Glomerulonephritis Flashcards

1
Q

What does the term Glomerulonephritis encompasses?

*includes 5 things

A
  • Caused by pathology in glomerulus
  • diagnosed on renal biopsy
  • causes CKD
  • can progress to kidney failure (except minimal change disease)
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2
Q

What Ix would you order for glomerulonephritis?

A
  • Bloods
    • FBC, U&E, LFT, CRP, Immunoglobulins, complement (C3,C4), autoantibodies (ANA, ANCA, andti-DSDNA, anti GBM)
  • Urinanalysis
    • MC&S
    • Bence Jones
    • A:CR/P:CR
    • RBC Cast
  • Imaging
    • CXR - pulmonary haemorrhage
    • Renal USS
  • Renal Biopsy (definitive)
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3
Q

What is Nephritic syndrome?

A

Group of sx, not diagnosis

  • Haematuria
  • Protenuria (<3.5g/24hrs)
  • Low GFR
  • Oliguria
  • HTN
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4
Q

What is Nephrotic syndrome?

A

Group of sx, not diagnosis

  • Proteinuria (>3g/day)
  • Peripheral oedema
  • Hypoalbuminamia (<30g/L)
  • Hypercholesterolaemia
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5
Q

What is interstitial nephritis?

What are the types of interstitial nephritis?

A
  • inflammation of spaces between cells and tubules
  • acute interstitial nephritis & chronic tubulointerstitial nephritis
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6
Q

What is glomerulosclerosis?

What causes golmeruosclerosis?

A
  • Pathological processes of scarring of tissue in the glomerulus
  • Any glomerulonephritis, obstructive uropathy, focal segmental glomeruloscelrosis
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7
Q

What causes nephrotic syndrome?

A
  • Primary renal disease
    • Minimal Chnage Disease (most common in children)
    • Membranous nephorpathy
    • Focal Segmental Glomerulosclerosis
    • Membranoproliferative GN
  • Secondary
    • DM
    • myeloma
    • amyloidosis
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8
Q

What causes proteinuria?

A
  • Damage to podocytes
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9
Q

How would you Mx nephrotic syndrome?

A
  1. Reduce odema
    • Fluid & salt restriction
    • Loop diuretics
    • Add thiazide if oedema persist
    • Aim 0.5-1kg/day weight loss
  2. Treat underlying cause
    • Corticosteroids - causes remission
    • Renal biopsy
  3. Reduce proteinuria
    • ACEi/ARB
  4. Treat complications
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10
Q

`What are the Cx of nephrotic syndrome?

A
  • Thromboembolism
    • Eg: Renal vein thrombosis, DVT
    • Px: anti thrombin 3 loss through filtration in kidneys
    • Tx: Warfarin, low dose LMWH
  • Infection
    • Eg: RTI, UTI, Cellulitis, CNS infection
  • Hyperlipidaemia
    • Px: hepatic synthesis due to low oncotic pressure and dec. lipid breakdown
    • Tx: Statin
  • HTN & CKD
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11
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal Change Disease

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12
Q

What is the Px Minimal Change DIsease?

A
  1. T cells release cytokines
  2. Damage foot processes of podocytes
  3. Effacement occurs
  4. Loss of charge barriers
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13
Q

What causes minimal change disease?

A
  • Idiopathic (most)
  • NSAIDs, lithium
  • Paraneoplastic
    • hodgkin’s lymphoma
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14
Q

How would you diagnose MCD?

A
  • Light microscope
    • normal
  • Electron microscope
    • effacemet (narrowing) of podocyte foot process
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15
Q

How would you treat MCD?

A
  • Prednisolone 1mg/kg - 4-16weeks
  • If relapse
    • cyclophosphamide
    • calcineurin inhibitors
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16
Q

What is the most common cause of nephrotic syndrome in adults?

A
  • Membranous nephropathy
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17
Q

What causes Membranous Nephropathy?

A
  • Primary
    • idiopathic
  • Seconary
    • malignancy: lung, breast, GI, prostate
    • infection: schistosomiasis, hepatitis b/c strep, malaria
    • immunological disease: SLE, RA, sarcoidosis, sjogren
    • drug: gold, penicillamine
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18
Q

How would you diagnose MN?

A
  • Bloods
    • Antiphospholipase A2 receptor antibody
  • Histology
    • Thickened GBM
    • IgG deposits
    • Spikes on silver stain
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19
Q

How would you tx MN?

A
  • ACEi/ARB in all
  • Corticosteroid + cyclophosphamide in high risk progression
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20
Q

When would you consider a patient having MN being high risk of progression?

A
  • porteinuria >4g
  • no response to ACEi/ARB after 6months
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22
Q

What is the commonest glmerulonephritis seen on renal biopsy?

A
  • Focal segmental glomerulosclerosis
23
Q

What causes FSGS?

A
  • Idiopathic
  • Seconday
    • HIV
    • Heroin
    • Lithium
    • Lymphoma
    • scarring due to other glomerulonephritis
24
Q

What are FSGS all at risk of?

A
  • CKD and Kidney Failure
  • high proteinuria worsens prognosis
25
How would you diagnose FSGS?
* Histology * focal sclerosis
26
How would you tx FSGS?
* ACEi/ARB in all * Corticosteroid * Calcineurin inhibitor * Rituximab & palsma exchange in renal transplant
27
28
How would you mx pt with renal biopsy? \*think pre and post procedure
* Pre-procedure * BP - follow local protocol * FBC - Hb\>9, plt\>100, clotting (pt&aptt \<1.2) * Consent * Explain complication * Stop anticoagulants * Post procedure * Bed rest min 4hrs * Monitor pulse, BP, sx and urine colour * Macroscopic haematuria settles - can discharge * Start anticoagulants
29
What is IgA N also known as?
Berger's disease
30
What is the most commonest primary glomerulonephritis in developed countries?
* IgA nephorpathy
31
How does IgA Nephropathy (Berger's Disease) present?
* Asymptomatic * non-visible haematuria * high BP * Proteinuria * slow progression to RF
32
How would you diagnose IgA N?
* Histology * IgA in mesangium cells
33
How would you tx IgA N?
* ACEi/ARB * Corticosteroid * Fish oil
34
What are the examples of diseases causing nephritic syndrome?
* IgA Nephropathy * Anti-GBM disease (goodpasture syndrome) * Post-streptococcal GN * ANCA associated vasculitis * Granulomatosis c polyangiitis * Microscopic polyangiitis * Eosinophilic granulomatosis c polyangiitis (churg strauss syndrome) * Thin basement membrane disease * Alport syndrome * Lupus Nephritis
35
What is anti-GBM disease previously known as?
* Goodpasture disease
36
What is the presentation of anti-GBM disease?
Renal pathology * Oliguria * Haematuria * AKI Lung pathology * SOB * Haemoptysis * pulmonary haemorrhage
37
What does the anti-GBM antibody target?
* T4 collagen found in glomerular and alveolar basement membranes
38
How would you diagnose anti-GBM disease?
* Blood * anti-gbm in circulation
39
How would you tx anti-gbm disease?
* Plasma exchange * corticosteroid * cyclophosphamide
40
anti-GBM disease and ANCA associated vasculitis (Wegener's granulomatosis) presents the same. How would you differentiate between the two?
* anti-GBM D: have anti-GBM antibodies * WG: have Anti Neutrophil Cytoplasmic Antibodies (ANCA)
41
How does post-streptococcal GN present?
* 2 weeks after throat infection * 3-6 weeks after skin infection * haematuria * oedema * high BP * oliguria
42
How would you diagnose and tx PSGN?
* + anti-strep antibodies (ASO titre) * low C3 * IgG, IgM, C3 deposition on biopsy * Self limiting * ACEi/ARB, low sodium diet * If ESRF - RRT
43
44
What causes rapidly progressive GN?
* ANCA vasculitis * lupus nephritis * anti-GBM disease * IgA N * MN
45
How would you diagnose RPGN?
* Histology * cresenteric GN
46
How would you tx RPGN?
* Corticosteroids * cyclophosphamide * plasma exchange - antiGBM/ANCA vasculitis * monoclonal antibodies - lupus nephritis
47
What is Henoch-Schonlein Purpura?
* Small vessel vasculitis & systemic variant of IgA N * IgA deposit in skin/joint/gut/kidney
48
How does HSP present?
* Purpuric rash on extensor surfaces * fitting polyarthritis * abdominal pain * nephritis
49
How would you diagnose HSP?
* Clinically * Skin * IgA * C3 * Renal biopsy
50
How would you tx HSP?
* same as IgA nephropathy
51
52
How would you briefly tx Glomerulonephritis? \*Think supportive therapy, immunosuppresive therapy, invasive therapy
* **supportive therapy** * Discuss with renal team * MDT approach * ACEi/ARB for proteinuria * BP control * Salt, water restriction and diuretics - if fluid overload * LMWH if hypoalbuminaemia * Statins for HCL * **Immunosuppresive therapy** * Oral corticosteroid, IV methylprednisolone, Cyclophosphamide, Tacrolimmus, Ciclosporin, Rituximab, MMF, Azathioprine * **Invasive therapy** * RRT * Plasma exchange for AAV, anti-GBM