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Glomerulonephritis Flashcards

1
Q

how does nephrotic syndrome arise

A

when the basement membrane in glomerulus becomes highly permeable
- proteinuria >3.5g of protein in 24 hrs = frothy urine
- hypoalbumiaemia < 30g per litre
- peripheral oedema
- hypercholesterolaemia

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2
Q

what are complications of nephrotic syndrome

A
  • higher risk of infection
  • VTE
  • progression of cKD
  • HTN
  • hyperlipidaemia
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3
Q

what is the most common cause of nephrotic syndrome in children

A

minimal change disease
- usually idiopathic
- treated w steroids

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4
Q

what are the most common causes of nephrotic syndrome in adults

A
  • FSGS: idiopathic or secondary to infection, malignancy, drugs
  • membranous nephropathy
  • HSP
  • infection e.g. HIV

  • membranoproliferative GN but more common in nephritic syndrome
  • amyloidosis/myeloma may have nephrotic range proteinuria but not necessarily other features
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5
Q

what are the features of nephritic syndrome

A
  • haematuria
  • oliguria
  • proteinuria
  • fluid retention
  • AKI
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6
Q

what is the most common cause of primary GN

A

IgA nephropathy or Berger’s disease

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7
Q

how does IgA typically present and what are investigatio findings

A
  • patient in 20s presenting w episodic gross haematuria or directly after URT, GI infection or strenuous infection
  • histology: IgA deposits in glomeruli and mesangial proliferation
  • normal C3,C4
  • asymptomatic microhaematuria w intermittent visible haematuria
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8
Q

what is the treatment of IgA nephropathy

A

supportive therapy
- ACEi/ARB for proteinuria/HTN

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9
Q

when does post-strep GN present and who does it commonly affect

A

weeks after Group A B haemolytic strep infection
- 1-2 wks post tonsilitis/pharyngitis
- 3-4 wks post impetigo/cellulitis
- affects children 3-12

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10
Q

what are investigation findings of PSGN

A
  • positive anti-strep antibodies (ASO titre)
  • low serum C3
  • biopsy: immune complex deposition IgG, IgM, C3
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11
Q

what is the treatment of PSGN

A

usually self-limiting but supportive therapy:
- ACEi/ARB for proteinuria/HTN
- low sodium diet
- if ESRF then RRT

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12
Q

give 3 examples of small vessel vasculitis aka ANCA associated cellulitis

A
  • granulomatosis w polyagiitis
  • microscopic polyangiitis
  • eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
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13
Q

granulomatosis with polyangiitis (GPA)
- key features
- investigation findings
- treatment

A
  • features: pulmonary and nasopharyngeal involvement e.g. nasal ulcers/polyps
  • investigation: c-ANCA, biopsy shows segmental necrotising GN
  • ✅: immunosuppression
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14
Q

microscopic polyangiitis
- key features
- investigation findings
- treatment

A
  • features: usually only mild resp symptoms
  • investigation: p-ANCA (MPO), biopsy shows segmental necrotising GN
  • ✅: immunosuppression
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15
Q

Churg-Strauss syndrome
- key features
- investigation findings
- treatment

A
  • features: asthma, allergic rhinitis, purpura, peripheral neuropathy
  • investigations: p-ANCA, eosinophilia, focal segmental necrotising GN
  • ✅immunosuppression
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16
Q

what happens in Goodpasture syndrome aka anti-GBM disease

A
  • anti-GBM antibodies against type IV collagen attack the glomerulus and pulmonary basement membranes
  • pulmonary haemorrhage + haemoptysis
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17
Q

what are the investigation findings of anti-GBM disease

A
  • anti-GBM antibodies
  • pulmonary infiltrates on CXR
  • biopsy: linear deposition of IgG along basement membrane
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18
Q

what is the treatment of Goodpasture’s syndrome

A
  • plasma exchange
  • immunosuppression e.g. cyclosphophamide
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19
Q

what is thin basement membrane disease due to

A
  • hereditary
  • abnormalities of type IV collagen
20
Q

what are the investigation findings of thin basement membrane disease

A
  • persistent microscopic haematuria - possible visible intermittent haematuria
  • biopsy: diffuse thinning of GBM
21
Q

what is the treatment of thin basement membrane disease

A
  • monitor renal function
  • supportive treatment
22
Q

what is alport syndrome

A

X-linked so usually affects males
- mutation in gene coding for type V collagen
- associated with hearing loss and abnormalities of the eyes
- often leads to ESRF

23
Q

what are the investigation findings of alport syndrome

A
  • persistent microscopic haematuria w intermittent visible haematuria
  • sensorineural hearing loss
  • biopsy: splitting of GBM and alternating thickening and thinning of GBM
  • genetic studies - FHx
24
Q

what is the treatment of alport syndrome

A
  • supportive treatment
  • RRT
  • renal transplant: can lead to Goodpasture’s
25
what are the investigation findings of lupus nephritis
- ANA & anti-dsDNA positive - biopsy: 6 different classes of lupus nephritis
26
what is the treatment of lupus nephritis
- supportive therapy - immunosuppressive therapy based on classification/presentation
27
what is supportive therapy in the management of GN
- If suspect GN – discuss with Renal team - MDT approach depending on underlying diagnosis - **ACEi/ARB** for proteinuria Control BP - **Salt and water restriction** if volume overloaded - **Diuretics** for fluid overload - If **hypoalbuminaemic** <20g/dl then higher risk for VTE – consider **therapeutic LMWH** - **Statins** for hypercholesterolaemia
28
what is immunosuppressive therapy in the management of GN
- Specific to cause of GN – decided by Renal team (+/- Respiratory / Rheumatology teams if lung or systemic involvement ) - Oral Corticosteroids, IV pulsed methylprednisolone, Cyclophosphamide, Tacrolimus, Ciclosporin, Rituximab, MMF, Azathioprine
29
what is invasive therapy in the management of GN
- **Renal replacement therapy**/haemodialysis for those in severe AKI or ESRF - **Plasma exchange** for AAV (with lung involvement), anti-GBM
30
what is one of the main complication of anti-GBM syndrome and what factors increase the risk of this
**pulmonary haemorrhage** * smoking * lower respiratory tract infection * pulmonary oedema * inhalation of hydrocarbons * young males
31
what are the causes of membranous nephropathy ## Footnote 5 categories
* **idiopathic**: due to anti-phospholipase A2 antibodies * **infections**: hepatitis B, malaria, syphilis * **malignancy** (in 5-20%): prostate, lung, lymphoma, leukaemia * **drugs**: gold, penicillamine, NSAIDs * **autoimmune diseases**: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
32
what is the managment of membranous nephropathy (3)
- all pt receive **ACEi/ARB**: shown to reduce proteinuria and improve prognosis - **immunosuppression**: combination of corticosteroid + another e.g. cyclophosphamide - **consider anticoagulation** for high-risk patients
33
what are the causes of FSGS
* idiopathic * secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy * HIV * heroin * Alport's syndrome * sickle-cell
34
in what setting is there a high recurrence rate of FSGS
renal transplant
35
what does renal biopsy of FSGS show
- focal and segmental sclerosis and hyalinosis on light microscopy - effacement of foot processes on electron microsocopy
36
what is the management of FSGS
steroids +/- immunosuppression
37
what does RPGN describe
a rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli
38
what are 2 main causes of RPGN
- Goodpasture's syndrome - Wegener's granulomatosis
39
what are the features of RPGN
- those of nephritic syndrome: haematuria + red cell casts, proteinuria, HTN, oliguria - features specfic to underlying cause: haemoptysis with Goodpasture's, vasculitic rash or sinusitis with Wegener's
40
what are differences between IgA nephropathy and PSGN
- IgA onset develops 1-2 days after URTI vs PSGN develops 1-2 weeks after URTI - PSGN associated low complement levels - main symptom in PSGN is proteinuria
41
when does Alport's syndrome usually present and what features may be present
- microscopic haematuria - progressive renal failure - bilateral sensorineural deafness - lenticonus: protrusion of lens surface into the anterior chamber - retinits pigmentosa
42
what is the treatment of proteinuria (2)
1. **ACEi or ARBs**: 1st line in pt w co-existent HTn + CKD 2. **SGLT-2 inhibitors**
43
how do SGLT2 inhibitors help in the management of proteinuria
- mainly act by blocking reabsorption of glucose in PCT which lowers the renal glucose threshold --> glycosuria - by blocking the co-transporter, they also reduce Na+ reabsorption --> natriuresis reduces the intravascular volume + BP - but also inc delivery of Na+ to the macula densa cells which normalises tubuloglomerular feedback and reduces intraglomerular pressure
44
how does nephrotic syndrome predispose to thrombosis
loss of antithrombin III, protein C & S with an associated rise in fibrinogn levels ## Footnote LMWH
45
how does anti-GBM disease present
the disease affects type IV collagen that is found in both the **kidneys** and the **lungs** which causes chest symptoms such as **haemoptysis, coughing and chest pain**

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