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Inflammation block > An intro to glomerular diseases > Flashcards

An intro to glomerular diseases Flashcards

1
Q

What is glomerulonephritis

A

-Glomerular inflammation
-Generally caused by immunological mediated injury to the glomeruli
-Pathogenic mechanism: deposition of circulating or in situ formation of immune; deposition of antiglomerular basement membrane abs
(These mechanisms activate secondary mechanisms that lead to the glomerular damage &inflammation)
-Pattern of injury and the clinical presentation will depend on the ‘target’ of the immune response

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2
Q

How can we classify glomerulonephritis

A
  1. ) PRIMARY eg membranous

2. ) SECONDARY- as part of a generalized disease eg SLE

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3
Q

How may someone with glomerular disease present?

A
  • hypertension
  • incidental finding of proteinuria
  • incidental finding of microscopic haematuria
  • Nephrotic syndrome
  • Progressive renal impairment
  • Acute kidney injury
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4
Q

What is nephrotic syndrome

A

A collection of symptoms due to kidney damage

  • hyperlipidaemia
  • Oedema( children=periorbital; adults=peripheral)
  • Hypoalbuminuaemia
  • Heavy proteinuria>3.5g per day
  • If you have 3+ protein on urine dipstick and someone with oedema, it’s almost always going to be nephrotic syndrome
  • A leak of protein through your kidney cos the podocyte pores(these usually hang onto protein) get disrupted and the protein leaks through into the urine freely
  • Basically an increase in protein leak associated with oedema
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5
Q

What may be a consequence or renal artery stenosis

A

renal hypertension

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6
Q

Why would you consider checking complements if a pt presents to you with incidental hypertension

A

To check for SLE

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7
Q

Why would you consider checking ANCA if a pt presents to you with incidental hypertension

A

To check for vasculitis

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8
Q

What is IgA nephropathy?

A
  • aka Berger’s disease
  • occurs when IgA lodges in your kidney
  • Results in local inflammation that, over time, may hamper your kidneys’ ability to filter wastes from your blood
  • Could cause and incidental finding of hypertension
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9
Q

What are some causes of secondary hypertension

A
  • endocrine causes

- renal artery stenosis

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10
Q

What are some non-glomerular causes of microscopic haematuria ?

A
  • Bladder tumours
  • Renal stones
  • Renal tumors
  • BPH
  • UTI
  • Renal injury
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11
Q

What are some of the primary glomerular causes of microscopic haematuria

A
  • IgA nephropathy
  • Alports
  • Thin basement membrane disease
  • Post infectious GN
  • Membranoproliferative GN
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12
Q

What are some of the secondary glomerular causes of microscopic haematuria

A
  • Henoch Scorlein Purpura (IgA vasculitis)
  • SLE
  • HUS
  • ANCA
  • Sickle nephropathy
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13
Q

Outline the pathogenesis of IgA nephropathy

A

-Glomerular deposition of IgA causing inflammation

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14
Q

Outline the clinical presentation of IgA nephropathy

A

Variable clinical presentation

  • Microscopic haematuria
  • Hypertension
  • Slowly progressive renal impairment
  • Rapidly progressive renal impairment
  • Nephrotic range proteinuria
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15
Q

What lab tests may be useful for IgA nephropathy

A
  • Raised serum IgA

- Renal biopsy shows mesangial proliferation with IgA deposition

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16
Q

How can we manage IgA nephropathy?

A
  • Control of BP

- Immunosuppression may be useful

17
Q

Outline the characteristics of Henoch Schonlein Purpura

A
  • Inflammation of the small blood vessels esp in kidneys,skin and gut
  • Most common in young children
  • IgA deposition in the kidney in a similar pattern to IgA nephropathy
  • Associated with a leucocytoclasic vasculitic rash
  • Variable prognosis, some fully recover with resolution of the rash and renal findings, others progress to ESKD
18
Q

Define leucocytoclasic

A

‘To be destroyed by WBCs’

-eg IgA vasculitis; the small vessels are destroyed by IgA antibodies

19
Q

What are the primary causes of nephrotic syndrome?

A
  • Membranous nephropathy
  • FSGS(focal segmental glomerulosclerosis)
  • MCGN (Mesangiocapillary glomerulonephritis)
  • Minimal change disease
20
Q

What are the secondary causes of nephrotic syndrome?

A
  • Diabetic nephropathy
  • SLE
  • Amyloidosis
  • Malignancy
  • Drugs
21
Q

What are the possible complications of nephrotic syndrome?

A
  • Protein malnutrition
  • Hypovolaemia
  • AKI (esp older pts with min change disease)
  • VTE
  • Infections
22
Q

Describe the management of nephrotic syndrome

A
  • Diuretics
  • ACE
  • Anticoagulation
  • Statin
  • Renal biopsy (in children minimal change disease is common so steroids are given before the biopsy)
23
Q

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

A

Minimal change disease (90%)

24
Q

What are the most common causes of nephrotic syndrome in adults

A 
FSGS(35%)
Membranous nephropathy(33%)
25
Q

What is minimal change disease?

A
  • Sudden onset oedema especially in children
  • Normal light microscopy
  • Foot process effacement of podocytes on EM
26
Q

Outline the causes of minimal change disease

A
  • Ideopathic(majority), esp kids
  • NSAIDs
  • Lithium,pellicinamine,pamidronate, sulfazalizine,immunizations
  • Paraneoplastic (Hodgkins lymphoma)
  • Infections (syphillis, TB, mycoplasma, Hep C)
  • Allergy
27
Q

What is FSGS

A
  • Focal segmental glomerulosclerosis
  • This is a lesion, not a disease
  • A lot of cases have nephrotic syndrome with it
  • Light microscopy shows focal and segmental areas of mesangial collapse and sclerosis
  • Very common in blacks
28
Q

What are the possible causes of FSGS?

A

-Idiopathic-usually presents with nephrotic syndrome

Secondary (non-nephrotic proteinuria, hypertension, microscopic haematuria and renal insufficiency more common presentations)

  • HIV infection(collapsing)
  • Reflux nephropathy
  • Massive obesity
  • Scaring from previous insult eg IgA, vasculitis, Lupus
  • Heroin
29
Q

What is membranous nephropathy

A
  • Most common cause of primary nephrotic syndrome in adults
  • Basement membrane thickening, little or no cellular expansion
  • Electron dense deposits in the GBM (represent immune deposits)
  • Ideopathic-antiPLA2 ab associated
  • Secondary- hepB, autoimmune diseases (inc SLE), thyroiditis, carcinomas, gold,penicillamine,captopril, NSAIDs
30
Q

Define exsanguination

A

severe loss of blood

31
Q

How can we treat hyperkalaemia ?

A
  • Calcium gluconate to protect your heart & prevent him getting arrhythmias
  • Insulin will drive K into cells (but you’re not removing the K you’re just moving it into a different compartment, so you then need to think about removing the K excess)
  • Dextrose to replace loss fluids & provide carbs for the body
  • It is the extracellular K that’s dangerous and can cause arrhythmias
32
Q

Outline ANCA positive vasculitis

A
  • Granulomatosis with polyangitis (GPA)
  • Microscopic polyangitis
  • Rapidly progressive GN with crescent formation
  • ANCA= anti neutrophil cytoplasmic abs and these have been shown to be pathogenic
33
Q

What is anti GBM disease

A
  • Auto antibodies to the glomerular basement membrane causing a rapidly progressive glomerular nephritis with crescent formation
  • Previously known as good pastures syndrome
  • Associated with anti GBM abs and alveolar basement membrane abs
  • Can cause absolute anuria with pulmonary haemorrhage (or only AKI or pulmonary haemorrhage)
34
Q

How can the colour of the urine on a urine dipstick be useful?

A
  • Visible haematuria
  • Frothy suggests proteinuria
  • Cloudy may suggest infection
  • Coca cola colour suggests rhabdomyolysis
35
Q

Why may the urine specific gravity be useful in a urine dipstick?

A
  1. ) high= increased conc of solutes in the urine eg glucose in diabetes or dehydration
  2. ) If low can suggest GN or diabetes insipidus (but non-specific and not greatly helpful)
36
Q

What blood tests may be useful in suspected glomerular disease?

A
  • Blood cultures
  • U&E, LFT, Bone profile
  • Virology
  • RF
  • C3 &C4
  • ANCA
  • Anti GBM
  • Myeloma screen (Igs,Electrophoresis & urine Bence-Jonce proteins)
37
Q

What is rheumatoid factor?

A

-Antibodies directed against the Fc portion of IgG (usually IgM)

38
Q

What are the different ways gomerular disease can present in

A
  1. ) Acute vs chronic
  2. ) Idiopathic vs secondary
  3. ) Incidental finding vs acute presentation
  4. ) Nephrotic (proteinuria) vs nephritic (haematuria)

Inflammation block (27 decks)

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