constellation of GN+ pulmonary hemorrhage

Disease: reserved for those with GN+ pulmonary hemorrhage+ anti-GBM antibodies

40
Q

What is the most common etiology of anti-GBM disease?

A

Idiopathic

41
Q

Goodpasture disease have renal involvement with clinical features of ***.

A

RPGN

42
Q

How is goodpasture disease diagnosed?

A

-Demonstration of anti-GBM antibodies in serum or kidney biopsy

There is a potential for ‘double positive anti-GBM and ANCA associated disease’ ** test for ANCA!

43
Q

What is the treatment for goodpasture disease?

A

Plasmapheresis and immunomodulating agents (prednisone and cyclophosphamide)

44
Q

What is Lupus nephritis?

A

-an immune complex mediated glomerular disease with Anti-ds DNA antibodies

45
Q

How is lupus nephritis diagnosed?

A

-Suspected by an abnormal urinalysis and elevation of serum creatinine, but diagnosis confirmed by renal biopsy

46
Q

What are the 3 systemic ANCA associated vasculitides with Pauci-immune GN?

A

1) GPA
2) Microscopic polyangitis
3) Eosinophilic granulomatosis with polyangitis

47
Q

What are the antibodies that produce tissue an vascular damage?

A

P-ANCI and C-ANCA

48
Q

What is GPA and what is it characterized by?

A

C-ANCA associated vasculitis of small-medium vessels characterized by granulomatous inflammation

49
Q

What are then renal manifestations of GPA?

A

RPGN is most common with crescentic necrotizing glomerulonephritis

50
Q

How does GPA affect the upper and lower airway?

A

Nasal and oral inflammation and saddle node deformity

51
Q

What is microscopic polyangitis (MPA)?

A

P- ANCA associated vasculitis of small-medium vessel that clinically appears similar to GPA

52
Q

What are the features that distinguish MPA from GPA?

A

MPA has absence of granuloma formation and has sparing of the upper respiratory tract

53
Q

What is eosinophilic granulomatosis with polyangitis (EGPA)?

A

P- ANCA associated vasculitis associated with asthma and esosinophilia

54
Q

What are the 3 disease phases of EGPA?

A

1) prodromal
2) eosinophilic infiltrative phase
3) vasculitis phase

55
Q

What is the prodromal phase of EGPA characterized by?

A

Atopic disease, allergic rhinitis, and asthma

56
Q

What is the treatment for Pauci-immune GN?

A
  • Referral
  • Immunposuppressants (corticosteroids)

*** prognosis is very poor w/o treatment

57
Q

What are the benign features of renal cysts?

A

Round and sharply demarcated with smooth walls, anechoic, and no enhancement with contrast

58
Q

What is poly cystic kidney disease?

A

An inherited disease that causes an irreversible decline in kidney function (may be both autosomal dominant or recessive)

59
Q

What do the majority of patients with PKD eventually require?

A

Dialysis or kidney transplant

60
Q

What is the most common genetic cause of CKD?

A

Autosomal dominant PKD (ADPKD)

61
Q

What are the two genes that account for most cases of ADPKD?

A

PKD1 and PKD2

62
Q

What is ADPKD characterized by?

A
  • Massive kidney enlargement

- Progressive decline in GFR (50% of patients will have ESRD by 60)

63
Q

What are some of the extra renal manifestations of ADPKD?

A

HTN, abdominal pain, and hepatic cyst

64
Q

What is the initial modality used for screening and diagnosis of ADPKD?

A

US

65
Q

How is ADPKD treated?

A
  • Tolvaptan
  • Dialysis and kidney transplant
  • strict BP control and low salt diet
66
Q

What are the two primary organ systemic affected in autosomal recessive PKD (ARPKD)?

A

Kidneys and hepatobiliary tract

67
Q

Who is ARPKD most common in and what is it caused by?

A
  • Primarily a disease of infants and children

- Mutation of PKHD1 gene

68
Q

What is ARPKD characterized by?

A

Bilaterally markedly enlarged kidneys and congenital hepatic fibrosis

69
Q

How is ARPKD diagnosed?

A

US- may be detected by routine pregnancy US after 24 weeks gestation

70
Q

What are the 6 etiologies of glomerulonephritis?

A

IgA nephropathy, Poststreptococcal GN, Anti-GBM, lupus nephritis, IgA vasculitis HSP, and Pauci immune GN

71
Q

What is glomerulonephritis?

A

A term given to those diseases that present in the nephritic spectrum and usually signifies an inflammatory process causing renal dysfunction

72
Q

A patient with IgA nephropathy has persistent proteinuria > 1g/day, elevated Cr and reduced GFR, or HTN. How should they be treated?

A

ACE or ARB

73
Q

What are the two diseases of the nephritic spectrum that present with RPGN?

A

Anti-GBM glomerulonephritis and pauci immune GN

Clinical Medicine 2 (22 decks)

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