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Renal (Year 2 GM) > Glomerular Disease (clinical) > Flashcards

Glomerular Disease (clinical) Flashcards

1
Q

What are features of glomerulonephritis?

A
  • Haematuria
  • Proteinuria
  • Hypertension
  • Renal insufficiency
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2
Q

What is the difference between nephrotic and nephritic syndrome?

A

Nephrotic - proteins in the urine

Nephritic - inflammation of the kidney

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3
Q

What is macroscopic and microscopic haematuria?

A
  • Macroscopic, tea- or cola colored or frank blood
  • Microscopic, =>5 RBC per high power field
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4
Q

What is the duration of haematuria?

A

Can be transient or persistent

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5
Q

What is the more likely syndrome for haematuria - nephritic or nephrotic syndrome?

A

Nephritic

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6
Q

What is the source of blood in the urine?

A

•Source: kidney, ureter, bladder, prostate, urethra

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7
Q

What is the finding of microscopy on persistent microscopic haematuria?

A

•In glomerulonephritis: persistent micorscopic haematuria, microscopy shows dysmorphic RBC (Mickey-mouse-like)

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8
Q

What are the types of proteinuria?

A
  • Glomerular or tubular
  • Albuminuria or proteinuria
  • Persistent or transient
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9
Q

Which is more common for proteinuria - nephritic syndrome or nephrotic syndrome?

A

They are equal

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10
Q

How do you determine proteinuria?

A

•Urine protein creatinine ratio or 24 hour urine collection

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11
Q

What is the definition of persistent proteinuria?

A

More than 1 gram/mmol creatinine

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12
Q

What is defined as hypertentsion?

A

Over 140/80

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13
Q

What condition is more likely to present with hypertension? Renal insufficiency? Nephritis or nephrotic syndrome?

A

Nephritis

Renal insufficiency can be mild or severe

May have slow or rapid deterioration

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14
Q

What are the features of nephritic state?

A
  • Active urine sediment: haematuria, dysmorphic RBCs, cellular casts
  • Hypertension
  • Renal impairment
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15
Q

What are the features of nephrotic syndrome?

A
  • Oedema
  • Proteinuria >3.5 g/day
  • Hypoalbuminemia
  • Hyperlipidemia
  • Can be caused by primary (idiopathic) glomerular disease or secondary glomerular diseases
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16
Q

What is the differential diagnosis for nephrotic syndrome?

A
  • Congestive Heart Failure (JVP raised, normal albumin, minimal proteinuria)
  • Hepatic Disease (abnormal LFTs, no proteinuria)
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17
Q

What are the different classifications of glomerulonephritis?

A
  • Aetiology: autoimmune, infection, malignancy, drugs, others
  • Primary versus secondary i.e. kidney alone or part of multisystem disease.
  • Morphological
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18
Q

What is the difference between proliferative and non-proliferative glomerulonephritis?

A

Proliferative: Excessive numbers of cells in the glomeruli - these include infiltrating leucocytes

Non-proliferative: Glomeruli look normal or have areas of scarring. They have normal numbers of cells

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19
Q

What is the definition of glomerulonephritis that is, diffuse, focal, global and segmental?

A
  • Diffuse: >50% of glomeruli affected
  • Focal: <50% of glomeruli affected
  • Global: all the glomerulus affected
  • Segmental: part of the glomerulus affected
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20
Q

Which glomerulonephritis syndrome causes urinary sediment abnormalitites and proteinuria?

A

IgA nephropathy

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21
Q

What types of glomerulonephritis cause nephrotic syndrome?

A

Minimal change disease

Membranous nephropathy

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22
Q

What types of glomerulonephritis cause a nephritic state?

A
  • Anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis
  • Post-infection glomerlunephritis
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23
Q

Look

A
24
Q

What are the different types of proliferative glomerulonephritis?

A
  • Diffuse proliferative - post-infective nephritis
  • Focal proliferative - mesangial IgA disease
  • Focal necrotizing (crescentic) nephritis
  • Membrano-proliferative nephritis
25
Q

What are the features of post-streptococcal glomerulonephritis?

A

Follows 10 - 21 days after infection typically of throat or skin

  • Most commonly with Lancefield group A Streptococci.
  • Genetic predisposition: HLA-DR, -DP, -DP.
26
Q

What are the drugs sued to treat post-infective glomerulonephritis?

A
  • Antibiotics for infection, debatable.
  • Loop diuretics such as frusemide for oedema
  • Vasodilator drugs (e.g. amlodipine) for hypertension
27
Q

What is the most common cause of glomerulonephritis?

A

IgA nephropathy

28
Q

What is IgA nephropathy characterised by?

A

IgA deposition in the mesangium and mesangial proliferation

29
Q

Who is IgA most common in?

A

2nd and 3rd decade of life

Men more commonly affected

30
Q

What is the prognosis of IgA nephroapthy?

A

•Up to 40% of cases can progress to end stage kidney disease.

31
Q

What is the presentation of IgA nephropathy?

A
  • Microscopic haematuria.
  • Micoscopic haematuria + proteinuria
  • In rare cases - Nephrotic syndrome (it usually presents with nephritic syndrome)
  • IgA crescentic glomerulonephritis
32
Q

What are the causes of crescentic glomerulonephritis?

A

ANCA associated - anti neutrophil cytoplasmic antibody assocaited:

  1. Microscopic polyangitis
  2. Granulomatosis with polyangitis
  3. Eosinophilic granulomatosis with polyangitis
  • Anti-glomerular basement membrane (GBM) e.g. anti-GBM nephritis or Goodpasture’s syndrome
  • Others:
    1. IgA vasculitis.
    1. post-infection glomerulonephritis.
    1. SLE
33
Q

What percentage of crescentic glomerulonephritis is caused by anti-GBM?

A

10-20%

34
Q

What is the presentation of antiGBM glomerulonephritis and goodpastures syndrome?

A
  • Nephritis (anti-GBM glomerulonephritis)
  • Nephritis+ lung haemorrhage (Goodpasture’s syndrome).

Two peaks: 3rd decade of life and 6th/7th decade of life

35
Q

How is Anti-GBM disease diagnosed?

A

•Diagnosed by demonstrating anti-GBM antibodies in serum and kidney

36
Q

How is anti-GBM treated?

A

•Treatment: aggressive immunesuppression: steroid, plasma exchange, and cyclophosphamide.

37
Q

Give examples of the possible immunosuppression treatment for crescentic glomerulonephritis management

A
  • Corticosteroids
  • Plasma exchange
  • Cytotoxic e.g. Cyclophosphamide
  • B-cell therapy e.g. Rituximab
  • Complement inhibitors
38
Q

What is the prognosis for crescentic glomerulonephritis?

A

•Prognosis is good provided treatment is started early enough

39
Q

Summary for proliferative glomerulonephritides

A
  • Present with nephritic syndrome
  • Blood on dipstix – variable proteinuria
  • Can cause rapid decline in renal function leading to dialysis
  • Early diagnosis and appropriate treatment
40
Q

What are the examples of non-proliferative glomerulonephritis?

A
  • Minimal Change Disease
  • Focal and segmental glomerulonephritis
  • Membranous Nephropathy
41
Q

What are the general measures in managing nephrotic syndrome management?

Oedema?

Hypertansion?

Risk of thrombosis?

Risk of infection?

Dyslipidaemia?

A
  • Treat oedema: salt and fluid restriction and loop diuretics.
  • Hypertension: use Renin-Angiotensin-Aldosterone-blockade.
  • Reduce risk of thrombosis: Heparin or Warfarin.
  • Reduce risk of infection e.g. pneumococcal vaccine.

Treat dyslipidemia e.g. statins

•Specific therapy towards cause of the non-proliferative glomerulonephritis

42
Q

What is the commonest form of non-proliferative glomerulopathy in children?

A

Minimal change nephrotic syndrome

43
Q

What is the onset of minimal change nephrotic syndrome?

A

Sudden onset of oedema - days

44
Q

Describe proteinuria in minimal change nephrotic syndrome

A

•Complete loss of proteinuria with steroids

45
Q

What is relapse rate for minmal change?

A

•Two thirds of patients relapse

46
Q

What is the treatment of minimal change?

A
  • Prednisolone – 1mg/kg for up to 16 weeks.
  • Once remission achieved , slow taper over 6 months.
  • Initial relapse treated with further steroid course.
  • Subsequent relapses treated with
  • Cyclophosphamide
  • Cyclosporin
  • Tacrolimus
  • Mycophenolate mofetil
  • Rituximab
47
Q

What is the prognosis for minimal change glomerulopathy?

A
  • Despite relapsing behaviour, prognosis is favourable.
  • Risk of end stage kidney disease is low.

Steroids toxicity as multiple exposure

48
Q

What is the presentation of focal and segmental glomerulonephritis?

A

Not a single disease - a syndrome with multiple causes

Presents with nephrotic syndrome

49
Q

What are the distinctive patterns of focal and segmental glomerulonephritis?

A

•Pathology reveals focal and segmental sclerosis with distinctive patterns e.g.

tip lesion, collapsing, cellular, perihilar, and not otherwise specified

Can be either primary or secondary

50
Q

What is the treatment for focal and segmental glomerulosclerosis?

A

•General measures, as previously described.

Generally steroid resistant

•Trail of steroids, positive response , even partial remission, carries better prognosis.

Alternative options: cyclosporin, cyclophosphamide, and Rituximab

51
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy

Most of the cases occur in isolation (idiopathic)

52
Q

What are the serological markers for membranous nephropathy?

A
  • Anti-phospholipase A2 receptor (PLA2R) antibody positive in 70% of idiopathic cases
  • Thrombospondin type 1 domain containing 7A (THSD7A).
53
Q

What are the secondary causes of membranous nephropathy?

A

Malignancies

SLE

Rhematoid arthritis

Drugs: NSAIDs, Gold, Penicillamine

54
Q

What is the treatent for membranous nephropathy?

A
  • General measures for at least 6 months.
  • Immunesuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function.
  • Cyclophosphamide and steroids (alternate months) for 6 months.
  • Cyclosporine.
  • Rituximab.
  • Resolves spontaneously in a third.
  • Prognosis good in treated patients whose proteinuria resolves
  • About 25% are on dialysis at 10 years
  • Can recur in renal transplants
55
Q

Summary for non-proliferative glomerulonephritis

A
  • Present with nephrotic syndrome.
  • Renal biopsy is key investigation.
  • Identify cause, if possible.
  • General measures are important in all cases.
  • Specific treatment as appropriate.
56
Q
A

Renal (Year 2 GM) (28 decks)

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