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Renal 2 > Glomerular Diseases > Flashcards

Glomerular Diseases Flashcards

1
Q

6 Findings of Nephritic Syndrome

A 
Proteinuria (not in nephrotic range usually)
Hematuria (often microscopic/dysmorphic)
Azotemia
Red Cell Casts
Oliguria
HTN
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2
Q

4 Findings of Nephrotic Syndrome

A

Proteinuria > 3.5g/day
Hypoalbuminemia
Hyperlipidemia
Edema

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3
Q

Rapidly Progressive Glomerulonephritis

A

Rapid loss of renal function: creatinine doubles (50% decrease in GFR) in =< 3 months, commonly have crescents on biopsy

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4
Q

4 Primary Glomerulonephritides (& classic presentation and age/racial group)

A 
Minimal Change Disease (children) - always nephrotic syndrome
Focal Segmental Glomerulosclerosis (AAs) - usually nephrotic syndrome or nephrotic range proteinuria
Membranous Nephropathy (Caucasians > 40yo) - nephrotic syndrome category
IgA Nephropathy (Asians and Hispanics) - intermittent gross hematuria or asymptomatic microhematuria
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5
Q

Minimal Change Disease Microscopy

A

Normal on light, normal on fluorescence (not immune mediated), effacement (fusion) of foot processes on EM

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6
Q

Focal Segmental Glomerulosclerosis (FSGS) Microscopy

A

Foci of scarring on light representing permanently injured and collapsed capillary loops, foot effacement on EM, normal on fluorescence (not immune mediated)

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7
Q

Membranous Neuropathy Findings

A

Thick, rigid membrane from immune deposits. Silver stain shows black SPIKES. SUBEPITHELIAL immune deposits, and diffuse immune deposits shown on fluorescence

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8
Q

IgA Neuropathy Microscopy

A

Mesangial proliferation from IgA deposition, but ICs only deposited in mesangium so that’s only place fluoro shows.

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9
Q

IgA Typical Presentation

A

Presents concurrently w/ upper respiratory infection (AT THE SAME TIME), patient develops gross hematuria. Post-Infectious Glomerulonephritis is 10-14 days after infection

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10
Q

3 Treatments for Primary Glomerulonephritides

A

Corticosteroids to reduce inf
Immunosupressants if Ab mediated
ACEis/ARB for reduction in proteinuria

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11
Q

Postinfectious Glomerulonephritis (6)

A

Usually after GAStrep, can be prevented by antibiotics. Recent URI or skin infection, but occurs a few weeks afterwards. Nephritic syndrome maybe gross hematuria. Usually resolves on its own w/in 6 wks. LOW COMPLEMENT levels that rise as disease resolves

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12
Q

Contrast of PostStrep GN vs. IgA Neph (3)

A

Delayed vs. immediate from URI
Nephritic syndrome vs. usually without, just gross hematuria
Usually resolves w/in 6 wks vs. persistent and recurrent hematuria

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13
Q

PostStrep GN Microscopy

A

Light: diffuse proliferative glomerulonephritis, just a shitload of cells everywhere w/ cap loops closed and some PMNs
Fluoro reveals granular IC and complement deposition
EM shows large SUBEPITHELIAL IC deposits called HUMPS (bigger than membranous neph spikes)

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14
Q

4 Secondary GN w/ Low Complements

A

Post-infectious GN
Membranoproliferative GN
Cryoglomulinemia
Lupus nephritis

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15
Q

Membranoproliferative GN (& clinical presentation)

A

Related to Hep C. Can occur by itself or w/ mixed cryglobulinemia. (both low complements)
Presents w/ nephritic syndrome or a mixture of asymptomatic proteinuria and hematuria (ALSO RBC CAST)

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16
Q

Cryoglobulinemia Clinical Presentation

A

Vasculitis w/ palpable purpura, little raised plaques on skin. Also arthralgias/weakness

17
Q

MPGN Microscopy

A

Basement membranes thick and may appear split (membrano), also called tram tracking. Also too many cells (proliferative)
EM confirms SUBENDOTHELIAL immune deposits. Also complements low

18
Q

Cryoglobulin microscopy

A

Sometimes precipitate inside capillary loops & looks like thrombi

19
Q

Size of Involved Vessels in Vasculitis

A

Small

20
Q

ANCA (& 2 types and targets)

A

Abs that activate neutrophils that contribute to vasculitis. C-ANCA stains cytoplasm and P stains perinuclear. Myeloperoxidase (MPO) is target of P and Proteinase 3 (PR3) is target of C

21
Q

ANCA-positive small vessel vasculitis (4 of them and renal presentation)

A

Granulomatosis w/ polyangitis (Wegener’s), Churg-Strauss, Microscopic polyangiitis, Isolated pauci-immune GN
Accompanied by crescentic, pauci-immune GN

22
Q

Granulomatosis w/ Polyangitis (flowchart description and clinical presentation)

A

ANCA +, small vessel vasculitis, with granuloma present but no asthma/eosinophilia. Often presents w/ chronic sinusitis and purulent/bloody nasal discharge that doesn’t resolve w/ antibiotics. NEPHRITIC

23
Q

Microscopic Polyangiitis

A

Clinical presentation similar to granulomatosis w/ polyangitis but no granuloma

24
Q

Isolated pauci-immune GN

A

Pathophys same as granulomatosis w/ polyangitis, but disease limited to kidney

25
Q

Churg-Strauss Syndrome

A

ANCA + small vessel vasculitis w/ history of allergic rhinitis/asthma leading to eosinophilic small vessel vasc. Tender nodules on skin too. Also pulmonary infiltrates

26
Q

ANCA + Small Vessel Vasculitis Microscopy

A

Pauci-immune GN (no fluoro, not nphils directly attacking)
Formation of cellular crescents w/ focal necrosis (pushing into edge of BC, compressing it)
Evidence of vasculitis
Churg Strauss Syndrome maybe eosinophilia

27
Q

Tx for Renal Involvement/Small Vessel Vasculitis (4)

A

Corticosteroids
Immunosupressants
ACEis/ARBs to treat HTN
Plasmapharesis to remove Abs if life-threatening

28
Q

Goodpasture’s Syndrome (what it is and 4 renal involvement presentations)

A

Anti-Glomerulobasement Disease - Abs cross react w/ other basement membranes and often present w/ lung hemorrhage:
Nephritic syndrome
Rapidly progressing (doubling serum creatinine less than 3 months)
Crescentic, necrotizing glomerulonephritis
Linear staining on immunofluorescence bc direct Ab attack on BM w/ IgG

29
Q

Alport Syndrome

A

Can appear similar to to Goodpasture’s bc Abs towards collagen. Usually not as serious

30
Q

Lupus Nephritis

A

Usually young women, can mimic any glomerular disease and every Ig stain/low complement are positive (full house). Positive ANA stain bc Anti-Nuclear Antibodies

31
Q

Diabetic Nephropathy (incidence stuff)

A

Most common cause, higher risk in T1 but way more T2s. Most develop around 20 years in T1, T2 harder to tell.

32
Q

Diabetic Nephropathy (2 lab findings)

A

Microalbuminuria (30-300 mg/g alb/cr)

Kimmelstiel-Wilson nodules on light microscopy, w/ thickened BMs but no ICs

33
Q

Diabetic Nephropathy Tx

A

Don’t really have it, just control diabetes/use ACEis and shit

34
Q

Amyloidosis

A

Two types: Primary (AL) w/ light chain and secondary w/ Amyloid A protein)

35
Q

Amyloidosis 3 Lab Findings and 2 Symptoms

A

Deposition of large, amorphous material on light micro
Congo red stain positive w/ apple green result
Electron microscopy w/ thin, randomly oriented fibers
Nephrotic syndrome and asymptomatic proteinuria

36
Q

Henoch-Schonlein Purpura

A

Looks like IgA nephropathy, but signs of vasculitis/purpura

37
Q

HIV Associated Nephropathy

A

Looks like FSGS, collapsing variant and has tubular reticular aggregates in glomerular endothelial cells

38
Q

2 Secondary GN that Mimic Primaries

A

Henoch-Schonlein Purpura and IgA Neph

HIV Associated Neph and FSGS

Renal 2 (11 decks)

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