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URINARY > Glomerular Disease (clinical) > Flashcards

Glomerular Disease (clinical) Flashcards

1
Q

in basic terms what is glomerular disease

A

Inflammatory disorders of the kidney.

Responsible for almost 30% of end-stage kidney disease.

Classified based on morphology.

Majority are attributed to autoimmune aetiologies

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2
Q

what are features of glomerulonephritis

A

haematuria
proteinuria
hypertension
renal insufficiency

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3
Q

what are the two types of haematuria and how are they classified

A

macroscopic - tea or cola coloured ruin or frank blood

microscopic - >5 RBC per high power field

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4
Q

what is the difference between nephrotic and nephritic syndromes

A

nephrotic

  • disease of the kidneys
  • loss of protein

nephritic

  • disease of the glomeruli
  • loss of protein AND whole RBC
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5
Q

how is haematuria seen in glomerulonephritis

A

persistent microscopic haematuria

miroscopy shows dysmorphic RBC (mickey mouse like)

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6
Q

what are the aspects of haematuria

A

Macroscopic or Microscopic,

Transient or persistent

Nephritic>nephrotic

Source: kidney, ureter, bladder, prostate, urethra

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7
Q

how is proteinuria seen in glomerulonephritis

A

persistent, proteinuria of more than 1 gram /mmol creatinine

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8
Q

what are the aspects of hypertension

A

> 140/80 mmHg

Nephritis > nephrotic

Renal insufficiency i.e. rising creatinine

  • Nephritic > nephrotic
  • Mild or severe
  • Slow or rapid deterioration
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9
Q

what comprises the nephritic state

A

Active urine sediment: haematuria, dysmorphic RBCs, cellular casts

Hypertension

Renal impairment

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10
Q

what comprises 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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11
Q

how would you make a differential diagnosis of nephrotic syndrome

A

Congestive Heart Failure (JVP raised, normal albumin, minimal proteinuria)

Hepatic Disease (abnormal LFTs, no proteinuria)

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12
Q

what three ways is glomerulonephritis classified

A
  1. Aetiology: autoimmune, infection, malignancy, drugs, others
  2. Primary versus secondary i.e. kidney alone or part of multisystem disease.
  3. Morphological
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13
Q

what are the 2 types of glomerulonephritis

A

proliferative and non-proliferative

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14
Q

what happens in proliferative glomerulonephritis

A

Excessive numbers of cells in glomeruli - these include infiltrating leucocytes

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15
Q

what happens in non-proliferative glomerulonephritis

A

Glomeruli look normal or have areas of scarring - they have normal numbers of cells

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16
Q

what does diffuse indicate in terms of the disease

A

Diffuse: >50% of glomeruli affected

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17
Q

what does focal indicate in terms of the disease

A

Focal: <50% of glomeruli affected

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18
Q

what does global indicate in terms of the disease

A

Global: all the glomerulus affected

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19
Q

what does segmental indicate in terms of the disease

A

Segmental: part of the glomerulus affected

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20
Q

what would be seen in IgA nephropathy

A

urinary sediment abnormalities

proteinuria

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21
Q

what would be seen in nephrotic syndrome

A

membraneous nephropathy - minimal change disease

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22
Q

what would be seen in a nephritic state

A

Anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis

Post-infection glomerulonephritis

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23
Q

what are the 4 types of proliferative glomerulonephritides

A
  1. diffuse proliferative - post infective
  2. focal proliferative - mesangial IgA disease
  3. focal necrotizing (cresentic) nephritis
  4. membrano-proliferati e
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24
Q

what happens in post-streptococcal glomerulonephritis

A

follows 10-21 days after infection typically of the throat or skin

most commonly Lancefield group A streptococci

genetic predisposition - HLA-DR, -DP

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25
Q

CASE 1: Six year old boy brought to GP generally unwell, dark urine

Puffy face, no rashes no oedema, BP 135/86mmHg

Had had a sore throat 2 weeks previously

What is the presumptive diagnosis

A

post-streptococcal nephritis

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26
Q

CASE 1: what investigations should be taken

A

Blood counts
urins sample

Hb 130g/L; WCC 11.3 x 109
Urea 11.2mmol/L, creatinine 160mmol/L
Urine microscopy RBC +++, casts +
Complement: low C3

27
Q

CASE 1: what treatments should he be given

A

Antibiotics for infection, debatable.

Loop diuretics such as frusemide for oedema

Vasodilator drugs (e.g. amlodipine) for hypertension

28
Q

what is the most common cause of glomerulonephritis world-wide

A

IgA nephropathy

  • most common in 2nd and 3rd decade of life
  • males more commonly affected
29
Q

how is IgA nephropathy characterised

A

by IgA deposition in the mesangium as well as mesangial proliferation

30
Q

how does IgA nephropathy present

A

Microscopic haematuria.

Microscopic haematuria + proteinuria

Nephrotic syndrome

IgA crescentic glomerulonephritis

31
Q

CASE 2: 30 male referred to the renal clinic by GP for incidental microscopic haematuria.

BP 150/90 mmHg.

Creatinine 80 µmol/L.

Urine dip: RBC+++, Protein ++.

Renal US: normal kidney size with no structural abnormalities

what is your differential diagnosis

A

IgA nephropathy

32
Q

CASE 2: what treatment could this man be started on straight away

A

ACE-I and antihypertensives for better BP control

33
Q

CASE 2: what investigation could be done to confirm the diagnosis of IgA nephropathy

A

renal biopsy

34
Q

CASE 2: what could you expect this man to need 10 years down the line

A

kidney transplant

35
Q

CASE 3: how could focal necrotising glomerulonephritis present clinically

A

increasing tiredness, anorexia, weight loss, rash on ankles and lower legs, bilateral basal crepitations

BP 150/85

36
Q

CASE 3: what would her urine dipstick show and what could her serum creatinine be

A

protein +++
blood ++
creatinine 640 micromol/L

37
Q

CASE 3: renal biopsy shows focal necrotising glomerulonephritis - what would the treatment be

A

High dose steroids, Cyclophosphamide,

plasma exchange

38
Q

what are the three types of crescentic glomerulonephritis

A
  1. anti-neutrophil cytoplasmic antibody (ANCA)-associated
  2. anti-glomerular basement membrane (anti-GBM) eg goodpastures syndrome
  3. others - IgA vasculitis, post-infectiom GN, SLE (lupus nephritis)
39
Q

what is anti-GBM disease and how is it diagnosed

A

rare disease caused by circulating anti-GBM

diagnosed by demonstrating anti-GBM antibodies in serum and kidney

40
Q

how does anti-GBM disease present

A

presents as nephritis
= anti-GBM glomerulonephritis

presents as nephritis AND lung haemorrhage
= goodpastures syndrome

41
Q

when does presentation of anti-GBM disease peak

A

Two peaks: 3rd decade and 6th/7th decade.

42
Q

what is the treatment for anti-GBM disease

A

aggressive immunesuppression
steroid,
plasma exchange, cyclophosphamide

43
Q

what is the general management plan for crescentic glomerulonephritis

A 
IMMUNOSUPPRESSION 
Corticosteroids
Plasma exchange
Cytotoxic e.g. Cyclophosphamide
B-cell therapy e.g. Rituximab
Complement inhibitors
44
Q

PROLIFERATIVE GN SUMMARY:
how does it present

what would a dipstick show

what can rapid decline lead to

A

nephritic syndrome

blood, variable proteinuria

rapid loss of renal function and dialysis

45
Q

what are the three types of non-proliferative GN

A

minimal change disease

focal and segmental GN

membranous nephropathy

46
Q

what is the management of nephrotic syndrome

A

GENERAL
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
specific therapy towards cause of non-proliferative GN

47
Q

how does minimal change nephrotic syndrome present

A

commonest in children

sudden onset fo oedema (days)

complete loss of proteinuria with steroids

48
Q

what is the treatment for minimal change disease

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
49
Q

what is the prognosis for minimal change disease

A

Despite relapsing behaviour, prognosis is favourable.

Risk of end stage kidney disease is low.

BUT risk of steroids toxicity as multiple exposure

50
Q

CASE 4: 22 year old woman presented with severe oedema which had developed suddenly over a week.

she was breathless and had left sided chest pain

urine dip ++++ protein

what is your differential diagnosis

A

minimal change disease (non-proliferative GN)

51
Q

CASE 4: what investigations would you want to do

A 
Urine protein creatinine ration 
Creatinine
Serum Albumin
Haemoglobin
Cholesterol
Pregnancy test
52
Q

CASE 4: investigation results-

Urine protein creatinine ration 400mg/mmol.

Creatinine 110 mmol/l (<110)

Serum Albumin 15 g/L (>35)

Haemoglobin 154 g/L

Cholesterol 9.2 mmol/l

Pregnancy test negative

what are general measures you may want to take

A

Salt and fluid restrictions.
Daily weights.
Loop diuretic e.g. Furosemide.
Thromboprophylaxis e.g. low molecular weight heparin.

53
Q

CASE 4: what is a typical treatment plan

A

Prednisolone 60 mg per day

Achieved remission after 8 weeks of treatment.

Diuretics and thromboprophylaxis stopped.

Prednisolone dose tapered over 6 months.

54
Q

what is the pathology of focal and segmental GLomerulosclerosis

A

focal and segmental sclerosis with distinctive patterns e.g.
tip lesion, collapsing, cellular, perihilar, and not otherwise specified

55
Q

how does focal and segmental GS present

A

nephrotic syndrome - not a single disease but a syndrome with multiple causes

can be primary (idiopathic) or secondary

56
Q

how does FSGS respond to steroids

A

steroid resistant

57
Q

what is the treatment for FSGS

A

General measures, as previously described.

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

**Alternative options: cyclosporin, cyclophosphamide
Rituximab

58
Q

CASE 5: 34 year old man presented with severe oedema which developed over 3 weeks

Investigations - severe nephrotic syndrome

what might a renal biopsy show

A

focal and segmental glomerulo sclerosis

59
Q

what is the commonest case of nephrotic syndrome in adults

A

membranous nephropathy

60
Q

what are serological markers of membranous nephropathy

A

Anti-phospholipase A2 receptor (PLA2R) antibody positive in 70% of idiopathic cases

Thrombospondin type 1 domain containing 7A (THSD7A).

61
Q

most cases of membranous nephropathy are idiopathic - what are some secondary causes

A

Malignancies

SLE

Rheumatoid arthritis.

Drugs: NSAIDs, gold, penicillamine

62
Q

what is the treatment 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.

63
Q

what is the prognosis for membraneous nephropathy

A

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

64
Q

NON-PROLIFERATIVE GN SUMMARY:

how does it present

what is the key investigation

what are the broad treatment guidelines

A

nephrotic syndrom

renal biopsy

general measures important in all cases - then specific treatment as appropriate

URINARY (27 decks)

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