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*Urinary System > Glomerular Disease (Clinical) > Flashcards

Glomerular Disease (Clinical) Flashcards

1
Q

4 features of glomerulonephritis? (HRHP)

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

Describe appearance of both microscopic and macroscopic haematuria

A

Macroscopic - tea/cola coloured or frank blood

Microscopic - blood not visible to naked eye; =>5 RBC per high power field

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3
Q

What is the basic difference between nephrotic and nephritic syndrome?

A

NEPHROTIC = loss of a lot of protein

NEPHRITIC = loss of a lot of blood

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4
Q

Which syndrome is more likely to involve haematuria?

A

Nephritic

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5
Q

Where can blood in haematuria come from?

A

Kidney

Ureter

Bladder

Prostate

Urethra

(anywhere in renal tract!)

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6
Q

In glomerulonephritis, persistent microscopic haematuria shows what on microscopy?

A

Dysmorphic ‘Mickey-mouse like’ RBCs

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7
Q

What are the 3 ways to classify proteinuria?

A
  • Glomerular or tubular (glomerular - from increased permeability of glomerular membrane; tubular - from reduced tubular function)
  • Albuminuria or proteinuria (both describe abnormal protein excretion in urine - one more focused on albumin)
  • Persistent or transient
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8
Q

Is protienuria more a nephrotic or nephritic syndrome?

A

They are equal (use urine dipstick to see what side its likely to be on)

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9
Q

What are the 2 ways to diagnose proteinuria?

A

Urine protein creatinine ratio

24 hr urine collection

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10
Q

In glomerulonephritis, what is the nature of proteinuria?

A

Persistent proteinuria of more than 1 gram/mmol of creatinine

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11
Q

What is the definition of hypertension?

A

>140/80mmHg

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12
Q

Is hypertension more a nephritic or nephrotic syndrome symptom?

A

Nephritic

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13
Q

Hypertension is usually found in renal insufficiency, how is RI diagnosed and what are the ways to classify it?

A

Rising creatinine !

  • Nephritic > nephrotic
  • Mild or severe
  • Slow or rapid deterioration
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14
Q

3 fetaures of nephritic state

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

4 features of nephrotic syndrome

A
  • Oedema
  • Proteinuria > 3.5g/day
  • Hypoalbuminaemia
  • Hyperlipidaemia
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16
Q

What 2 things can nephrotic syndrome be caused by?

A

Primary (idiopathic) glomerular disease - only glomerulus

Secondary glomerular disease - other parts of body e.g. lupus, SLE

(diabetes is most common cause)

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17
Q

2 differential diagnoses for nephrotic syndrome? How to differentiate them?

A
  • Congestive Heart Failure (JVP raised, normal albumin, minimal proteinuria)
  • Hepatic disease (abnotmal LFTs, no proteinuria)
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18
Q

3 ways to classify glomerulonephritis?

A
  • Aetiology*: autoimmune, infection, malignancy, drugs, others
  • Primary v secondary* i.e. kideny alone or part of multisystem disease
  • Morphological*
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19
Q

Define proliferative vs non-proliferative glomerulonephritis

A

Proliferative = excessive numbers of cells in glomeruli; these include infiltrating leukocytes

Non-proliferative = glomeruli look normal or have areas of scarring; they have normal numbers of cells

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20
Q

How is diffuse glomerulonephritis defined?

A

>50% of glomeruli affected

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21
Q

How is focal glomerulonephritis defined?

A

<50% of glomeruli affected

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22
Q

How is global glomerulonephritis defined?

A

All of glomerulus affected

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23
Q

How is segmental glomerulonephritis defined?

A

Part of glomerulus affected

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24
Q

What glomerulonephritis syndrome causes urinary sediment abnormalities and proteinuria?

A

IgA nephropathy

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25
Q

What types of glomerulonephritis are associated with nephrotic syndrome?

A

Minimal change disease

Membranous nephropathy

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26
Q

What types of glomerulonephritis are associated with nephritic state?

A

Anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis

Post-infection glomerulonephritis

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27
Q

Say whether it is associated with nephrotic syndrome or nephritic syndrome, and to what extent: minimal change disease, membranous nephropathy, FSGS, mesangioproliferative GN, membranoprolferative GN, diffuse proliferative GN, crescentic GN

A

Top 3 - non-proliferative; more protein

Bottom 3 - proliferative; more blood

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28
Q

What are the 4 types of proliferative glomerulonephritides?

A
  • Diffuse proliferative - post-infective nephritis
  • Focal proliferative - mesangial IgA disease
  • Focal necrotizing (crescentic) nephritis - most advanced; aggressive injury
  • Membrano-proliferative nephritis
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29
Q

What is the hallmark of post-infective glomerulonephritis on electron microscopy?

A

‘sub-endothelial hump’

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30
Q

What does post-strep GN usually follow?

A

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

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31
Q

What type of bacteria is associated with post-strep GN? Is there another component to it?

A

Most commonly Lancefield group A Streptococci

Genetic predisposition: HLA-DR, -DP

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32
Q

Case 1: 6 yr old boy generally unwell, dark urine, puffy face, no rashes, no oedema, BP 135/86mmHg, sore throat 2 weeks prev; what is presumptive diagnosis?

A

Post-streptococcal nephritis

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33
Q

Case 1: what would be relevant investigations? What might the results be?

A

Hb 130g/L; WCC 11.3 x 109

Urea 11.2mmol/L, creatinine 160umol/L (high for a 6 yr old)

Urine microscopy RBC+++, casts +

Complement: low C3

These combined with hypertension indicate NEPHRITIC

34
Q

What is a urinary cast?

A

microscopic cylindrical structure produced by kidney and present in the urine in certain disease states; form in the distal tubule and collecting ducts then dislodge and pass into the urine

made up of white blood cells, red blood cells, kidney cells, or substances such as protein or fat - content of a cast can help tell you decide whether your kidney is healthy or abnormal

35
Q

Treatment for post-infective glomerulonephritis?

A

Abx debatable !
Loop diuretic such as frusemide for oedema

Vasodilator drugs e.g. amlodipine for hypertension

36
Q

What is the commonest cause of glomerulonephritis worldwide?

A

IgA nephropathy

37
Q

What is IgA nephropathy characterised by?

A

IgA deposition in mesangium and mesangial proliferation

38
Q

What demographic is IgA nephropathy most common in?

A

2nd and 3rd decade of life; males more commonly affected

39
Q

What is the prognosis for IgA nephropathy?

A

Up to 40% can progress to end stage kidney disease

(slow disease - progresses over decades)

40
Q

4 possible features of an IgA nephropathy presentation?

A
  • Microscopic haematuria*
  • Micrscopic hamaturia + proteinuria*
  • Nephrotic syndrome* (probability of end stage KD increased)
  • IgA crescentic glomerulonephritis*
41
Q

Histology of segmental necrosis - intense glomerulus inflammation (from intense inflammation of capillaries leading to rupture)

A
42
Q

Histology of crescent formation; glomerulus is circled

A
43
Q

3 broad causes of crescentic glomerulonephritis?

A
  • Auto-neutrophil cytoplasmic antibody (ANCA)-associated
  • Anti-glomerular basement membrane (GBM) (10-20%)
  • Others e.g. IgA vasculitis; post-infection glomerulonephritis; SLE
44
Q

Give the types of ANCA-associated causes for crescentic glomerulonephritis (3) (hint - all … with polyangitis

A
  1. Microscopic polyangitis
  2. Granulomatosis with polyangitis
  3. Eosinophilic granulomatosis with polyangitis

(aggressive, v sick people, hypekalaemia, v high creatinine)

45
Q

Give an example of an anti-GBM-associated cause of crescentic glomerulonephritis

A

Anti-GBM nephritis (Goodpastures syndrome)

46
Q

Case 3: 60 yr old woman 3 month histoy of increasing tiredness, anorexia, weight loss

Physical exam - rash on both ankles + lower legs and bilateral basal crepitations; BP 150/85

Urine dipstix: protein +++ and blood ++

Serum creatinine 640umol/L

ANCA positive w MPO-ANCA of 134 units/L

What might you want to do next?

A

Renal biopsy

47
Q

What might the renal biopsy from case 3 show? What is the treatment?

A

Focal necrotizing glomerulonephritis

Treatment = high does steroids, cyclophosphamide, plasma exchange

48
Q

What is Anti-GBM?

A

Rare disease caused by circulating anti-GBM (autoantibodies which are targeted to the basement membrane, which is part of the wall of these capillary blood vessels in the kidneys and lungs; commonly affects kidneys +/- lungs)

49
Q

What 2 things can anti-GBM present as?

A
  • Nephritis (anti-GBM glomerulonephritis)
  • Nephritis + lung haemorrhage (Goodpasture’s syndrome)
50
Q
A
51
Q

What are the 2 peaks in age that people develop anti-GBM disease?

A

3rd decade

6th/7th decade

52
Q

How is anti-GBM diagnosis confirmed?

A

By demonstrating anti-GBM antibodies in serum and kidney

53
Q

Treatment for anti-GBM disease?

A

Aggressive immunosuppression: steriod, plasma exchange and cyclophosphamide

54
Q

General management of crescentic glomerulonephritis is immunosuppression and prognosis is good provided treatment is started early enough, what is used in the immunosuppressive treatment (5)?

A
    • Corticosteroids*
    • Plasma exchange*
    • Cytotoxic e.g. cyclophosphamide*
    • B-cell e.g. rituximab*
    • Complement inhibitors*
55
Q

Summary - proliferative glomerulonephritides - 4 points:

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
56
Q

3 broad types of non-proliferative glomerulonephritis?

A
  • Minimal change disease
  • Focal and segmental glomerulonephritis
  • Membranous nephropathy
57
Q

Name 5 general measures for management of nephrotic syndrome

A

Treat oedema (salt + fluid restriction and loop diuretics)

Hypertension (RAAS-blockade)

Reduce thrombosis risk (heparin or warfarin)

Reduce infection risk (e.g. pneumococcal vaccine)

Treat dyslipidemia (e.g. statins)

58
Q

In addition to the general measures for nephrotic syndrome; give another therapy that should be involved

A

Specific therapy towards cause of the non-proliferative glomerulonephritis

59
Q

Commonest form of nephrotic syndrome in children?

A

Minimal Change Nephrotic Syndrome

60
Q

Descibe onset of minimal change nephrotic syndrome?

A

Sudden onset of oedema - days

61
Q

What fraction of MCNS patients relapse?

A

2/3rds

62
Q

Treatment for minimal change disease (and first relapse)?

A
  • PREDNISOLONE - 1mg/kg for up to 16 weeks
  • Once remission acheieved - slow taper over 6 months
  • Initial relapse treated with further steroid course
63
Q

Following initial relapse, what are subsequent relapses treated with in minimal change disease?

A
  • Cyclophosphamide (immunosuppression)
  • Cyclosporin (immunosuppression)
  • Tacrolimus (T-cell specific calcineurin inhibitor - similar immunosuppressive actions with cyclosporine)
  • Mycophenolate mofetil (inhibits T- and B-cells - immunosuppression)
  • Rituximab (monoclonal antibody - immunosuppression)
64
Q

Prognosis for minimal change disease?

A

Despite relapse behaviour - prognosis now favourable

Risk of end stage KD now low

Steroids toxicity from multiple exposure

65
Q

Case 4 - 22 yr old woman; severe oedema suddenly developed over a week

Breathless + LS chest pain

Urine dip ++++ protein

A

Urine protein creatinine ration 400mg/mmol

Creatinine 110mmol/l (<110)

Serum albumin 15g/L (>35)

Haemoglobin 154 g/L

Cholesterol 9.2 mmol/L

Pregnancy test negative

66
Q

General measures for case 4?

A

Salt and fluid restrictions

Daily weights

Loop diuretic e.g. furosemide

Thromboprophylaxis e.g. low molecular weight heparin

67
Q

As case 4 progresses what is treatment?

A

Predisnolone 60mg per day

(remission after 8 wks; diuretics + thromboprophylaxis stopped; predisnolone dose tapered over 6 months)

68
Q

Is focal and segmental glomerulonephritis a single disease?

A

NO, rather a syndrome with multiple causes (can be primary (idiopathic) or secondary)

69
Q

What does focal and segmental glomerulonephritis present with?

A

Nephrotic syndrome

70
Q

What is the chance of focal and segmental GN progressing to end stage KD?

A

High

71
Q

Histology of focal/segmental GN - podocytes are dying, as they die chance of recovery is less and less

A
72
Q

Treatment for focal/segmental glomerulosclerosis?

A

General measures (prev described)

Trial of steroids - +ve response, even partial remission, carries better prognosis

Alternatively - immunosuppression e.g. cyclosporin, cyclophosphamide, Rituximab

73
Q

Commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy

74
Q

Majority of cases of membranous nephropathy occur in what?

A

Isolation (idiopathic)

75
Q

2 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)
76
Q

Name 4 secondary causes of membranous nephropathy

A
  • Malignancies
  • SLE
  • Rheumatoid arthritis
  • Drugs: NSAIDs, gol, penicillamine
77
Q

Histology of membranous nephropathy

A
78
Q

Treatment for membranous nephropathy? In what circumstances woud immunosuppression be implemented?

A
  • General measures for at least 6 months
  • Immunosuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function

Cyclophosphamide and steroids (alternate months) for 6 months; Cyclosporine; Rituximab

  • 1/3rd resolve spontaneously
79
Q

Prognosis for membranous nephropathy?

A

Good in treated patients whose proteinuria resolves

About 25% on dialysis at 10 yrs

Can recur in renal transplants

80
Q

Case history 6:

  • 66 year old man presented with cough,breathlessness, and peripheral oedema.
  • He smokes 20 cpd.
  • Urine dip: Proteinuria ++++
  • Urine protein creatinine ration 580mg/mmol.
  • Serum albumin 20 g/L.
  • Serum creatinine 135mmol/l
  • Renal biopsy: confirms membranous nephropathy.
A
  • CT chest/abdomen/pelvis: suggestive of lung cancer.
  • Bronchoscopy and biopsy confirm squamous cell carcinoma.
  • General measures for nephrotic syndrome.
  • No immunesuppression.
  • Partial remission following radiotherapy
81
Q

Summary for non-proliferative glomerulonephritis - 5 points:

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
82
Q

Summary:

A
  • Glomerulonephritis is an important cause of end stage renal disease
  • Different types of glomerulonephritis present in different ways and differ in prognosis
  • Precise diagnosis depends on renal biopsy and the results influence management

*Urinary System (26 decks)

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