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Renal > Glomerular Disease: Presentations, Etiologies and Comps > Flashcards

Glomerular Disease: Presentations, Etiologies and Comps Flashcards

1
Q

Severity of glomerular disease and likelihood of progression can be predicted by what finding?

A

Degree of proteinuria

*Any form of glomerular disease can lead to nephrotic syndrome, as indicated by the degree of proteinuria

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2
Q

What is the most common form of glomerulonephritis?

A

IgA nephropathy (Berger disease)

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3
Q

What are the common signs and symptoms of all forms of glomerulonephritis (aka nephritic syndrome)?

A
  • UA shows hematuria
  • Dysmorphic red cells
  • Red cells casts
  • Urine sodium and FeNa are low
  • Azotemia
  • Oliguria
  • Hypertension
  • Edema e.g. periorbital
  • Mild proteinuria
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4
Q

What is the presentation of PSGN?

A

Signs and symptoms of glomerulonephritis 1-3 weeks after streptococcal pharyngitis or skin infection (impetigo).

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5
Q

What is Alport syndrome? What is the presentation of Alport syndrome?

A

Alport syndrome is a congenital defect in type IV collagen that results in:

  • Glomerular disease
  • Sensorineural hearing loss
  • Visual disturbance from loss of collagen fibers that hold the lens of the eye in place
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6
Q

What is the presentation of PAN? With what is it associated?

A

Besides the presentation of glomerulonephritis, PAN presents with:

  • Vasculitis signs and symptoms
  • GI: abdominal pain, bleeding, nausea, vomiting, pain after eating
  • Neuro: mononeuritis multiplex, stroke (even in a young person)
  • Skin: ulcers, digital gangrene, and livedo reticularis
  • Cardiac disease in 1/3 of pts (even in young pts)
  • Virtually every organ can be affected but the lung is spared

PAN is assoc. w/ hepatitis B

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7
Q

How does kidney disease present in SLE?

A
  • Severe disease presents as membranous glomerulonephritis

- Long-standing disease may scar the kidney, showing glomerulosclerosis on biopsy

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8
Q

Amyloid is an abnormal protein associated with what? How does it cause kidney disease?

A
  • Myeloma
  • Chronic inflammatory diseases
  • Chronic infections
  • RA
  • IBD

There is also a primary form of amyloidosis in which an abnormal protein is produced for unknown reasons. The kidney is the primary target of this protein.

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9
Q

Which diseases give large kidneys on sonogram and CT scan?

A
  • Amyloid nephropathy
  • HIV nephropathy
  • Polycystic kidney disease
  • Diabetes
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10
Q

How does Goodpasture syndrome present? How does it differ from Wegener’s granulomatosis?

A

Goodpasture presents with lung and kidney problems, but there is NO upper respiratory involvement as there is in WG. Also, there are no signs or symptoms of systemic vasculitis (no skin, joint, GI, eye, or neuro involvement) as there are in WG.

Goodpasture and WG also present with anemia due to chronic blood loss from hemoptysis.

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11
Q

What is the presentation of IgA nephropathy (Berger disease)? How do you distinguish it from poststreptococcal glomerulonephritis?

A

Recurrent episodes of gross hematuria 1-2 days after a mucosal infection, including pharyngitis and viral gastroenteritis.

PSGN occurs 1-3 weeks after pharyngitis (or impetigo).

*There are no unique physical findings in IgA nephropathy.

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12
Q

What does biopsy reveal in glomerulonephritis?

A

Hypercellular, inflamed glomeruli; inflammation is due to immune complex deposition that activates complement; C5a attracts neutrophils, which mediate damage.

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13
Q

What are the complications of PSGN?

A

May progress to RPGN in adults; rarely progresses in children.

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15
Q

What do serum studies show in PSGN?

A

Elevated ASO and anti-DNase B titers; decreased complement

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16
Q

What does glomerular biopsy show in PSGN with:

  • LM
  • EM
  • IF
A
  • LM: glomeruli are enlarged and hypercellular, neutrophilic infiltration, “lumpy bumpy” appearance
  • EM: subepithelial immune complex humps
  • IF: granular appearance due to IgG, IgM, and C3 deposition along the GBM and mesangium
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17
Q

What are the causes of rapidly progressive (crescentic) glomerulonephritis (RPGN)?

A
  • PSGN (adults only)
  • DPGN
  • Goodpasture syndrome
  • Wegener granulomatosis
  • Microscopic polyangiitis
  • Churg-Strauss syndrome
18
Q

What is seen on LM of a glomerular biopsy in RPGN?

A

Crescent-moon shape; crescent consists of fibrin and plasma proteins with glomerular parietal cells, monocytes, and MPs.

19
Q

How can you figure out the cause of RPGN?

A

All causes show crescentic shape on LM; otherwise:

  • PSGN can be figured out through the HPI
  • DPGN if Hx of SLE or if EM shows subendothelial IC deposition
  • IF shows linear deposits in Goodpasture syndrome but is negative for other causes
  • ANCA test: Out of the IF negative (pauci-immune) causes, WG is c-ANCA positive, while microscopic polyangiitis and CSS are p-ANCA positive
  • Of the p-ANCA positive causes, CSS is associated with granulomatous inflammation, eosinophilia, and asthma, whereas MP is not
20
Q

What type of HSR is Goodpasture syndrome? To what are the antibodies directed at?

A

GPS is a type II HSR with antibodies to type IV collagen in the glomerular basement membrane and alveolar basement membrane.

21
Q

How are GPS and WG similar? How are they different?

A

Both cause lung and kidney disease (RPGN) and present with hemoptysis and hematuria.

Differences:

  • GP shows linear deposits on IF, whereas WG is IF negative
  • GP has anti-type IV collagen antibodies, whereas WG has c-ANCA antibodies
  • GP may show ocular signs and symptoms due to damage of type IV collagen in the eye
  • WG has nasopharyngeal/URI Sx e.g. otitis media, sinusitis, nasal ulcers, whereas GP does not
22
Q

Other than HPI, how can you distinguish between PSGN and DPGN as the cause of RPGN?

A

Electron microscopy: PSGN shows subepithelial IC deposition (seen as little humps), whereas in DPGN it is subendothelial (seen as a bigger mass).

23
Q

What are the causes of diffuse proliferative glomerulonephritis (DPGN)?

A

SLE and membranous proliferative glomerulonephritis (MPGN)

24
Q

What is seen in DPGN with:

  • LM
  • EM
  • IF
A
  • LM: “wire-looping” of capillaries
  • EM: subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition
  • IF: granular
25
Q

What in seen on kidney biopsy in Berger disease with:

  • LM
  • EM
  • IF
A
  • LM: mesangial proliferation
  • EM: mesangial IgA deposits
  • IF: IgA-based IC deposits in the mesangium
26
Q

What is seen on biopsy in Alport syndrome?

A

The mutation in type IV collagen results in split basement membrane.

27
Q

How does Alport syndrome present? How is the presentation different from other causes of glomerulonephritis?

A

Glomerulonephritis, deafness (sensorineural hearing loss), and less commonly, cataracts from damage to the lens.

Alport syndrome can be distinguished by presenting as isolated hematuria withOUT proteinuria or red cell casts.

28
Q

What is the inheritance pattern in Alport syndrome?

A

X-linked dominant

29
Q

What are the common signs and symptoms of all causes of nephrotic syndrome?

A
  • Massive proteinuria > 3.5 g/day; frothy urine
  • Hyperlipidemia and hypercholesterolemia
  • Edema (due to hypoalbuminemia causing decreased oncotic pressure, along with increased aldosterone)
  • Hypogammaglobulinemia with increased risk of infection
  • Hypercoagulable state (due to AT III loss) with increased risk of thromboembolism
  • Fatty casts
30
Q

What the causes of focal segmental glomerulosclerosis?

A
  • Usually idiopathic
  • HIV infection
  • Drugs: heroin, interferon, pamidronate, rapamycin
  • Massive obesity
  • Chronic kidney disease
  • Sickle-cell disease
  • Minimal change disease that didn’t resolve even with treatment

Renal (3 decks)

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