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Clinical Med - Nephrology > Glomerular Disease / Nephrotic / Nephritic > Flashcards

Glomerular Disease / Nephrotic / Nephritic Flashcards

1
Q

Proteinuria (>3.5g), Lipiduria, Fatty Casts, Edema, and HTN are all presentation of ______ syndrome

A

Nephrotic

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2
Q

Hematuria, RBC Casts, HTN, and Edema are all presentations of ______ syndrome.

A

Nephritic

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3
Q

When working up glomerulonephritis or nephrotic/nephritic syndromes…….

What would ANCA test for?

Anti-GBM?

ASO Titers?

SPEP/UPEP?

A

ANCA: Vasculitis, Wegner’s

Anti-GBM: Goodpasture’s

ASO: Strep

SPEP/UPEP: Multiple Myeloma

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4
Q

___ ________ is the most common lesion that causes primary glomerulonephritis.

This typically occurs 2-4 days after a URI of GI infection that results in the overproduction of an immune complex

A

IgA Nephropathy (Berger Disease)

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5
Q

Is IgA Nephropathy a nephritic or nephrotic syndrome?

Proliferative or non-proliferative glomerulonephritis?

A

Nephritic

Proliferative

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6
Q

What is seen on histology in IgA Nephropathy?

This is also diagnostic

A

Large, Globular IgA deposits in the mesangium

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7
Q

What is the classic presentation of a patient with IgA Nephropathy?

A

Hematuria following a recent URI

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8
Q

Could microscopic hematuria and mild proteinuria be seen in IgA Nephropathy?

A

Yes

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9
Q

If a patient with IgA Nephropathy was becoming HTN, which anti-hypertensive medications would you recommend?

A

ACEi

ARB

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10
Q

If a patient with CVD and IgA Nephropathy developed HLD, what medication class would you recommend?

A

Statin

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11
Q

_________ glomerulonephritis is the cause of 1/3rd of all non-DM associated nephrotic syndromes and is commonly idiopathic.

However, it is also associated with Hep B, SLE, Malignancy, and NSAIDs.

A

Membranous Glomerulonephritis (MGN)

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12
Q

Is Membranous Glomerulonephritis (MGN) a nephritic or nephrotic syndrome?

Proliferative or non-proliferative glomerulonephritis?

A

Nephrotic

Non-Proliferative

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13
Q

What is commonly seen on histology in a patient with MGN?

A

Diffuse thickening of the glomerular basement membrane

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14
Q

What may been seen on histology in a patient with immune mediated MGN?

A

Diffuse, Granular IgG deposition in the capillary walls

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15
Q

If you were to preform a silver stain on a patient with MGN, what may you see that would be diagnostic?

A

Spike Appearance

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16
Q

T:F: MGN is mostly idiopathic so it is NOT important to rule out secondary causes?

A

False

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17
Q

What transmembrane receptor expressed in the podocytes has been identified as a major antigen in idiopathic MGN?

A

Phospholipase A2 receptor

The M-type phospholipase A2 receptor (PLA2R)

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18
Q

How is MGN treated in patients who are most at risk for developing progressive disease?

What are these risk factors?

A

Immunosupressants

  1. Older age at presentation
  2. Male
  3. Nephrotic Proteinuria (>8-10 g/day)
  4. Increased sCr at presentation
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19
Q

What percentage of patients with MGN will develop ESRD?

A

1/3rd

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20
Q

On histology…..

A lobular Appearance
Increased Glomerular Cellularity
Mesangial Expansion
Narrow Capillary Lumens
An a thickening of glomerular capillary walls

Would all indicate _____________ glomerulonephritis

A

Membranoproliferative

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21
Q

Is membranoproliferative glomerulonephritis a nephritic or nephrotic syndrome?

Proliferative or non-proliferative glomerulonephritis

A

Nephritic

Proliferative

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22
Q

T/F: Membranoproliferative glomerulonephritis is classifed as being mediated by immune complexes and complex dysregulation that ultimately leads to endothelial injuries

A

True

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23
Q

When working up membranoproliferative glomerulonephritis what is important to rule out?

A

Hep B

Hep C

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24
Q

What is the most common cause of acute nephritis in children?

Particularly what a result of what?

A

Post-Infectious Glomerulonephritis

Group A, Beta-Hemolytic Streptoccocus

(Often referred to as PSGN)

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25
Q

Is post-infectious glomerulonephritis a nephritic or nephrotic syndrome?

Proliferative or non-proliferative glomerulonephritis

A

Nephritic

Proliferative

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26
Q

How soon after a strep infection would you expect to see PSGN to manifest?

A

10-14 days

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27
Q

PSGN histology appears as diffuse proliferative disease that is often describe as a “______ _____” appearance.

A

Starry Night

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28
Q

T/F: PSGN can present as asymptomatic microscopic hematuria?

A

True

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29
Q

PSGN can present in a full blown nephritic syndrome…

What are the symptoms of this?

A 
Red-Brown Urine
Proteinuria (up to nephrotic levels) 
Edema
HTN
AKI
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30
Q

What labs are most diagnostic for PSGN?

A

ASO Titers and Low Serum Compliment

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31
Q

How is PSGN treated and managed?

A

Supportive Care

Abx (Considered)

32
Q

Rapidly Progressive GN is diagnosed by a _______ formation on biopsy.

What are TWO examples RPGN?

A

Crescentric

Goodpasture’s
Henoch-Schonlein Purpura

33
Q

RPGN on histology can present as a cellular crescent or fibrotic crescent appearance.

Which has the worse prognosis?

A

Fibrotic

34
Q

_________ _______ is a RPGN that effects Type IV collagen of the kidney and is commonly associated with manifestations in the lungs

A

Goodpasture’s Disease

35
Q

Other than a crescentric appearance, what would be seen on histology in a patient with Goodpasture’s?

A

Linear Deposition of IgG in Anti-GBM antibodies

36
Q

What is the treatment of choice for Goodpasture’s Disease?

What medications are often given in combination with this?

A

Plasmaphoresis

PO Prednisone

Cyclophophamide (Immunosupression)

37
Q

T/F: If left untreated, Acute GN due to Goodpasture’s has a good prognosis

A

False

Very poor prognosis if left untreated

38
Q

Patients with Goodasture’s Disease often present with proteinuria, does this reach nephrotic range?

A

No

39
Q

Would you expect to see dysmorphic RBCs and WBCs in Goodpasture’s Disease?

A

Yes

40
Q

_______-_______ _______ is an IgA vasculitis which is the most common form of vasculitis in children?

A

Henoch-Schonlein Purpura (HSP)

41
Q

What is the most common presentation in a patient with Henoch-Schonlein Pupura (HSP)?

What else may be present?

A

Palpable Purpura (WITHOUT thrombocytopenia or coagulopathy)

Arthritis
Abdominal Pain
Renal Disease

42
Q

T/F: Leukocytoclastic vasculitis with IgA Immune complexes is charateristic of HSP

A

True

43
Q

Treatment of HSP can be breakdown into two categories (Supportive and Symptomatic)….

What is involved in each?

A

Supportive:

IVF
Rest

Symptomatic:

Treat joint pains with NSAIDs and Acetaminophen

44
Q

_____ ______ _______ results in 90% of nephrotic disease in children and is an idiopathic disease of the podocytes.

A

Minimal Change Disease

45
Q

Should you expect to see immune deposits on histology in a patient with minimal change disease?

A

No

46
Q

Would you expect to see diffuse effacement of the foot processes in minimal change disease?

A

Yes

47
Q

Although minimal change disease is primarily idiopathic…..

What medications are associated with minimal change disease?

A

NSAIDs
COX2
Lithium
Bisphosphinates

48
Q

What CA is commonly seen with minimal change disease?

A

Hodgkin’s Lymphoma

49
Q

If minimal change disease were a result of infection….

How would this be treated?

A

Vaccinations

50
Q

How does minimal change disease clinically present?

What would you see on UA?

A

Abrupt onset of drastic edema and weight gain

UA: High levels of proteinuria

51
Q

Is a biopsy warranted to work up minimal change disease?

When would it be warranted?

A

No, it is primarily diagnosed clinically

If a patient was unresponsive to therapy

52
Q

How is minimal change disease treated without immunosupressants?

What is used as immunosupression therapy?

A

Without immunosupression…..

Low NA+ diet
Diuretics
ACEi

Immunosupression….

Prednisone

53
Q

______ ________ __________ is a disease of the ppdocytes that is classified as non specific trapping of immunoglobulin C3 and IgM not thought to be pathogenic.

It is associated with circulating factor: Soluble Urokinase Receptor (SuPAR)

A

Focal Segmental Glomerulosclerosis (FSGS)

54
Q

In African Americans, FSGS involves what gene?

Which chromosome is this gene found on?

A

APOL1 Gene

Chromosome 22

55
Q

How does FSGS commonly present/manifest?

A

Proteinuria
Microscopic Hematuria
HTN
Renal Insufficiency

56
Q

What is the most determinate factor in the prognosis of FSGS?

A

Response to therapy

57
Q

Is FSGS treated with immunospressive therapy?

What is primarily used?

A

No

Glucocorticoids

58
Q

T/F: Kidney transplant is a curative treatment option for FSGS

A

False

FSGS returns to the transplanted kidney up to 40% of the time

59
Q

What are FOUR causes of Secondary Glomerulonephritis?

A

DM
SLE
HIV
Amyloidosis

60
Q

Would you expect to see diabetic nephropathy in Type 1 or 2 DM?

A

Type 1 DM

61
Q

What is the classic clinical manifestation of diabetic nephropathy?

A

Microalbuminuria (30-300 mg/d) n the setting of CKD

62
Q

If a patient developed macroalbuminuria (>300 mg), what would they be more at risk of developing?

A

ESRD

63
Q

What are unique features of diabetic nephropathy of histology?

What lesion is unique to diabetic nephropathy?

A

Mesangial Expansion
Glomerular Basement Membrane thickening
Glomerular Sclerosis

Kimmelstiel-Wilson Lesion

64
Q

How is diabetic nephropathy manged/treated?

A
  1. BG Control
  2. BP Control (ACEi, ARB, Diuretics)
  3. Avoid NSAIDs
  4. Low Na+ Diet
65
Q

_______ _______ ________ is a cause of secondary glomerulonephritis that is a chronic inflammatory disease of unknown cause that can affect the skin, joints, kidneys, lungs, nervous system, serous membranes,and/orother organs of the body

A

Systemic Lupus Erythematosis (SLE)

66
Q

SLE results in renal disease when Anti-____ imune complexes form and deposit in the ______ and _________ space.

A

Anti-DNA

Mesangium
Subendothelial Space

67
Q

How would SLE renal disease present on histology

A

Renal Artery Hyalinosis
Increased mesangial matrix
Cellular proliferation
Thickening of glomerular capillary walls

68
Q

How is SLE and renal disease treated?

A

Glucocorticoids in combination with…..

Mycophenolate Mofetil (MMF)

or

Cyclophosphamide

69
Q

If a patient with SLE nephritis relapses, what could be used?

A

Prednisone

+

MMF or Azathioprine

70
Q

___-_______ ______ is an infection of the kidney epithelial cells by HIV and expression of the HIV gene within the cells.

A

HIV-associated nephropathy (HIVAN)

71
Q

In a patient with HIVAN….

What is the CD4 count often?

Would they have a nephritic or nephrotic range of proteinuria?

A

CD4 count was often less than 200 (64%)

Nephrotic Range (~4.1 g/day)

72
Q

T/F: HAART is used in HIVAN treatment

A

True

Although no randomized trials have specifically examined this

73
Q

If a patient with HIVAN also had HTN, what would you recommend as treatment?

A

ACEi

ARB

74
Q

________ is a cause of secondary glomerulonephritis that is characterized by extracellular deposition of beta-sheet fibrils that can lead to organ dysfunction and death

A

Amyloidosis

75
Q

If the following was seen on histology what would it indicate….

Nodular amorphous material extending into the mesangium and into the capillaries

A

Renal Amyloid

76
Q

T/F: In primary renal amyloid, the degree of proteinuria can be > 20g

A

True

77
Q

What is used to treat secondary renal amyloid?

A

Colchicine

Tx underlying Inflammatory Process

Clinical Med - Nephrology (7 decks)

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