Renal > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

(37 cards)

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1
Q

Glomerulonephritis definition

A

inflammatory diseases involving the glomerulus and tubules

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2
Q

Nephrotic syndrome features:

A

“protein leac” (lipidaemia,oedema, albumin down, chol increases)

  1. Proteinurea (>3.5g in 24 hours)
  2. hypoalbuminaemia (<25g/l)
  3. peripheral oedema
  4. Hyperlipidaemia - total cholesterol >10mmol/l

Albumin is lost in the urine, due to gaps in podocytes allowing proteins to escape.

Oedema - due to loss of albumin, intravascular oncotic pressure decreases, fluid moves out of vessels

Hyperlipidaemia- hypoalbuminaemia, liver compensates by increasing production of lipids, hence causing hyperlipidaemia

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3
Q

Causes of Nephrotic syndrome

A

Primary

  • minimal change glomerulonephritis - the most common cause of nephrotic syndrome in children
  • membranous glomerulonephritis
  • focal segmental glomerulosclerosis - the most common cause of nephrotic syndrome in adults

Secondary

  • ​D - diabetes
  • A - Amyloidosis
  • V- vasculitis
  • I - infections (syphillus, hep B_
  • D- drugs

(SLE, malignancy, HIV)

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4
Q

Nephritic syndrome features

A

Blood +++ (microscopic or macroscopic)

Red cell casts- distinguishing features, form in nephrons and indicate glomerular damage

  1. Haematuria
  2. proteinuria (small amount)
  3. hypertension
  4. low urine volume <300ml/day
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5
Q

Causes of nephritic syndrome

A

Post sterptococcal glomerulonephritis - appears weeks after URTI

IgA nephropathy - appears within a day or two after URTI

Rapidly progressive glomerulonephritis (cresentic glumerulonehritis)

  • Good pastures - anti-GBM Ab against basal membrane antigens
  • vasculitic disorder- wegners, microscopic polyangitis
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6
Q

Tests for Glomerulonephritis

A

U&Es - creatinine for renal impairment

FBC- anaemia, infection

ESR, CRP- markers of inflammation (infectious cause_

EP and IG - IgA increased in IgA nephropathy EP rules out myeloma

Serum biochemistry- renal function, liver function, bone profile, lipids, glucose

Autoantibodies and complement

  • ANCA- wegers granulomatosis + polyarterial nodosum
  • Anti-GBM - good pastures
  • ANF- lupus

Urinalysis, Urine PCR

  • RBC casts, proteinuria

Coagulation screen

  • biopsy (are they able to clot)

Imaging - CXR, US

  • infection, pulmonary renal syndrom

LFTs (albumin levels)

GI - diabetes, commonest cause of all nephrotic syndromes

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7
Q

Feautures of IgA nephropathy

A
  • Commonest cause of GN in the world
  • may be secondary to:
    • Henoch-schloen purpura
    • cirrhosis
    • coeliac disease
  • may present with one or all
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8
Q

IgA nephropathy Clinical presentation

A
  • Haematuria - increased destruction of GBM
  • proteinuria
  • hypertension
  • renal impairment
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9
Q

Diagnosis of IgA nephropathy

A
  • Electronmicroscopy - shows immune complexes in the GBM
  • Immunofluorescence- shows IgA deposition
  • Light microscopy- proliferation of mesangium
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10
Q

Pathophysiology of IgA nephropathy

A
  1. overproduction of IgA could be triggered by infection
  2. IgA deposition in the mesangium + C3 deposition
  3. Lysis of mesangium - Proliferation and activation of mesangial cells causing production of matrix - inducing glomerulosclerosis and scarring
  4. result is tubular loss, glomerulosclerosis and hypertensive damage
  5. Spillage of protein and blood cells into the urine
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11
Q

Treatment of IgA nephropathy

A
  • No specific treatment
  • Anti-hypertensives, ACE inhibitors
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12
Q

Outcomes of IgA nephropathy

A
  1. resolution
  2. Perists
  3. progression to ESRF 1/3
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13
Q

Membranous Glomerulonephropathy Clinical feautres

A
  • proteinuria without haematura
  • hypertension
  • renail impairment
  • Nephrotic syndrome!
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14
Q

Pathophysiology of Membranous glomerulonephritis

A
  1. Trigger may be Ag from tumour, infections, drugs
  2. Production of immune complexes, stuck in GBM
  3. alters GBM charg, permeability selectivity and thickened GBM
  4. Results in glomeruloscerlosis, tubular loss and hypertensive damage
  5. leads to loss of protein in urine = hallmark
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15
Q

Features of membranous GN

A
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16
Q

Treatment of membranous GN

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A

Non specific therapy

  • diuretics - furosemide
  • ACE inhibitors - reduce proteinuria
  • Statins
  • consider anticoagulation -because of the hypervoagulable state associate with nephrotic syndrome

Specific

combination of

  • prednisolone - dampen IC
  • chlorambucil

No proven specific treatment wait for 6 months first due to rule of 30%

Rituximab has shown to be successful

17
Q

Outcome of membranous GN

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A
  • 1/3 get resolution
  • 1/3 peristent
  • 1/3 progression to ESRF
18
Q

Porticelli regimen

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A

1 month of chorampuci/cyclophosphamide then 1 month prednisolone for 6 month period

treatment of membranous GN

19
Q

Cresentic GN definition/ causes

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A

Group of nephropathys associated with crescents on biopsys and with rapid progression to ESRF over a few weeks

Causes

  • Goodpastures
  • polyarteritis nodosa
  • Wegeners granuloatosis
20
Q

Goodpastures Pathophysiology

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A
  1. Production of Anti-bodies against GBM plus Bm in lung (pulmonary renal syndrome)
  2. Deposition of Ab/complemet activation
  3. causes destruction of glomerular cells, proliferation of epithelial cells, crecent formation
  4. results in glomerulscerlosis, tubular loss and hypotensive damage
21
Q

Good pastures clinical features

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A
  • Nephritic syndrome
  • Haematuria
  • Proteinruia
  • Hypertension
  • Renal impairment
22
Q

Outcome of goodpastures

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A

all will progress unless treated

23
Q

Treatment of goodpastures syndrome

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A

cytotoxic drugs to reduce antibody production

24
Q

Pathophysiology of wegeners granulomatosis

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A
  1. Necrotising granulomas of midline structures - nose, lungs, kidneys
  2. Necrotising vasculitis
  3. Nasal symptoms- bleeding, stuffiness and deafness
  4. Pulmonary symptoms - flitting opacities, pulmonary haemorrhage
  5. Crescentric glomerulonephritis - RPGN

Associated with anti-neutrophil antbody (ANCA)

25
Treatment of wegeners granulomatosis
Steroids, cytotoxics and spetrin Rituximab is also effective - fever side effects Untreated mortaility is 95% within one year
26
Post-infectious GN pathophysiology
1. Post infection - stretococcal 2. Production of AB/IC 3. Deposition of ab/ic in mesangium and all throughout kidney 4. complement is activated 5. Reversible destriction of glomerular cells, proliferation of epithelial cells, crescent formation
27
Clinical features of Post-infectious GN
* haematuria * proteinuria * renal impairment
28
Treatment of post infectious GN
* self-limiting * antibiotic therapy
29
Minmal change features
* commonest form of GN in children * nephrotic syndrome
30
minimal change diagnosis
* lightmicroscopy will appear normal * Electronmicroscopy - foot long procces, disruption to filtration barrier * immunofluroscence - shows C3 and IgM deposition
31
Pathogenesis and cause of minimal change
T-cell mediated, cytokine mediated Targets glomerulus, epithelial cells and GBM charge Idiopathic but may be secondary to malignancys (lymphomas)
32
Treatment of minimal change disease
Curable * high dose steroids - prednisolone * cyclophosphamide- if they go into relapse * cyclosporine- if the above doesnt work- steroid resistant or continually relapsing
33
Diabetic nephropathy incidence
**Incidence** * Affects 35% of type 1 and increases rates of type 2 * Only affects a subset-not everyone * Occurs after 10 years of diabetes
34
Clinical features of diabetic nephropathy
**Clinical features** * **​**Proteinuria and microalbuminaemia for years * Hypertension (Nephrotic syndrome) * Progressive ESRF * Most patients die of CVD before ESRF * ESRF
35
Histology and EM findings
Histology: * Primarily endothelial dysfunction/damage affecting the glomerulus. * Leads to nodular deposition of matric substance glomerulosclerosis- **Kimmelstiel-Wilson nodu**le * As the disease advances - GBM thickening with abnormal BM tht is leaky to protein EM: glomerulular is uniformly thickened
36
Treatment of diabetic nephropathy
Treatment: ACEi limit proteinuria and control BP. No specific therapy.
37
Prevention of diabetic nephropathy
Glycaemic control in early years and BP control is imperative
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