Glomerular and Vascular Disorders Flashcards
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What are some basic examples of first-line therapy needed for HTN in glomerular disease?
BP recs for adult patients? Pregnancy?
Meds, etc.
- 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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What are some basic examples of first-line therapy needed for proteinuria in glomerular disease?
- 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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What are some basic examples of first-line therapy needed for HLD in glomerular disease?
- 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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What are some basic examples of first-line therapy needed for nephrotic edema in glomerular disease?
What should you do for furosemide-resistant edema?
- 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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You are at an increased risk for what in nephrotic syndrome patients?
What lab level does this occur at?
Increased thromboembolism
Albumin < 2.5
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When do you give full dose prophylactic AC for TE in nephrotic syndrome?
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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Why do you need a higher dose of heparin in nephrotic patients?
Heparin depends on antithrombin III, which may be lost in the urine in NS patients
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What infection can spontaneously occur in nephrotic patients with ascites? Treatment should include?
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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What prophylactic abx should be used for high-dose steroids or other IS is prescribed?
TMP-SMX (dapson or atovaquone in sulfa-allergic)
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What is the specific deficiency in IgA nephropathy?
IgA1 with galactose deficient at the hinge region
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Where do the immune complexes in IgAN deposit?
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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How is the time frame different between IgAN and PIGN?
IgAN will be days after an infection
PIGN will be weeks later
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What’s another name for systemic IgA vasculitis?
What are the clinical criteria?
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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What do you see on histopathology for IgAN?
LM? IF? EM?
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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What does the MEST-C classify? What is the definition?
Primary IgAN
Mesangial hypercellularity
Endocapillary hypercellularity
Segmental sclerosis
Tubular atrophy and interstitial fibrosis
Crescents
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What parts of the MEST-C criteria are associated with the worst prognosis?
Which ones may be improved with immunosuppression?
M1, S1, >= T1, and >= C1 are associated with worse prognosis
E1 and C1 may be improved with immunosuppression
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When should you start RAASi in IgAN?
Should you use aldosterone blockers? Why?
RAASi is recommended in proteinuria > 0.5 with or without HTN
Aldo blockers may be considered for antiproteinuric and antifibrotic effects
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In primary IgAN, when should you consider advancing treatment after supportive care?
What is the next step in therapy?
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
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For the following primary IgAN variants - how should you treat them?
Nephrotic IgAN with minimal change on biopsy?
Treat as minimal change disease
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For the following primary IgAN variants - how should you treat them?
IgAN with AKI in the absence of common reversible causes?
Repeat kidney biopsy if AKI persists for ≥ 2 weeks to rule out rapidly progressive (RP) IgAN.
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For the following primary IgAN variants - how should you treat them?
RP IgAN?
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.
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For the following primary IgAN variants - how should you treat them?
Secondary IgAN?
Evaluate and treat secondary causes
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For the following primary IgAN variants - how should you treat them?
IgAV?
For patients at high risk for CKD progression despite maximal supportive care: treat with corticosteroids as described above for primary IgAN.
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For the following primary IgAN variants - how should you treat them?
IgAN in pregnancy planning?
For patients with high CKD progression risk, consider a 6-month course of immunosuppression to optimize proteinuria prior to conception.
