UT/Nephro > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

(42 cards)

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1
Q

Proliferative vs non-proliferative glomerulonephritis

A

Proliferative (nephritic): inflammation in the glomerulus causes recruitment / proliferation of cells - hematuria + proteinuria
Non-proliferative (nephrotic): structural injury causes damage to the filtration barrier - proteinuria (>3.5 g/L)

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2
Q

Types of proliferative GNs (nephritic) (6)

A

-Mesangial proliferative GN (IgA nephropathy)
-Diffuse proliferative GN (post-infectious, SLE)
-Membranoproliferative glomerulonephritis (MPGN - Hep C)
-RPGN (anti-GMB disease, Goodpasture’s, etc.)
-Vasculitits (ANCA-associated)
-Hereditary nephritis

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3
Q

What is the most common proliferative and non-proliferative GN?

A

Proliferative: mesangial (IgA)
Non-proliferative: diabetic nephropathy

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4
Q

Presentation of mesangial proliferative GN

A

Gross hematuria during or immediately after infection

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5
Q

Histology of mesangial proliferative GN

A

-IgA deposits
-Mesangial proliferation

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6
Q

What is Henoch-Schonlein purpura

A

A disease with identical histology to mesangial proliferative GN, but it is systemic (arthritis, GI issues, etc.)

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7
Q

Types of diffuse proliferative GNs (2)

A

-Lupus
-Post-infectious GN (PIGN)

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8
Q

Serology features of lupus (3)

A

-↓C3 + ↓C4
-ANA (+)
-dsDNA (specific for renal disease)

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9
Q

Classes of lupus nephritis (6)

A

1: normal light microscopy but IF (+)
2: mesangial proliferation
3: focal proliferative
4: diffuse proliferative - worst prognosis
5: membranous
6: glomerulosclerosis - end stage

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10
Q

Features of PIGN (5)

A

-Presents 10-21 days post-infection
-Gross hematuria (“tea” / “cola” coloured urine)
-Edema
-Hypertension
-↓C3

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11
Q

Histology of PIGN (3)

A

-PMN infiltration
-Proliferation (mostly mesangial)
-IgG / C3 deposits on IF

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12
Q

Pathogens most commonly associated with PIGN

A

Adults: S. aureus
Kids: GAS

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13
Q

Features of membranoproliferative GN (MPGN) (2)

A

-↓C3
-Associated with autoimmune diseases, monoclonal proteins, and infections (esp Hep C)

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14
Q

Histology of MPGN (3)

A

-Lobular appearance to glomeruli
-Double contoured BM
-Granular IgG staining on IF

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15
Q

General features of RPGN (3)

A

-Crescents in >50% of glomeruli
-Tubular range proteinuria
-Rapid decline in kidney function

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16
Q

Types of RPGN (3)

A

Type I: anti-GBM disease
*If lung (hemoptysis) + kidney involvement - Goodpasture’s disease
Type II: due to immune-complex diseases like SLE, PIGN, IgA
Type III: associated with ANCA

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17
Q

Histology patterns of the 3 types of RPGNs

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A

Type I: smooth linear IgG staining, necrotizing GN, patchy podocyte effacement
Type II: granular staining
Type III: no staining (pauci-immune), ecrotizing GN, patchy podocyte effacement

18
Q

p-ANCA vs c-ANCA

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A

p-ANCA: MPO (+) - microscopic polyangiitis (MPO)
c-ANCA: PR3 (+) - granulomatosis + polyangiitis

19
Q

Investigations to order when a proliferative GN is suspected (6)

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A

-ANA (can add anti-dsDNA for renal SLE)
-ANCA
-Anti-GBM Ab
-C3 + C4
-Renal biopsy
-ASOT (if post-strep GN suspected)

20
Q

Types of non-proliferative GNs (nephrotic) (6)

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A

-Diabetic nephropathy
-Minimal change disease (MCD)
-Membranous GN (MGN)
-Focal segmental glomerulosclerosis (FSGS)
-Paraprotein deposition disease
-Pre-eclampsia

21
Q

Approach to non-proliferative GNs (6)

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A
  1. Rule out diabetes (A1c)
  2. Exclude paraprotein-related disease (protein electrophoresis)
  3. If female, exclude pregnancy - pre-eclampsia
  4. Histology
    -Minimal change disease= podocyte foot effacement
    -Membranous GN= thick GBM, IgG deposits, anti-PLA2R (serology)
    -Focal segmental glomerulosclerosis (FSGS)= sclerotic lesions, global podocyte effacement
  5. Serology (SLE, Hep B, HIV) + med review
22
Q

Nephroprotection with diabetic nephropathy

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A

ACEi (start when microalbuminuria is present or non-diabetic but ptroteinuria >1-2 g/day) - help prevent progression to CKD

23
Q

Histology of diabetic nephropathy (4)

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A

-Glomerulosclerosis
-Nodules
-Think GBM
-Diffuse podocyte effacement

24
Q

Stages of diabetic kidney disease (5)

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A

Hyperfiltration: <30 mg/day (urinary albumin)
-Microalbuminuria: 30-300 mg/day
-Macroalbuminuria: >300 mg/day
-Overt nephropathy: GFR 15-60
-ESRD: GFR <15

25
Minimal change disease (MCD) is most common in what age group?
**Peds** - 80% of non-proliferative GNs are MCD
26
Features of MCD (2)
-Normal GFR -Podocyte foot effacement
27
Management of MCD
Steroids
28
Presentation of membranous GN (MGN) (2)
-↓ GFR -Hypertension
29
MGN can be associated with what? (5)
-SLE -Drugs -Malignancy -Hepatitis B -Syphilis
30
Serological marker of MGN
**Anti-PLA2R** (if primary MGN)
31
Common complication of MGN
**Venous thrombosis** - look for signs of DVT
32
Management of MGN (2)
In high risk groups + those with CKD: -Cytotoxic drugs -Steroids
33
Signs of focal segmental glomerulosclerosis (FSGS) (1)
**Glomerulosclerosis on histology** - associated with low renal mass and hyperperfusion of remaining nephrons
34
FSGS may be associated with what?
HIV
35
What are praraproteins and how can they cause GN?
**Monoclonal proteins (light or heavy chain)** resulting from proliferation of one clone of plasma cells - can have toxic effects on renal tubules and/or cause overflow proteinuria
36
Diseases associated with paraproteins (4)
-Multiple myeloma (MM) -Light chain deposition disease -Amyloidosis -Waldenstorm's macroglobulinemia
37
Diagnosis of paraprotein-related disorders
**Serum and urine protein electrophoresis** *Note that a urine dipstick may be normal despite monoclonal protein excretion because it only detects albumin
38
When might pre-eclampsia cause GN?
In the third trimester of pregnancy
39
Common features associated with nephrotic syndrome (proteinuria >3.5 g/day)
-**Hypoalbuminemia** (lost in urine) -**Edema** (low oncotic pressure + salt retention) -**Hyperlipidemia** - higher risk of thrombosis (esp in MGN) -**Hypogammaglobulinemia** (low IgG)
40
What is Alport syndrome?
A familial GN characterized by **visual + auditory defects** - poor prognosis *Caused by mutations in genes encoding components of type IV collagen
41
What is benign familial hematuria
A familial GN where there is a thin GBM but no other defects - excellent prognosis
42
Common cause of hematuria in children
**Hypercalciuria** - need to check urine calcium
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