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Priya's Board Review > Glomerular and Vascular Disorders > Flashcards

Glomerular and Vascular Disorders Flashcards

1
Q

glom #BRB

What are some basic examples of first-line therapy needed for HTN in glomerular disease?

BP recs for adult patients? Pregnancy?
Meds, etc.

A
  • Lifestyle modifications: salt restriction, weight control, exercise, stop smoking
  • BP < 120
  • Pregnancy < 140/90 (glom disease and proteinuria)
  • ACE or ARB (if safely tolerated); 2nd line MRA, loop/thiazide diuretics (help BP, reduce hyperK, enhance antiproteinuric effects of RAASi)
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2
Q

glom #BRB

What are some basic examples of first-line therapy needed for proteinuria in glomerular disease?

A
  • First-line: ACEi or ARB
  • Consider nondihydropyridine CCBs (diltiazem) for those who can’t tolerate RAASi
  • Sodium intake < 2g
  • Second-line: MRA
  • Watch protein intake in nephrotic range proteinuria
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3
Q

glom #BRB

What are some basic examples of first-line therapy needed for HLD in glomerular disease?

A
  • Statins should be used per ASCVD guidelines (GFR<60 and UACR > 30 are risk factors)
  • Statins have not been proven to reduce CV events in NS
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4
Q

glom #BRB

What are some basic examples of first-line therapy needed for nephrotic edema in glomerular disease?

What should you do for furosemide-resistant edema?

A
  • IV loop diuretics
  • Switch to torsemide or bumetanide; add a thiazide, thiazide-like, and/or MRA to the loop
  • For continued resistance: amiloride (use this with high-degree proteinuria), acetazolamide, IV loops, UF, or HD
  • Sodium < 2g
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5
Q

glom #BRB

You are at an increased risk for what in nephrotic syndrome patients?
What lab level does this occur at?

A

Increased thromboembolism
Albumin < 2.5

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6
Q

glom #BRB

When do you give full dose prophylactic AC for TE in nephrotic syndrome?

A

Albumin <2-2.5 AND one of the following:
- Proteinuria >10g/d, BMI > 35, family Hx of TE, CHF class 3/4, recent abdominal or ortho surgery, or prolonged immobilization

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7
Q

glom #BRB

Why do you need a higher dose of heparin in nephrotic patients?

A

Heparin depends on antithrombin III, which may be lost in the urine in NS patients

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8
Q

glom #BRB

What infection can spontaneously occur in nephrotic patients with ascites? Treatment should include?

A

SBP may occur
Empiric abx should include benzylpenicillin (pneumococcal infx)

For recurrent SBP, consider monthly IVIG daily x4d for IgG levels > 600 (limited evidence)

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9
Q

glom #BRB

What prophylactic abx should be used for high-dose steroids or other IS is prescribed?

A

TMP-SMX (dapson or atovaquone in sulfa-allergic)

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10
Q

glom #BRB #iga

What is the specific deficiency in IgA nephropathy?

A

IgA1 with galactose deficient at the hinge region

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11
Q

glom #BRB #iga

Where do the immune complexes in IgAN deposit?

A

Immune complex deposition in the mesangium
The ICs activate complement and other pathways that lead to mesangial cell proliferation, matrix deposition, glomerular injury, and tubulointerstitial fibrosis

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12
Q

glom #BRB #iga #pign

How is the time frame different between IgAN and PIGN?

A

IgAN will be days after an infection
PIGN will be weeks later

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13
Q

glom #BRB #iga

What’s another name for systemic IgA vasculitis?

What are the clinical criteria?

A

Systemic IgA vasculitis is HSP.

Purpura or petechiae (lower limb) and at least 1 of the following:
- abdominal pain
- histopathology
- arthritis or arthralgia
- renal involvement

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14
Q

glom #BRB #iga

What do you see on histopathology for IgAN?
LM? IF? EM?

A

LM: mesangial expansion and hypercellularity, segmental and/or global glomerulosclerosis, endocapillary hypercellularity, crescents
IF: mesangial IgA is more dominant (or co-dominant) with others (IgG, IgM a/o C3); lambda typically > than kappa

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15
Q

glom #BRB

What does the MEST-C classify? What is the definition?

A

Primary IgAN
Mesangial hypercellularity
Endocapillary hypercellularity
Segmental sclerosis
Tubular atrophy and interstitial fibrosis
Crescents

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16
Q

glom #BRB #iga

What parts of the MEST-C criteria are associated with the worst prognosis?
Which ones may be improved with immunosuppression?

A

M1, S1, >= T1, and >= C1 are associated with worse prognosis
E1 and C1 may be improved with immunosuppression

17
Q

glom #BRB #iga

When should you start RAASi in IgAN?
Should you use aldosterone blockers? Why?

A

RAASi is recommended in proteinuria > 0.5 with or without HTN
Aldo blockers may be considered for antiproteinuric and antifibrotic effects

18
Q

glom #BRB #iga

In primary IgAN, when should you consider advancing treatment after supportive care?
What is the next step in therapy?

A

Persistent proteinuria > 1g/day after 6 months of maximal supportive care.

Oral prednisone at 0.8–1.0 mg/kg/d × 2 mo, then reduce by 0.2 mg/kg/d per month for the next 4 mo, or
Intravenous bolus of 1 g methylprednisolone × 3 d at months 1, 3, and 5, followed by oral prednisone at 0.5 mg/kg/d on alternate days × 6 mo

19
Q

glom #brb #iga

For the following primary IgAN variants - how should you treat them?

Nephrotic IgAN with minimal change on biopsy?

A

Treat as minimal change disease

20
Q

glom #brb #iga

For the following primary IgAN variants - how should you treat them?

IgAN with AKI in the absence of common reversible causes?

A

Repeat kidney biopsy if AKI persists for ≥ 2 weeks to rule out rapidly progressive (RP) IgAN.

21
Q

glom #brb #iga

For the following primary IgAN variants - how should you treat them?

RP IgAN?

A

CYC and corticosteroids similar to the treatment of ANCA-associated vasculitis (AAV).
RTX has NOT been shown to be effective in this IgAN subset.

Clinically, RP IgAN is defined as ≥50% decline in eGFR over 3 months or less after excluding reversible causes [e.g., pre- and post-kidney causes]. Having crescents without a concomitant decline in kidney function does not define RP IgAN.

22
Q

glom #brb #iga

For the following primary IgAN variants - how should you treat them?

Secondary IgAN?

A

Evaluate and treat secondary causes

23
Q

glom #brb #iga

For the following primary IgAN variants - how should you treat them?

IgAV?

A

For patients at high risk for CKD progression despite maximal supportive care: treat with corticosteroids as described above for primary IgAN.

24
Q

glom #brb #iga

For the following primary IgAN variants - how should you treat them?

IgAN in pregnancy planning?

A

For patients with high CKD progression risk, consider a 6-month course of immunosuppression to optimize proteinuria prior to conception.

25
Q

glom #brb #iga

For the following primary IgAN variants - how should you treat them?

IgAN in children?

A

Most pediatric nephrologists treat children with proteinuria > 1 g/d and mesangial hypercellularity (Oxford M1) with RAASi + corticosteroids.

Children with RP IgAN have a poor outcome. Treatment with corticosteroids and oral CYC may be considered (limited data).

26
Q

glom #brb #iga

What is the IS therapy for non-nephrotic proteinuria IgAN patients?

A

The benefits of steroids have not been proven

27
Q

glom #brb #iga

When is immunosuppressive therapy NOT recommended in patients with IgAN?

A

Not recommended in eGFR < 30 (not in the setting of AKI or if you have a high-quality sample that shows CKD)

Risks and benefits of using immunosuppression must be discussed in patients with eGFR < 50 due to the increased likelihood of adverse effects.

28
Q

glom #brb #vasculitis

What are the names of the different vasculitis disorders of large-sized vessels?
Age association?

A

Aorta –> renal artery
Granulomatous arteritis: giant cell (>50yo) and Takayasu (< 50yo)

29
Q

glom #brb #vasculitis

Which one is associated with polymyalgia rheumatica: giant cell or Takayasu arteritis?
Which one is associated with more renal involvement?

A

Giant cell is associated with PMR.
Takayasu is associated with more renal involvement.

30
Q

glom #brb #vasculitis

What are the names of the different vasculitis disorders of medium-sized vessels?
Age association?
Which one has mucocutaneous lymph node involvement?
Which has more renal involvement?

A

Renal artery → interlobar artery → arcuate artery

Necrotizing arteritis: PAN and Kawasaki

PAN: usually adults and without mucocutaneous lymph nodes; microaneurysms look like “beads on a chain” on an angiogram

Kawasaki: usually children with mucocutaneous lymph node involvement

PAN has more renal involvement; renal involvement in Kawasaki is uncommon

31
Q

glom #brb #vasculitis #pan

PAN is associated with what kind of infection?

A

Hepatitis B (or other infections)

32
Q

glom #brb #vasculitis #pan

Where is PAN involved in histopathology? Where do lesions exclude PAN?
What kind of lesions do you see in the arteries?

A

Renal artery, interlobar, arcuate, interlobular arteries
Involvement of capillaries, arterioles, and venous beds excludes PAN

Nodular inflammatory lesions and aneurysms; you may see pseudoaneurysms

Priya's Board Review (19 decks)

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