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Stage 2: Inflammation > Glomerular Disease > Flashcards

Glomerular Disease Flashcards

1
Q

What does glomerular inflammation lead to?

A

Blood and protein in the urine (normally should leave protein and blood in glomerular capillaries)

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2
Q

How can complement affect glomerular pathology?

A

Complement consumption can affect glomerular pathology

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3
Q

Describe the effects of immune complexes

A
  • Promote activation and deposition of complement, opsonisation and phagocytosis
  • They can either circulate and cause problems in organs in which they are deposited or form in situ
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4
Q

Which diseases have immune complex deposition as a key feature?

A

SLE an cryoglobulinaemia (autoimmune diseases)

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5
Q

What is glomerulonephritis?

A
  • Glomerular inflammation generally cause by immunological injury to the glomeruli
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6
Q

What is primary glomerulonephritis?

A

Antibody targeted to a specific part of the glomerulus e.g. membranous

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7
Q

What is secondary glomerulonephritis?

A

Glomerulonephritis as part of a generalised disease e.g. SLE

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8
Q

Describe the pathogenic mechanism of glomerulonephritis

A
  • Deposition of circulating or in situ formation of immune complexes
  • OR deposition of antiglomerular basement membrane antibodies
  • These mechanisms activate secondary mechanisms that lead to the glomerular image and inflammation
  • Pattern of injury and clinical presentation will depend on the ‘target’ of the immune response
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9
Q

What are different ways that glomerular disease can present?

A

1) (Incidental) hypertension
2) Incidental finding of microscopic haematuria
3) Incidental finding of proteinuria
4) Nephrotic syndrome
5) Progressive renal impairment
6) AKI

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10
Q

What questions would you ask in the history to find out about glomerular disease?

A

1) Any history of diabetes, lupus, other systemic illness, hormonal, structural causes e.g. congenital deformities e.g. aortal co-optation esp. in young patients
2) Any rashes or joint pains?
3) Drug history- recent changes, some can be associated with onset of nephrotic syndrome
4) Systemic symptoms? e.g. fever, haemoptysis
5) Recent angiography?

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11
Q

What might you see on examination of someone with suspected glomerular disease?

A
  • Renal bruits

- Rashes or evidence of active joint inflammation

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12
Q

What investigations might you do in someone with suspected glomerular disease?

A

1) Bloods - U&E, FBC, CRP, albumin, bone profile, LFT, blood culture
2) C3/C4 complement levels - might be low in SLE
3) Myeloma screen -immunoglobulins, protein electrophoresis (blood and urine) and urine Bence-Jones proteins
4) Virology - Hep B/C and HIV associated with nephrotic syndrome
5) RF
6) ANA, dsDNA, ANCA, anti-GBM
7) Urine dipstick
8) Urine PCR or 24h urine collection for protein
9) Cholesterol - tends to be high in nephrotic syndrome
10) Consider cryoglobulins (if have vasculitic rash)

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13
Q

What imaging would you do in someone with suspected glomerular disease?

A
  • Renal ultrasound esp. if confirmed blood, urine or renal symptoms
  • Patients with nephrotic syndrome often have AKI and risk of renal vein thrombosis so check for this on US early
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14
Q

What are other causes of secondary hypertension other than glomerular disease that should be considered?

A
  • Endocrine causes
  • Renal artery stenosis
  • Hypertension itself can cause blood in urine and glomerular pathology
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15
Q

What are non-glomerular causes of microscopic haematuria esp. in older men and women?

A

1) Bladder tumours
2) Renal stones
3) Renal tumours
4) BPH
5) UTI
6) Renal injury

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16
Q

What are primary glomerular causes of microscopic haematuria (glomerular inflammation making it leaky)?

A

1) IgA nephropathy
2) Alports - genetic abnormalities of collagen, X linked but does occur in females, associated with deafness, FH
3) Thin BM disease
4) Post infectious glomerulonephritis
5) Membranoproliferative glomerulonephritis

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17
Q

What investigation results would indicate membranoproliferative glomerulonephritis?

A
  • Low complement levels

- Maybe RF positive

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18
Q

What are secondary glomerular causes of microscopic haematuria?

A

1) Henoch Scorlein Purpura
2) SLE
3) HUS (more acute presentation)
4) ANCA associated vasculitis
5) Sickle nephropathy

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19
Q

What is ANCA associated vasculitis usually associated with?

A

Decline in renal function

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20
Q

What is the cause of IgA nephropathy?

A
  • Glomerular deposition of IgA causing inflammation within glomeruli
  • In situ IgA being deposited bc of antigens in the kidneys
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21
Q

What is the (variable) clinical presentation of IgA nephropathy?

A

1) Microscopic haematuria
2) Hypertension
3) Slowly progressive renal impairment, progressive renal scarring - CKD/ESRF
4) Rapidly progressive renal impairment (crescentic IgA)
5) Nephrotic range proteinuria - can cause nephrotic syndrome

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22
Q

What investigation results would show IgA nephropathy?

A

1) Raised serum IgA

2) Renal biopsy - mesangial proliferation with IgA deposition

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23
Q

How would you manage IgA nephropathy?

A
  • Control of BP to prevent further scarring
  • Immunosuppression may be beneficial in some cases e.g. steroids with rapidly progressive renal impairment and nephrotic range proteinuria
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24
Q

Describe the features of Henoch Schonlein Purpura (systemic IgA)

A
  • Inflammation of the small blood vessels esp. in kidney, skin and gut
  • Depositions of IgA in kidney in similar pattern to IgA nephropathy
  • Depositions of IgA in skin leading to skin lesions
  • Most common in young children were can get transient illness
  • Associated with leucocytoclastic vasculitis rash
  • Variable prognosis - some fully recover with resolution of the rash and renal findings, others progress ESRD
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25
Q

What disease should you think of in a young patient with oedema?

A

Nephrotic syndrome (CV disease unlikely)

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26
Q

What investigation results would you have in nephritic syndrome?

A
  • Urine dipstick - 3+ protein ± haematuria
  • Often preserved renal function with low albumin
  • High cholesterol
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27
Q

What are the clinical features of nephrotic syndrome?

A

1) Heavy proteinuria > 3.5g per day
2) Hypoalbuminaemia (low serum albumin)
3) Oedema - children periorbital, adults peripheral
4) Hyperlipidaemia

28
Q

Why does oedema occur in nephrotic syndrome?

A

Because of the low oncotic pressure the vasculature holds onto fluid worse than normal

29
Q

What are primary causes of nephrotic syndrome?

A

1) Membranous nephropathy
2) Focal segmental glomerulosclerosis (FSGS)
3) MCGN
4) Minimal change disease - most common cause in children many are treated without having a biopsy with steroids

30
Q

What are secondary causes of nephrotic syndrome?

A

1) Diabetic nephropathy
2) SLE
3) Amyloidosis
4) Malignancy
5) Drugs

31
Q

What are causes of nephrotic syndrome in < 15 years?

A

1) Minimal change disease
2) FSGS
3) Mesangial proliferative glomerulonephritis

32
Q

What are causes of nephrotic syndrome in 15-40 years?

A

1) FSGS
2) Minimal change disease
3) Membranous nephropathy (incl. lupus), diabetic nephropathy
4) Pre-eclampsia
5) Post infectious GN

33
Q

What are causes of nephrotic syndrome in > 40 years?

A

1) FSGS
2) Membranous nephropathy
3) Diabetic nephropathy
4) Minimal change disease
5) IgA nephropathy
6) Primary amyloidosis
7) Post infectious GN

34
Q

Why does hyperlipidaemia occur in nephrotic syndrome?

A

Decrease in oncotic pressure stimulates hepatic lipoprotein synthesis resulting in a high cholesterol to maintain oncotic pressure

35
Q

What are potential complications of nephrotic syndrome?

A

1) Protein malnutrition
2) Hypovolaemia despite fluid overload - consider in patients presenting with AKI and nephrotic syndrome
3) AKI esp. in older patients with minimal change disease
4) VTE esp. DVT, PE, renal vein thrombosis esp. membranous with < 10g proteinuria per day, give prophylaxis at certain level
5) Infections - low IgG due to urinary loss?

36
Q

How do you manage nephrotic syndrome?

A

1) Diuretics
2) ACEi - protects kidney, reduces BP and proteinuria
3) Anticoagulation
4) Statin (depends how long remission will take)
5) Renal biopsy - in children MCD common so steroids given before biopsy

37
Q

What are the features of minimal change disease?

A
  • Sudden onset oedema esp. in children
  • Normal renal function (elderly may have AKI)
  • Risk of relapse (30%)
  • Foot process effacement of podocytes
  • Would do biopsy in adults
38
Q

What are causes of minimal change disease/diseases associated?

A

1) Majority idiopathic esp. children
2) Drugs e.g. NSAIDs, lithium, penicillamine, pamidronate, sulfazalizine, immunisations
3) Hodgkin’s lymphoma
4) Infections e.g. syphilis, TB, mycoplasma, Hep C
5) Allergy (30% of cases describe history of allergy) e.g. asthma, hay fever
6) SLE, T1D, adult polycystic kidney disease, HIV nephropathy

39
Q

Describe FSGS

A
  • FSGS is a lesion, not disease (pathological diagnosis not clinical)
  • Focal and segmental areas of mesangial collapse and sclerosis
  • 35% of cases of nephrotic syndrome in adults
  • There are a number of identified circulating factors and podocyte mutations associated with the development of FSGS
40
Q

How does FSGS present?

A

1) Idiopathic/primary FSGS - nephrotic syndrome
2) Secondary FSGS - non-nephrotic proteinuria, hypertension, microscopic haematuria and renal insufficiency (nephrotic syndrome less common)

41
Q

What are causes of secondary FSGS?

A

1) HIV infection (collapsing)
2) Reflux nephrology
3) Massive obesity
4) Scarring from previous insult e.g. IgA, vasculitis, lupus
5) Heroin
6) Steroid/steroid resistant?

42
Q

What are the features of membranous nephropathy?

A
  • Most common cause of primary nephrotic syndrome in adults
  • BM thickening, little or no cellular expansion
  • Electron dense deposits in glomerular BM (represent immune deposits)
  • Treatment = immunosuppression
43
Q

What are the causes of membranous nephropathy?

A

1) Idiopathic - antiPLA2 antibody associated
2) Secondary - Hep B, autoimmune diseases (SLE), thyroiditis, carcinomas (esp. elderly), gold, penicillamine, captopril, NSAIDs

44
Q

What are the features of mesangiocapillary glomerulonephritis (MCGN)?

A
  • Associated with immune complex deposition (immunoglobulins detected on histology)
  • e.g. chronic infections, autoimmune diseases, monoclonal gammopathies
  • Associated with complement dysregulation (often genetic)
45
Q

What are the features of cryoglobulinaemia?

A
  • Circulating immune complexes which precipitate out in the cold
  • Often MCGN on renal biopsy
  • Associated with rash (livedo reticularis) and Raynaud’s
  • Arthralgia and myalgia
46
Q

What are other causes of nephrotic syndrome?

A

1) Monoclonal gammopathies incl. myeloma/MGRS (always consider these as cause of renal disease)
2) Diabetes
3) SLE (membranous)
4) Post infectious glomerulonephritis

47
Q

What should you always consider with absolute anuria?

A

Obstruction (post-renal cause) e.g. large prostate (need to do fluid assessment)

48
Q

What might be causes of haemoptysis in the context of glomerular disease?

A
  • Pulmonary renal syndrome

- ANCA positive vasculitis

49
Q

What are the priorities if someone has low sats, high potassium and acidosis?

A

Treat the hyperkalaemia (and acidosis) and hypoxia

50
Q

What would a normal heart size but bilateral infiltrates suggest?

A

More than just fluid i.e. blood

51
Q

What is a key ECG feature of hyperkalaemia?

A

Broad QRS complex

52
Q

What are the differentials of someone with acute onset anuria, SoB, high K, haemoptysis for 24h, high RR, low sats, high creatinine and acidosis, pale (and other features)?

A

1) Pulmonary renal syndrome
2) Pneumonia with AKI
3) Endocarditis with pulmonary oedema (endocarditis causes antibodies on heart valve which break off and embolise around the body)
4) Any cause of AKI associated with pulmonary oedema due to fluid overload (pre, post, intrinsic renal)

53
Q

What are the features of ANCA positive vasculitis (granulomatosis with polyangiitis - GPA)?

A
  • Microscopic polyangiitis (MPA)
  • Rapidly progressive glomerulonephritis with crescent formation
  • ANCA = pathogenic anti neutrophil antibodies
  • Can cause similar changes on high microscopy to endocarditis but v different treatment
54
Q

What are the causes of pulmonary renal syndrome?

A

1) Anti GBM disease
2) ANCA vasculitis
3) Lupus with pulmonary haemorrhage

55
Q

What are the features of anti GBM disease (goodpasture’s syndrome- GPS)?

A
  • Autoantibodies to the glomerular BM causing a renal pulmonary glomerulonephritis with crescent formation
  • Associated with anti-GBM antibodies and alveolar basement membrane antibodies
  • Can cause absolute anuria with pulmonary haemorrhage (or only AKI/pulmonary haemorrhage) or ESRF
  • Only way to treat is to get rid of antibodies either with plasma exchange or immunosuppression
56
Q

What are causes of haematuria?

A

1) Malignancy
2) Renal stones
3) Prostatitis
4) Trauma
5) ‘Inflammation’ in the urinary tract incl. UTI, renal TB
6) Active inflammation in the glomerulus for any reason
7) Kidney infarction
8) Polycystic kidney disease
- Remember menstruation in women
- (beeturia)
- (rhabdomyolysis - myoglobin)

57
Q

What are causes of proteinuria?

A

1) Diabetes
2) Hypertension
3) Obesity
4) UTI
5) Glomerulonephritis
6) Polycystic kidney disease
7) Myeloma and amyloidosis
8) SLE
- (rarely urological tumour)

58
Q

What does urine specific gravity indicate?

A
  • If high incl. concentration fo solutes in urine e.g. glucose in diabetes or dehydration
  • If low can suggest glomerulonephritis or diabetes insipidus (but non specific)
59
Q

What should you do if proteinuria is positive?

A

Send urine for PCR or 24h collection for protein

60
Q

What might the observation of urine indicate?

A

1) Visible haematuria
2) Frothy - proteinuria
3) Cloudy - infection
4) Coca Cola colour suggested rhabdomyolysis (damaged skeletal muscle leading to release of myoglobin in urine)

61
Q

What are rheumatoid factors?

A

Antibodies (usually IgM) directed against the Fc position of IgG

62
Q

What does nephrotic mean?

A

Proteinuria

63
Q

What does nephritic mean?

A

Haematuria

64
Q

What are differentials of rash + renal impairment?

A

1) ANCA vasculitis
2) HSP (Henoch Schonlein Purpura)
3) Cryoglobulinaemia
4) Endocarditis
5) Lupus
6) Meningococcal sepsis
7) Drug reaction
8) Atheroembolic

65
Q

What are trash feet?

A
  • Cardiac disease
  • Angiogram causes cholesterol deposits to be released
  • These burst through to the skin causing discrete small rashes on feet and associated with eosinophilia and renal impairment as emboli can go to kidney as well

Stage 2: Inflammation (39 decks)

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