DIT review - Renal 2 Flashcards

1
Q

Describe the general characteristics of nephritic syndrome

A
  • Proteinuria < 3.5 g/day
  • Hematuria and RBC casts
  • Azotemia – increased serum BUN and Creatine
  • Hypertension – salt retention with periorbital edema
  • Oliguria
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2
Q

What are the different types of nephritis syndrome

A

Post-strep glomerulonephritis

IgA nephropathy (Berger disease)

Alport Syndrome

Rapidly Progressive Glomerulonephritis

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3
Q

What type of strep infection precedes PSGN

A

Skin or pharynx

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4
Q

Where will you see immune complex deposits in PSGN + what other things will be seen on biopsy

A
  • Hypercellular glomeruli
  • Neutrophils
  • EM: Immune deposits – subepithelial humps
  • IF: “starry sky” granular appearance (“lumpy bumpy”)
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5
Q

What labs will you find in PSGN?

A
  • Decreased C3 levels (complement is activated and used up)
  • Anti-streptolysin O titer to prove that there was a previous Strep infection
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6
Q

What disease is associated with IgA nephropathy

A
  • Associated with Henoch-Schonlein purpura
    • Palpable purpura on butt and legs
    • Arthralgias
    • Abdominal pain
    • Renal disease
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7
Q

Where will you see deposits in IgA nephropathy + what else will you see on biopsy?

A
  • IgA immune complex deposited in mesangium
  • Proliferation of mesangial cells
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8
Q

Describe the presentation of IgA nephropathy

A
  • Presents as hematuria with RBC casts following a mucosal infection
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9
Q

What is the cause of Alport syndrome

A
  • Due to defect in Type IV collagen (basement membrane)
    • Leads to splitting of the basement membrane longitudinally
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10
Q

Presentation of Alport syndrome

A
  • Presents as isolated hematuria, sensory hearing loss, and ocular disturbances
    • “Can’t see, can’t pee, can’t hear high C”
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11
Q

What is the characteristic finding in rapidly progressive glomerulonephritis

A
  • Characterized by crescents in Bowman space
    • Crescents comprised of fibrin and macrophages
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12
Q

What are the subtypes of RPGN?

A

Goodpasture

Granulomatosis with polyangiitis (Wegener)

Microscopic polyangiitis

Diffuse proliferative glomerulonephritis

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13
Q

Finding in Goodpasture (presentation, IF)

A
  • Type II HSR – antibodies against glomerular basement membrane
  • Linear IF pattern
  • Affects kidneys and the lungs (alveolar basement membrane)
  • Presents as hematuria + hemoptysis
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14
Q

How do you differentiate Wegener’s from Microscopic polyangiitis

A

Wegener’s - cANCA

Microscopic polyangiitis - pANCA

Both have negative IF

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15
Q

What disease is associated with Diffuse proliferative glomerulonephritis

A

Lupus - most common type of renal disease in SLE

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16
Q

Describe the biopsy of diffuse proliferative glomerulonephritis

A
  • Anti-dsDNA seen subendothelially and within mesangium
  • Granular IF
  • Light microscopy – deposits make basement membrane look thick – “wire looping” of capillaries
    • THINK: wire lupus
  • Often presents as nephrotic + nephritic syndrome
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17
Q

What are the general characteristics of nephrotic syndrome

A
  • Proteinuria > 3.5 g/day
  • Hypoalbuminemia – protein lost in urine
  • Edema – decreased oncotic pressure due to hypoalbuminemia
  • Increased risk of infection – loss of immunoglobulin in urine
  • Increased risk of thrombosis – loss of antithrombin III
  • Hyperlipidemia – liver tries to make more lipoproteins in order to make up for decreased oncotic pressure
18
Q

What are the types of nephrotic syndrome?

A

Foot process effacement: Minimal change disease, focal segmental glomerulosclerosis

Immune deposition: Membranous nephropathy, Membranoproliferative glomerulonephritis

Other: Diabetes, Amyloidosis

19
Q

Describe biopsy of Minimal change disease (H&E, EM, IF)

A
  • H&E – normal
  • EM – foot process effacement
  • IF – negative
20
Q

What is the most common cause of nephrotic syndrome in children and adults

A

Children - minimal change disease

Adults - Focal segmental glomerulosclerosis

21
Q

What is a trigger for minimal change disease

A

Infections or immunizations

22
Q

What populations are associated with focal segmental glomerulosclerosis

A
  • Most common cause of nephrotic syndrome in African Americans and Latinos
  • More prevalent in HIV patients
23
Q

Describe the biopsy of focal segmental glomerulosclerosis

A
  • H&E – focal (affects some glomeruli), segmental (affects part of glomerulus)
  • EM – foot process effacement
  • IF – negative
24
Q

What kidney diseases are associated with Lupus

A

Diffuse proliferative glomerulonephritis (nephritic)

Membranous nephropathy (nephrotic)

25
Q

Describe biopsy of membranous nephropathy

A
  • H&E – thickening of basement membrane
  • EM – “spike and dome” appearance with subepithelial deposits
  • IF – granular
26
Q

Describe biopsy of membranoproliferative glomerulonephritis

A
  • Type I:
    • Biopsy:
      • H&E – thick basement membrane with “tram track” appearance
        • Due to mesangium proliferating between the basement membrane
        • THINK: membranoproliferative = membrane proliferating = 2 membranes
      • EM – subendothelial deposits
      • IF – granular
    • Associated with HBV and HCV
  • Type II:
    • Aka Dense deposit disease
    • Associated with C3 nephritic factor (autoantibody that stabilizes C3 convertase, leading to over-activation of complement, inflammation, and low levels of circulating C3)
27
Q

Describe biopsy of Diabetic nephropathy

A
  • Will show sclerosing of the mesangium with Kimmelstie-Wilson nodules (round acellular nodules)
28
Q

Where in the glomerulus are deposits in amyloidosis

A

Within the mesangium

29
Q

Describe the disorder associated with each renal cast:

  • RBC cast
  • WBC cast
  • Bacterial cast
  • Epithelial cell cast
  • Waxy cast
  • Hyaline cast
  • Fatty cast
  • Granular cast
A
  • RBC casts à glomerular damage (e.g. glomerulonephritis)
  • WBC casts - acute pyelonephritis (kidney infection)
  • Bacterial casts - pyelonephritis
  • Epithelial cell casts - acute tubular necrosis, toxic ingestions
  • Waxy casts - end stage renal disease/chronic renal failure
  • Hyaline casts (solidified mucoproteins secreted by tubular epithelial cells) - normal, dehydration
  • Fatty casts - nephrotic syndrome
  • Granular (“muddy brown”) casts - chronic renal disease, acute tubular necrosis
30
Q

What is the most common kidney stone

A

Calcium stones

31
Q

Are calcium stones radiopaque or radiolucent?

A

Radiopaque (can be seen on X-ray)

32
Q

Risk factors for calcium stones

A
  • Hypercalcemia/hypercalciuria
    • Cancer, increased PTH, ethylene glycol (calcium oxalate), increased vitamin C (calcium oxalate)
33
Q

What type of stone is a struvite stone?

A

Ammonium magnesium phosphate stone

34
Q

What is a major contributor to the formation of ammonium magnesium phosphate stones?

A

Urease (+) bacteria - Proteus, Klebsiella, Staph

  • Recall:
    • Urea is broken down by urease into NH3 and CO2
    • NH3 converted to NH4+ which can combine with magnesium and phosphate
35
Q

What type of stones can form staghorn calculi?

A

Struvite stones (ammonium magnesium phosphate)

Cystine stones

36
Q

Are struvite stones radiopaque or radiolucent?

A

Radiopaque

37
Q

What are risk factors for uric acid stones?

A
  • Associated with hyperuricemia and gout, acidic pH
38
Q

Are uric acid stones radiopaque or radiolucent?

A
  • Radiolucent
    • Not seen on X-ray
    • Seen on US and CT
39
Q

Treatment of uric acid stones?

A

Treat with alkalinization of the urine

40
Q

Disorder associated with cystine stones

A
  • Associated with cystinuria (defective COLA transporter in proximal convoluted tubule)
41
Q

Treatment of cystine stones?

A

Alkalinizing urine

42
Q
A