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Renal 3 Flashcards

1
Q

What is the mechanism of action of acetazolamide?

A

Inhibits carbonic anhydrase –> increased excretion Na HCO3 + diuresis + decreased total body stores of HCO3

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2
Q

What are the clinical uses for acetazolamide? (5)

A
  1. glaucoma
  2. metabolic alkalosis
  3. altitude sickness
  4. urine alkalization
  5. pseudotumor cerebri
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3
Q

What are the toxicities of acetazolamide?

A

–hyperchloremic metabolic acidosis

–NH3 toxicity

–paresthesias

–sulfa allergy

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4
Q

LM: segmental sclerosis and hyalinosis

IF: negative

EM: effacement of podocyte foot processes

diagnosis?

A

Focal segmental glomerulosclerosis

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5
Q

LM: segmental sclerosis and hyalinosis

IF: negative

EM: effacement of podocyte foot processes

diagnosis?

A

Focal segmental glomerulosclerosis

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6
Q

LM: diffuse capillary and GBM thickening

IF: granular

EM: spike and dome appearance with subepithelial deposits

Diagnosis?

A

Membranous nephropathy

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7
Q

Focal segmental glomerulosclerosis

What would we see on LM, IF, and EM?

A

LM: segmental sclerosis and hyalinosis

IF: negative

EM: effacement of podocyte foot processes

diagnosis?

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8
Q

What is the treatment for membranous nephropathy? What is the response to this treatment?

A

Steroids.

Poor response; my progress to chronic renal disease

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9
Q

LM: normal glomeruli; lipid seen in PCT cells

IF: negative

EM: effacement of podocyte foot processes

Diagnosis?

A

Minimal change disease

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10
Q

What are the possible causes/triggers of minimal change disease?

A
  1. recent infection
  2. immunization
  3. immune stimulus
  4. may be associated with Hodgkin lymphoma
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11
Q

What disease process is the nephrotic presentation of SLE?

A

membranous nephropathy

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12
Q

What is the cause of the granular IF and “spike and dome” on EM for membranous nephropathy?

A

subepithelial immune complex deposition

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13
Q

LM: congo red stain shows apple-green birefringence under polarized light

Diagnosis?

A

amyloidosis

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14
Q

Briefly describe the pathophysiology of how systemic amyloidosis causes nephrotic syndrome.

A

amyloid deposition in the mesangium

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15
Q

LM: tram-track appearance

IF: granular, subendothelial immune complex deposits

Diagnosis?

A

membranoproliferative glomerulonephritis

Type 1

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16
Q

With what co-morbidities/disease is membranoproliferative glomerulonephritis Type 1 associated?

A

Hep b

Hep C

May also be idiopathic

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17
Q

With what co-morbidities/disease is membranoproliferative glomerulonephritis Type 2 associated?

A

Associated with C3 nephritic factor

(stabilizes C3 convertase –> decreased serum C3 levels)

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18
Q

Why do we see “tram-tracking” in membranoproliferative glomerulonephritis Type 1?

A

GBM splitting caused by mesangial growth.

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19
Q

LM: mesangial expansion, GBM thickening, eosinophilic glomerulosclerosis (Kimmelstiel-Wilson lesion)

Diagnosis?

A

Diabetic glomerulonephropathy

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20
Q

Membranous nephropathy

What would you see on LM, IF, and EM?

A

LM: diffuse capillary and GBM thickening

IF: granular

EM: spike and dome appearance with subepithelial deposits

Diagnosis?

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21
Q

Minimal change disease

What would you see on LM, IF, and EM?

A

LM: normal glomeruli; lipid seen in PCT cells

IF: negative

EM: effacement of podocyte foot processes

Diagnosis?

22
Q
  1. recent infection
  2. immunization
  3. immune stimulus
  4. may be associated with Hodgkin lymphoma

These are the potential triggers for which nephrotic syndrome?

A

What are the possible causes/triggers of minimal change disease?

23
Q

amyloidosis

What would you see on LM?

A

LM: congo red stain shows apple-green birefringence under polarized light

Diagnosis?

24
Q

membranoproliferative glomerulonephritis

Type 1

What would you see on LM and F?

A

LM: tram-track appearance

IF: granular, subendothelial immune complex deposits

Diagnosis?

25
Diabetic glomerulonephropathy What would you see on LM?
LM: mesangial expansion, GBM thickening, eosinophilic glomerulosclerosis (Kimmelstiel-Wilson lesion) Diagnosis?
26
How does diabetes lead to glomerulonephropathy?
nonenzymatic glycosylation of the GBM --\> increased permeability and GBM thickening nonenzymatic glycosylation of efferent arterioles --\> increased GFR --\> mesangial expansion
27
LM: mesangial proliferation EM: mesangial immune complex deposits IF: IgA immune complex deposits in mesangium Diagnosis?
Ig A nephropathy | (Berger disease)
28
How does IgA nephropathy usually present?
Often presents with URI or acute gastroenteritis Episodic hematuria with RBC casts
29
What is Alport syndrome?
A mutation in Type IV collagen --\> thinning and splitting of the GBM. Most commonly X-linked
30
With what symptoms is Alport syndrome associated?
glomerulonephritis deafness less commonly, eye problems
31
LM: wire-looping of capillaries IF: granular EM: subendothelial and sometimes intramembranous IgG immune complexes, often with C3 deposition
Diffuse proliferative glomerulonephritis
32
What is the most common cause of death in patients with SLE?
diffuse proliferative glomerulonephritis
33
What are the two most common causes of diffuse proliferative glomerulonephritis?
SLE membranoproliferative glomerulonephritis
34
Cresent formation in the Bowman's space/glomerulus on H&E/LM is indicative of what disease process?
rapidly progressive glomerulonephritis There are multiple causes of RPGN; the clinical picture and IF can help make the specific diagnosis
35
H&E: cresent formation in the Bowman's space IF: linear Diagnosis?
Goodpasture's Syndrome
36
What is the classic presentation of Goodpasture syndrome? What is the disease process?
In Goodpasture syndrome, **antibodies** are made **against the collagen (type IV)** in the **glomerular** and **alveolar basement membranes** presents as **hematuria** and **hemoptysis**, classically in young, adult males.
37
H&E: cresent formation in the Bowman's space IF: granular Diagnosis?
post-streptococcal glomerulonephritis diffuse proliferative glomerulonephritis
38
H&E: cresent formation in the Bowman's space IF: negative (pauci-immune) Diagnosis?
Wegener granulomatosis microscopic polyangiitis Churg-Strauss syndrome
39
H&E: cresent formation in the Bowman's space IF: negative (pauci-immune) c-ANCA positive Diagnosis?
Wegener granulomatosis
40
H&E: cresent formation in the Bowman's space IF: negative (pauci-immune) p-ANCA positive granulomatous inflammation, eosinophilia, asthma Diagnosis?
Churg-Strauss syndrome
41
H&E: cresent formation in the Bowman's space IF: negative (pauci-immune) p-ANCA positive No granulomatous inflammation, eosinophilia, or asthma Diagnosis?
microscopic polyangiitis
42
LM: glomeruli enlarged and hypercellular IF: granular, lumpy-bumpy appearance (IgG, IGM, C3 deposition along GBM and mesangium) EM: subepithelial humps (IC) Diagnosis?
post-streptococcal glomerulonephritis
43
What is the classic hx for post-streptococcal glomerulonephritis?
Peripheral and periorbital edema, dark urine, and hypertension approximately two weeks after group A ß-hemolytic streptococcal infection of the pharynx or skin (impetigo). increased anti-DNase B titers and decreased complement levels.
44
What are the classic symptoms in nephritic syndromes?
azotemia oliguria hypertension (due to salt retention) proteinuria (\<3.5g/day) hematuria and RBC casts in the urine
45
What are the symptoms of nephrolithiasis (kidney stones)?
Colicky pain that radiates to the groin unilateral flank tenderness hematuria
46
Ig A nephropathy (Berger disease) What would we see on LM, IF, and EM?
LM: mesangial proliferation EM: mesangial immune complex deposits IF: IgA immune complex deposits in mesangium Diagnosis?
47
Diffuse proliferative glomerulonephritis What would we see on LM, IF, and EM?
LM: wire-looping of capillaries IF: granular EM: subendothelial and sometimes intramembranous IgG immune complexes, often with C3 deposition
48
Goodpasture's Syndrome What would we see on LM and IF?
H&E: cresent formation in the Bowman's space IF: linear Diagnosis?
49
Wegener granulomatosis microscopic polyangiitis Churg-Strauss syndrome What would we see on LM and IF?
H&E: cresent formation in the Bowman's space IF: negative (pauci-immune) Diagnosis?
50
Wegener granulomatosis What would we see on LM and IF? How would you distinguish this diagnosis from microscopic polyangiitis or Churg-Strauss syndrome?
H&E: cresent formation in the Bowman's space IF: negative (pauci-immune) c-ANCA positive Diagnosis?
51
Churg-Strauss syndrome What would you see on LM and IF? How would you distninguish this from Wegener granulomatosis? How would you distninguish this from microscopic polyangiitis?
H&E: cresent formation in the Bowman's space IF: negative (pauci-immune) p-ANCA positive granulomatous inflammation, eosinophilia, asthma Diagnosis?

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