CVPR: Renal > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

(28 cards)

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1
Q

Nepritic syndromes characteristics/signs

A
  • classic presentation of pts w/glomerulonephritis
  • reduction of GFR ==> elevated serum creatinine
  • hematuria + dysmorphic RBCs and/or RBC casts + proteinuria
    • WBCs also possible
  • hypertension + edema
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2
Q

Typical renal-limited diseases associated w/glomerulonephritis

A
  • IgA nephropathy
  • Anti-GBM disease
  • Membranoproliferative glomerulonephritis (MPGN)
  • Renal limited vasculitis (ANCA associated)
  • Hemolytic-uremic syndrome
  • C3 glomerulopathy/Dense deposit disease
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3
Q

Typical systemic diseases associated w/glomerulonephritis

A
  • Henoch-Schönlein Purpura
  • Goodpasture’s syndrome
  • Lupus nephritis
  • ANCA associated vasculitis
  • Infection associated
  • Post-infectious
  • Endocarditis/shunt nephritis
  • Cryoglobulinemia
  • Immunoglobulin deposition diseases
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4
Q

Common labs/serology evaluation in glomerulonephritis

A
  • lab: CBC, electrolyte, 24-hour urine, liver fxn tests
  • serology:
    • C3 (complement) levels
    • antistreptolysin (ASO) titer
    • ANA, ANCA, cryoglobulins, anti-GBM
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5
Q

Pulmonary-renal syndrome definition

A
  • patients presenting w/glomerulonephritis + pulmonary hemorrhage
  • e.g. in Goodpasture’s or ANCA-associated vasculitis
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6
Q

Blood tests + disease associations in glomerulonephritis

A

ANA, Anti-DS DNA

Lupus

C3, C4

See table

Blood cultures

Bacterial endocarditis

ASO

Post-infectious

Hepatitis C

Cryoglobulinemia

Hepatitis B

Membranoproliferative glomerulonephritis

Anti-neutrophil cytoplasmic antibodies (ANCA)

Pauci-immune vasculitis

Anti-GBM antibodies

Anti-GBM disease, Goodpasture’s syndrome

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7
Q

Pathophysiology of proteinuria in glomerulonephritis

A
  • direct damage to glomerular capillary wall via immunologic mechanisms ==> increased protein filtration
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8
Q

Pathophysiology of reduction of GFR in glomerulonephritis

A
  • reduced GFR <== acute, inflammatory process w/in glomerulus
  • ==> glomerular vasocontsriction/occlusion or thrombosis ==> decreased filtration surface area
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9
Q

Pathophysiology of active urine sediment in glomerulonephritis

A
  • excretion of RBCs, WBCs, or casts <== glomerular inflammation + disruption of GBM
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10
Q

Pathophysiology of edema/hypertension in glomerulonephritis

A
  • edema <== increase in tubular reabsorption of salt + water <== reduced glomerular perfusion w/normal tubular fxn ==> expansion of ECF volume
  • HTN <== salt + water retention
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11
Q

Epidemiology/etiology: Post-infectious glomerulonephritis

A
  • occurs 2-3 wks after Group A strep infection
  • most common in children
  • may occur w/acute or subacute active infections
  • mediated by Ab response to strep ==> immune complex deposition + activation of complent @ glomeruli
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12
Q

Pathology/Clinical Presentation: Post-infectious glomerulonephritis

A
  • light microscope: proliferative + exudative w/inflitration of PMNs and monocytes
  • Immunofluorescence: IgG + C3 deposits @ subendothelial, mesangial, subepithelial
  • clinical present:
    • edema + sudden weight gain + HTN
    • hematuria + proteinuria
    • decreased GFR
    • Positive ASO titer
    • decreased C3 w/normal C4
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13
Q

Diagnosis/Tx: Post-infectious glomerulonephritis

A
  • Dx: nephritic syndrome + positive streptozyme + low C3
  • Tx: supportive
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14
Q

Epidemiology/etiology: IgA Nephropathy

A
  • most common; usually males 15-35
  • mediated by deposition of IgA complexes @ mesangium ==> activation of mesangial cells ==> cell proliferation
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15
Q

Pathology/Clinical: IgA Nephropathy

A
  • light: increase in mesangial cell number/matrix
  • IF: IgA, IgG, C3 @ mesangium
  • Clinical:
    • usually asymptomatic
    • often increased hematuria w/onset of viral illness
    • systemic sx possible
    • skin w/IgA deposits = Henoch-Schonlein purpura
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16
Q

Epidemiology/etiology: MPGN

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A
  • MPGN = mesangial proliferation + thickeneing of GBM
  • epidemiology = associated w/systemic illness or idiopathic<== adolescents + female > male
17
Q

Pathology/Pathogenesis: MPGN

Study These Flashcards
A
  • LM: thick basement membrane, mesangial cell proliferation + lobulated appearance
    • Deposits @ capillary walls, mesangium: C3, IgG
  • EM: subendothelial + mesangial deposits
  • Pathogenesis: trapping of circulating immune complexes
18
Q

Clinical Presentation: MPGN

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A
  • acute glomerulonephritis or nephritic syndrome
  • early HTN
  • common test results: Hep C infection w/HCV and RNA in blood + cryoglobulins
    • RF
    • low complement (C3 & C4)
19
Q

Tx/Prognosis: MPGN

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A
  • poor prognosis ==> end-stage renal disease
  • sometimes steroids
  • Hep C + ==> anti-viral
20
Q

Pathology: Anti-GBM disease

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A
  • Ab binds to type IV collagen w/in GBM ==> linear IgG deposits ==> glomerulonephritis
  • Abs ==> complement activation + PMN infiltration
  • crescent formation + rapid loss of renal fxn
21
Q

Clinical Presentation/Tx/Prognosis: Anti-GBM disease

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A
  • pulmonary hemorrhage + iron deficiency anemia + nephritis
  • Tx: steroids + immunosuppresion + plasma exchange ==> increases renal survival
22
Q

Pathology/Pathogenesis: Pauci-Immune Renal Vasculitis

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A
  • PIRV=small vessel vasculitis involving the kidney but w/out immune-complex deposition
  • Path: fibrinoid necrosis + crescents
  • Pathogen:
    • ANCA (anti-neutrophil cytoplasmic Ab) positive
23
Q

Clinical Presentation/Tx: Pauci-Immune Renal Vasculitis

Study These Flashcards
A
  • Can present @ skin, lungs, GI (and renal)
    • w/lungs = pulmonary-renal syndrome
  • nephritic pattern of renal disease
  • Tx: immunosuppresive drugs; steroids + cyclophosphamide or rituximab
    • possible: plasma exchange; dialysis
24
Q

Pathology/Pathogenesis: Lupus Nephritis

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A
  • Path: immune-complexes @ mesangium, subepithelium, subendothelium w/lumpy-bumpy pattern
  • Pathogen: autoantibody disease e.g. ANA (Anti-nuclear antibody)
25
Clinical Presentation/Tx: : Lupus Nephritis
* Renal signs: heamturia, proteinuria * either nephritic or nephrotic * Tx: steroids + cyclophosphamide
26
Clinical Presentation/Tx: Cryoglobulinemia
* Systemic sx: palpable purpura, arthralgias, generalized weakness * Urine: Proteinuria, hematuria * Labs: low C4, cryoglobulins, RF * Tx: antiviral (w/Hep C) * rituximab if lymphoproliferative disease * plasmapheresis
27
Pathology/Pathogenesis: Cryoglobulinemia
* Path: immune-complex glmerulonephritis * memranoproliferative pattern of injury + subendothelial immune deposition * Pathogen: Cryoglobulins = frequently associated w/Hep C infection * cooling blood ==\> immune complex formation
28
Characteristics of Henoch-Schonlein purpura (HSP)
* clinical: * skin lesions (palpable purpura) * arthritis * GI involvement * glomerulonephritis * path: * focal proliferative necrotizing glomerulonephritis w/crescent formation * mesangial + cap wall deposits of IgA
CVPR: Renal
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