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Clinical Med II > Exam 3 - Glomerulonephritis & Cystic Disease of Kidney > Flashcards

Exam 3 - Glomerulonephritis & Cystic Disease of Kidney Flashcards

1
Q

What is a general description of Glomuerular disease?

A

Damage to the major components of the glomerulus

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2
Q

What is the difference between primary and secondary glomerular disease?

A

Primary = Glomerular injury is limited to the kidney

Secondary = Renal abnormalities result from a systemic disease

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3
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?

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4
Q

What is the etiology of Glomerulonephritis?

A

Deposition of immune complexes in the glomerulus

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5
Q

RBC casts are pathognomonic for what disorder?

A

Glomerulonephritis

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6
Q

The following clinical findings should cause concern for what?

  • RBC casts
  • Dysmorphic RBCs
  • Cola-colored urine
  • Proteinuria < 3.0 g/day
  • Elevated creatinine, decreased GFR
  • Oliguira
  • Edema
  • HTN
A

Nephritic Syndrome

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7
Q

What is commonly characterized morphologically by extensive crescent formation?

A

Rapidly Progressive Glomerulonephritis (RPGN)

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8
Q

Is hematuria more associated with the nephritic or nephrotic spectrum?

A

Nephritic

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9
Q

Are the following urine findings associated with extraglomerular or glomerular hematuria?

  • Red or pink color
  • Clots present
  • Proteinuria usually absent
  • Normal RBC morphology
  • No RBC casts
A

Extraglomerular

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10
Q

Are the following urine findings associated with extraglomerular or glomerular hematuria?

  • “Cola-colored”
  • No clots
  • Proteinuria may be present
  • Dysmorphic RBC morphology
  • RBC casts present
A

Glomerular

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11
Q

What is the most common cause or primary glomerularnephritis in the world?

A

IgA Nephropathy “Berger Disease”

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12
Q

When are the peak incidences of IgA Nephropathy?

A

2nd and 3rd decades of life

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13
Q

IgA depositions in the glomerular mesangium are seen on biopsy, what should you suspect?

A

IgA Nephropathy

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14
Q

What are clinical features/classic presentation seen with IgA Nephropathy?

A

Gross hematuria following shortly after a URI (1-2 days after onset of illness)

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15
Q

Which patients are likely to progress to ESRD with IgA Nephropathy?

How are these patients treated?

A

Those with persistent proteinuria > 1 g/day, elevated serum Cr, HTN

Treat with an ACE-I or ARB

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16
Q

What is the cause of Poststreptococcal GN (PSGN)?

A

Caused by nephritogenic strains of group AB-hemolytic strep

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17
Q

What are clinical features/classic presentation seen with PSGN?

A

Nephritic spectrum symptoms starting 1-3 weeks after infection

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18
Q

How is PSGN diagnosed?

A
  • Clinical presentation
  • Low complement (C3)
  • Documentation of recent GAS infection (elevated ASO titers and/or positive throat or skin cultures)
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19
Q

What is the classic tetra associated with IgA Vasculitis (HSP)?

A
  • Rash (palpable purpura)
  • Arthralgias
  • Abdominal pain
  • Renal disease
20
Q

A child presents with nephritic spectrum symptoms 1-3 weeks after a GAS infection. What should you suspect?

A

PSGN

21
Q

A 27 year old presents with nephritic spectrum symptoms 1-2 days post URI. What should you suspect?

A

IgA Nephropathy

22
Q

A child presents with post-URI with purpura, joint pain, abdominal discomfort, and noted renal dysfunction on labs. What should you suspect?

A

IgA Vasculitis (HSP)

23
Q

What is the etiology of Anti-GBM Antibody (Goodpasture) Disease?

A

Antibodies are directed against an antigen intrinsic to the GBM

24
Q

While the terms are used interchangeably, what is the difference in nomenclature between Goodpasture Syndrome and Goodpasture Disease?

A

Goodpasture Syndrome:
GN + pulmonary hemorrhage

Goodpasture Disease:
GN + pulmonary hemorrhage + anti-GMB antibodies

25
Q

If your patient is positive for anti-GBM antibodies in serum or kidney biopsy, what else should you check for?

A

Potential for “double-positive anti-GBM and ANCA-associated disease”

Need to also test for ANCA as many patients can present with both

26
Q

What is the treatment for Anti-GBM Antibody (Goodpasture) Disease?

A

Plasmapheresis + immunosuppressive agents (prednisone and cyclophosphamide)

27
Q

Pauci-Immune Glomerulonephritis includes what three systemic ANCA-associated vasculitides?

A
  • Granulomatosis with polyangiitis (GPA)
  • Microscopic polyangiitis (MPA)
  • Eosinophilic granulomatosis with polyangiitis (EGPA)
28
Q

What is the triad of GPA?

A
  • Upper respiratory symptoms
  • Lower respiratory symptoms
  • GN
29
Q

What are some upper/lower airway symptoms associated with GPA?

A
  • Nasal or oral inflammation
  • Saddle nose deformity
  • Dyspnea
  • Hemoptysis
30
Q

What are common renal manifestations associated with GPA?

A

Cresentic necrotizing GN

31
Q

Is GPA more associated with C-ANCA or P-ANCA?

A

C-ANCA

32
Q

How does MPA differ from GPA in regards to presentation.

A

Spares upper respiratory tract and has no granuloma formation

33
Q

How does EGPA differ from MPA and GPA?

A

EGPA is associated with asthma and eosinophilia

34
Q

What are the three phases of EGPA?

A
  • Prodromal phase (atopic triad)
  • Eosinophilic infiltrative phase
  • Vasculitic phase
35
Q

What will serology show in Lupus Nephritis?

A

+ Anti-Ds DNA titers

36
Q

What are some features of a benign renal cyst?

A

Round and sharply demarcated with smooth walls and no enhancement with constrast

37
Q

What is the etiology of polycystic kidney disease (PKD)?

A

Inherited disease that causes an irreversible decline in kidney function

38
Q

What is the most common genetic cause of PKD?

A

Autosomal dominant PKD

39
Q

What are common manifestations of ADPKD?

A
  • Renal HTN
  • Abdominal/flank pain
  • Hematuria
  • Hepatic cysts
40
Q

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

A

Ultrasound

41
Q

What is required for definitive diagnosis of ADPKD?

A

Genetic testing

42
Q

What is the management for ADPKD?

A
  • Strict BP control, low-salt diet
  • Supportive care
  • Tolvaptan
  • Dialysis or kidney transplant
43
Q

What populations does ARPKD primarily affect?

A

Infants and children

44
Q

What is the mechanism of ARPKD?

A

Mutation of the PKHD1 gene

45
Q

What organ systems are primarily affected in ARPKD?

A

Kidneys and hepatobiliary tract (hallmark)

46
Q

While both ADPKD and ARPKD are associated with bilateral markedly enlarged kidneys, progressive renal impairment, and HTN, what distinguishes ARPKD?

A

ARPKD is characterized by congenital hepatic fibrosis which will leads to portal HTN

Clinical Med II (17 decks)

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