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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
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
post-streptococcal nephritis
26
CASE 1: what investigations should be taken
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
CASE 1: what treatments should he be given
Antibiotics for infection, debatable. Loop diuretics such as frusemide for oedema Vasodilator drugs (e.g. amlodipine) for hypertension
28
what is the most common cause of glomerulonephritis world-wide
IgA nephropathy - most common in 2nd and 3rd decade of life - males more commonly affected
29
how is IgA nephropathy characterised
by IgA deposition in the mesangium as well as mesangial proliferation
30
how does IgA nephropathy present
Microscopic haematuria. Microscopic haematuria + proteinuria Nephrotic syndrome IgA crescentic glomerulonephritis
31
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
IgA nephropathy
32
CASE 2: what treatment could this man be started on straight away
ACE-I and antihypertensives for better BP control
33
CASE 2: what investigation could be done to confirm the diagnosis of IgA nephropathy
renal biopsy
34
CASE 2: what could you expect this man to need 10 years down the line
kidney transplant
35
CASE 3: how could focal necrotising glomerulonephritis present clinically
increasing tiredness, anorexia, weight loss, rash on ankles and lower legs, bilateral basal crepitations BP 150/85
36
CASE 3: what would her urine dipstick show and what could her serum creatinine be
protein +++ blood ++ creatinine 640 micromol/L
37
CASE 3: renal biopsy shows focal necrotising glomerulonephritis - what would the treatment be
High dose steroids, Cyclophosphamide, | plasma exchange
38
what are the three types of crescentic glomerulonephritis
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
what is anti-GBM disease and how is it diagnosed
rare disease caused by circulating anti-GBM diagnosed by demonstrating anti-GBM antibodies in serum and kidney
40
how does anti-GBM disease present
presents as nephritis = anti-GBM glomerulonephritis presents as nephritis AND lung haemorrhage = goodpastures syndrome
41
when does presentation of anti-GBM disease peak
Two peaks: 3rd decade and 6th/7th decade.
42
what is the treatment for anti-GBM disease
aggressive immunesuppression steroid, plasma exchange, cyclophosphamide
43
what is the general management plan for crescentic glomerulonephritis
``` IMMUNOSUPPRESSION Corticosteroids Plasma exchange Cytotoxic e.g. Cyclophosphamide B-cell therapy e.g. Rituximab Complement inhibitors ```
44
PROLIFERATIVE GN SUMMARY: how does it present what would a dipstick show what can rapid decline lead to
nephritic syndrome blood, variable proteinuria rapid loss of renal function and dialysis
45
what are the three types of non-proliferative GN
minimal change disease focal and segmental GN membranous nephropathy
46
what is the management of nephrotic syndrome
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
how does minimal change nephrotic syndrome present
commonest in children sudden onset fo oedema (days) complete loss of proteinuria with steroids
48
what is the treatment for minimal change disease
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
what is the prognosis for minimal change disease
Despite relapsing behaviour, prognosis is favourable. Risk of end stage kidney disease is low. BUT risk of steroids toxicity as multiple exposure
50
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
minimal change disease (non-proliferative GN)
51
CASE 4: what investigations would you want to do
``` Urine protein creatinine ration Creatinine Serum Albumin Haemoglobin Cholesterol Pregnancy test ```
52
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
Salt and fluid restrictions. Daily weights. Loop diuretic e.g. Furosemide. Thromboprophylaxis e.g. low molecular weight heparin.
53
CASE 4: what is a typical treatment plan
Prednisolone 60 mg per day Achieved remission after 8 weeks of treatment. Diuretics and thromboprophylaxis stopped. Prednisolone dose tapered over 6 months.
54
what is the pathology of focal and segmental GLomerulosclerosis
focal and segmental sclerosis with distinctive patterns e.g. tip lesion, collapsing, cellular, perihilar, and not otherwise specified
55
how does focal and segmental GS present
nephrotic syndrome - not a single disease but a syndrome with multiple causes can be primary (idiopathic) or secondary
56
how does FSGS respond to steroids
steroid resistant
57
what is the treatment for FSGS
General measures, as previously described. Trial of steroids, positive response , even partial remission, carries better prognosis. **Alternative options: cyclosporin, cyclophosphamide Rituximab
58
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
focal and segmental glomerulo sclerosis
59
what is the commonest case of nephrotic syndrome in adults
membranous nephropathy
60
what are serological markers of membranous nephropathy
Anti-phospholipase A2 receptor (PLA2R) antibody positive in 70% of idiopathic cases Thrombospondin type 1 domain containing 7A (THSD7A).
61
most cases of membranous nephropathy are idiopathic - what are some secondary causes
Malignancies SLE Rheumatoid arthritis. Drugs: NSAIDs, gold, penicillamine
62
what is the treatment for membranous nephropathy
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
what is the prognosis for membraneous nephropathy
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
NON-PROLIFERATIVE GN SUMMARY: how does it present what is the key investigation what are the broad treatment guidelines
nephrotic syndrom renal biopsy general measures important in all cases - then specific treatment as appropriate

URINARY (27 decks)

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