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Block 34 - Metabolic > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Describe how nephrotic syndrome often presents.

A

As a triad/ tetrad or manifestations:

1) proteinuria (>3g/24 hours)
2) Hypoalbuminaemia
3) Oedema
4) Dyslipidaemia (specifically hypercholesterolaemia)

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2
Q

Give a basic description of the pathophysiology in nephrotic syndrome.

A

Inflammation and damage to the glomerulus, specifically to podocytes. Damaged podocytes = protein loss.

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3
Q

1) In nephrotic syndrome, why can there be an increased risk of infection.
2) What causes hypoalbuminaemia in nephrotic syndrome?
3) How can hypercholesterolaemia occur in nephrotic syndrome?

A

1) Because antibodies are proteins which can be lost in urine in nephrotic syndrome.
2) Loss of albumin from circulating blood.
3) Hypoalbuminaemia causes the liver to produce more proteins (albumin AND cholesterol).

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4
Q

How does oedema occur in nephrotic syndrome?

A

Hypoalbuminaemia > reduced plasma oncotic pressure > water and electrolytes move into interstitium (less proteins = increased osmotic gradient) > oedema.

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5
Q

In nephrotic syndrome, what causes decreased GFR?

A

Oedema > hypovolaemia > reduced venous return to the heart > less volume pumped to the body > decreased renal blood flow > decreased GFR.

** Inflammation already in the glomerulus contributes to decreased GFR.

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6
Q

What is the consequence of decreased GFR in nephrotic syndrome?

A

Decreased GFR > renin released > RAAS unregulated > salt and water retention > increased BP > further oedema due to hypoproteinaemia.

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7
Q

Give the 3 reasons as to why you would investigate nephrotic syndrome.

A

1) Assess severity.
2) To confirm the diagnosis
3) To differentiate between types and causes.

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8
Q

List the investigations you would carry out in suspected nephrotic syndrome.

A

1) Urine dipstick
2) Urinalysis with microscopy
3) Bloods
4) Nephritis screen and serological studies
5) Radiology (USS) and renal biopsy

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9
Q

In nephrotic syndrome why would you carry out a urine dipstick and urinalysis?

A

To look for protein, glucose, nitrites, leukocytes, BJPs and cellular casts.

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10
Q

In nephrotic syndrome, which blood tests would you order?

A

FBC, U&Es. LFTS, creatinine, urea, CRP, glucose, lipid profile, ESR.

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11
Q

What tests are involved in the nephritic screen and serological studies for nephrotic syndrome?

A

1) Autoimmune screen (ANA, dsDNA, ANCA, complement - C3/C4), anti-GBM antibodies).
2) Serum free light chains
3) Syphilis serology
4) Hep B, Hep C and HIV serology

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12
Q

In a patient with nephrotic syndrome, what types of changes might you see on the biopsy with:

1) light microscopy
2) immunofluorescence
3) electron microscopy

A

1) General changes
2) Antibody/ immune complex stains
3) Detailed changes to the glomerulus.

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13
Q

Describe steps for the general management of nephrotic syndrome.

A

1) Lifestyle advice
2) Treat the cause
3) Treat HTN and hypercholesterolaemia.
4) Fluid and salt restriction
5) Diuresis
6) ACEis/ ARBs
7) Prophylactic antigoaculation
8) Immunotherapy
9) Dialysis if severe

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14
Q

For each manifestation below, name the associated signs and symptoms:

1) Dyslipidaemia
2) Hypoalbuminaemia
3) Oedema
4) Proteinaemia

A

1) Xanthalasma and xanthomata
2) Tiredness, leukonychia striata, oedema.
3) Peripheral oedema, pulmonary oedema, pleural effusion (these may cause breathlessness).
4) Frothy urine.

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15
Q

Name 6 complications of nephrotic syndrome.

A

1) HTN
2) AKI
3) Infection
4) VTE
5) CKD
6) Hyperlipidaemia

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16
Q

1) In nephrotic syndrome, what are 2 mechanisms of the injury to podocytes?
2) What could happen in the damaged area of the glomerular capsule also includes the glomerular basement membrane>

A

1) Immune complex deposition or complement protein activation.
2) Blood can also leak into the filtrate.

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17
Q

Name the 4 primary causes of nephrotic syndrome.

A

1) Minimal change disease
2) Membranous glomerulonephritis
3) Focal segmental glomerulonephritis
4) Membranoproliferative glomerulonephritis

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18
Q

Name 6 causes of secondary nephrotic syndrome.

A

1) Diabetic nephropathy
2) SLE
3) Amyloidosis
4) Hep C/ Hep B/ HIV
5) Myeloma
6) Pregnancy

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19
Q

1) What is the most common cause of nephrotic syndrome in children?
2) What is the most commonnephrotic syndrome overall?
3) What is the most common cause of nephrotic syndrome in adults?

A

1) Minimal change disease
2) Diabetic nephropathy.
3) Focal segmental glomerulosclerosis

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20
Q

1) What percentage of adult nephrotic syndrome is caused by minimal change disease?
2) In minimal change disease, what changes are seen on:

a) light microscopy
b) immunofluorescence
c) electron microscopy

A

1) about 25%.
2a) minimal change seen (as per the name)
2b) occasional IgM immunoglobulins.
2c) effacement of podocytes and podocyte foot processes.

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21
Q

In membranous glomerulonephritis, what changes are seen on:

a) light microscopy
b) immunofluorescence
c) electron microscopy

A

a) mesangial expansion and capillary wall thickening
b) IgG and C3 proteins
c) GBM thickening due to sub epithelial deposits (‘spikes’ can be seen upon silver staining due to these deposits).

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22
Q

Describe the deposits that can be seen on electron microscopy of a renal biopsy in membranous glomerulonephritis.

A

In idiopathic disease, these deposits are made up of IgG4, but they are made up of other IgG deposits in secondary disease (due to malignancy infection, immunological disease or drugs).

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23
Q

What is the mechanism of damage in membranous glomerulonephritis?

A

Immune deposits damage the podocytes, allowing proteins to be filtered through.

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24
Q

What is present in 70-80% patients with idiopathic membranous glomerulonephritis?

A

Anti-phospholipase A2 receptor antibody.

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25
Q

Describe the basic treatment for membranous glomerulonephritis.

A

BP control
Immunosuppression in those at high risk of progression
Treatment of the underlying cause in secondary disease (here, it is possible for proteinuria to remit).

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26
Q

Describe the basic treatment for minimal change disease.

A 
Prednisolone initially (1mg/kg for 4-16 weeks)
Longer term immunosuppression (cyclophosphamide/ calcineurin inhibitors) for frequent relapses.
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27
Q

In focal segmental glomerulosclerosis, what changes are seen on:

a) light microscopy
b) immunofluorescence
c) electron microscopy

A

a) focal segmental sclerosis within the glomerulus
b) no abnormalities
c) GBM thickening

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28
Q

1) Why does FSGS result in decreased urine output?
2) Why does proteinuria occur in FSGS?
3) Name 3 secondary causes of FSGS.

A

1) Because of the decrease in filtration to parts of the glomerulus.
2) Because sclerosis can lead to damage in surrounding podocytes.
3) HIV, heroin use, lithium use, lymphoma or kidney scarring due to other GN.

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29
Q

Describe the basic treatment for FSGS.

A

BP control
Corticosteroids are 1st line in primary idiopathic disease
Calcineurin inhibitors are 2nd line in primary idiopathic disease
Plasma exchange/ Rituximab can be used for recurrence of FSGS in transplants

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30
Q

Where is membranoproliferative glomerulonephritis more common and why?

A

More common in low and middle income countries due to infection.

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31
Q

Name the 2 types of membranoproliferative glomerulonephritis and describe them.

A

1) Immune complex associated: driven by increased or abnormal immune complex deposition in the kidney and complement activation.
2) C3 glomerulonephropathy: due to a genetic or acquired defect in the alternate complement pathway.

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32
Q

1) What is seen upon renal biopsy in membranoproliferative glomerulonephritis?
2) What distinguishes immune-complex associated disease from C3 glomerulonephropathy?

A

1) A proliferative glomerulonephritis with electron dense deposits.
2) Immunoglobulin deposits seen in immune complex associated disease.

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33
Q

Describe the basic treatments for membranoproliferative glomerulonephritis.

A

BP control
Treat underlying cause in immune complex disease
Immunosuppression if no underlying cause found and there is a progressive decline in renal function.
There are currently no treatments to block or modify C3 activation

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34
Q

What is nephritic syndrome often caused by?

A

An immune response triggered by infection or other disease which causes inflammation in the glomerulus. Often, the capillary endothelium and basement membrane are damaged.

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35
Q

What can cause red blood cell casts to be present in urine in nephritic syndrome?

A

Inflammation can cause bleeding into the kidney tubules which can cause red blood cell casts to be present in the urine.

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36
Q

What causes a sterile pyuria in nephritic syndrome?

A

Due to glomerular inflammation, white blood cells are usually recruited to the area and can leak through capillaries, causing a sterile pyuria (WBCs present but no infection).

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37
Q

1) What can cause oliguria and a potential AKI in nephritis syndrome?
2) What is another sign of nephritic syndrome which is caused by decreased GFR?

A

1) Inflammation that occurs in the glomerulus reduces the GFR by reducing fluid moving through.
2) Azotemia (retention of urea) or hypertension due to up regulation of RAAS.

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38
Q

Name 8 possible signs of nephritis syndrome.

A 
Proteinuria (typically <3.5g/24 hours)
Haematuria
Azotemia
RBC casts (acanthocytes)
Oliguria
Antistreptolysin O titres
HTN
Sterile pyuria (presence of leukocytes but no infection).
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39
Q

Name 7 possible causes of Nephritic syndrome.

A

1) Rapidly progressive glomerulonephritis
2) Anti-GBM disease (Goodpastures disease)
3) ANCA associated GN
4) Immune complex GN
5) Membranoproliferative GN
6) Henoch-Schönlein Purpura
7) Alport syndrome

40
Q

1) Generally, what is nephrotic syndrome due to?

2) Generally, what is nephritic syndrome due to?

A

1) It is normally proteinuria due to podocyte pathology.
2) It is haematuria ± proteinuria due to inflammatory damage (if a GN process causes scarring, this is what leads to the addition of proteinuria to haematuria).

41
Q

1) What is the most serious form of glomerulonephritis?
2) Describe the damage caused by RPGN.
3) Name 3 diseases which cause RPGN.

A

1) RPGN.
2) Diffuse, proliferative and crescentic.
3) Anti-GBM disease, small vessel/ ANCA vasculitis and immune complex GN (such as SLE).

**IgA nephropathy and membranous GN can ‘transform’ to become more rapidly progressive.

42
Q

1) When does RPGN occur?

2) What is RPGN characterised by?

A

1) When any aggressive GN rapidly progresses to renal failure over days or weeks.
2) Loss of GFR >/= 50% with the presence of extensive glomeruli-crescents. It rapidly progresses to renal failure over days/ weeks.

43
Q

1) In RPGN what causes crescents to form in glomeruli?
2) In RPGN, rupturing of the glomerular capillary wall causes what 4 types of cells to accumulate within the Bowman’s space?
3) What does inflammation in the Bowman’s space then lead to?

A

1) Crescents are formed after the rupturing of the glomerular capillary wall.
2) Macrophages, fibroblasts, fibrin and epithelial cells.
3) Inflammation causes cytokine release, promoting proliferation of parietal cells, signifying severe injury.

44
Q

Describe the basic treatment for RPGN.

A

Corticosteroids and cyclophosphamide.

Further treatment depends on the aetiology.

45
Q

Describe the basic pathophysiology go anti-GBM disease (good pastures disease).

A

Auto-antibodies (anti-GBM antibodies) are produced to type IV collagen which is present in glomerular and alveolar basement membranes.

46
Q

How does anti-GBM disease often present?

A

As acute renal disease (oliguria/ anuria, haematuria, AKI, renal failure) with crescent formations as well as with lung diseases such as pulmonary haemorrhage (SOB and haemoptysis).

** A small proportion will have isolated lung presentations.

47
Q

In anti-GBM disease, what can be seen upon immunofluorescence of a renal biopsy?

A

Linear deposition of antibodies along the glomerular basement membrane.

48
Q

Describe the basic treatment for anti-GBM disease.

A

Plasma exchange to remove antibodies, corticosteroids and cyclophosphamide.

49
Q

1) What does ANCA stand for?
2) What does ANCA associated GN cause?
3) In ANCA associated GN, what can be seen upon immunofluorescence?

A

1) Anti-neutrophil cytoplasmic antibody.
2) Pauci-immune necrotising crescentic GN.
3) Few or not immune deposits (as per the pathological term ‘Pauci’ which is latin for meaning few or little).

50
Q

Which type of glomerulonephritis accounts for the majority of RPGN cases?

A

ANCA associated glomerulonephritis.

51
Q

Name 3 types of ANCA associated glomerulonephritis.

A

1) Granulomatosis with polyangitis (Wegener’s granulomatosis)
2) Eosinophilic granulomatosis with polyangitis (Churg-strauss syndrome)
3) Microscopic polyangitis

**They are all forms of renal vasculitis.

52
Q

1) What are ANCAs produced by and what do they target?

2) What are the two main types of ANCA?

A

1) Produced by plasma cells to target proteins with neutrophil granules and/or monocyte lysosomes.
2) Perinuclear ANCA (pANCA) and cytoplasmic ANCA (cANCA).

**atypical ANCA (X-ANCA also exists).

53
Q

What do the following anti-neutrophil cytoplasmic antibodies act against:

1) pANCA
2) cANCA

A

1) Target myeloperoxidase in proteins which activates neutrophilic granules.
2) Target neutrophil peroxidase/proteinase 3 which activates macrophage and monocyte lysosome functions as well as neutrophils.

54
Q

What is the overall result of the action of the ANCAs?

A

Activation of macrophages and neutrophils causes renal vasculitis.

55
Q

1) Which disease are pANCAs most commonly seen in?
2) Which disease are cANCAs most commonly seen in?
3) The presence of which type of ANCA is associated with ulcerative colitis in 80% of patients?

A

1) Microscopic polyangitis.
2) Granulomatosis with polyangitis.
3) atypical ANCAs (X-ANCA). **Can also be associated with Crohn’s disease but only in 20% patients.

56
Q

Name 5 clinical presentations of ANCA associated GN.

A

1) Malaise
2) Myalgia
3) Arthralgia
4) Flu-like symptoms
5) AKI

57
Q

1) In ANCA associated GN, what causes acute inflammation and necrosis?
2) Which cells infiltrate the damaged area as 2nd line after neutrophils in ANCA associated GN?
3) What chronic changes occur in ANCA associated GN as a result of the inflammation?

A

1) Extravasation and infiltration of neutrophils.
2) Monocytes.
3) Scarring and fibrosis.

58
Q

Describe the basic management principles for ANCA associated GN.

A

Induction of remission using steroids and rituximab/ cyclophosphamide and then maintenance therapy with azathioprine, mycophenalate or rituximab for at least 12 months.

59
Q

What distinguishes immune complex glomerulonephritis from other forms of glomerulonephritis?

A

Immune deposits in the glomeruli which stain upon immunofluorescence.

**Serologic and histological findings will point to the underlying disease.

60
Q

Name the 3 types of immune complex GN.

A

1) IgA nephropathy
2) Post-streptococcal GN
3) Lupus nephritis

61
Q

Describe the pathophysiological mechanism which underlies all types of immune complex GN.

A

Immune complex deposition in the glomerulus which activates the classical complement pathway resulting in inflammation and low levels of C3 and C4.

62
Q

1) Describe the immune complex deposits in IgA nephropathy.

2) Describe a typical presentation of IgA nephropathy.

A

1) Mesangial and glomerular capillary IgA deposits.
2) Asymptomatic non-visible haematuria OR episodic visible haematuria usually occurring within 12-72 hours of an infection.

63
Q

1) What is the commonest primary GN in high income countries?
2) Give two signs of IgA nephropathy.
3) What does renal biopsy in IgA nephropathy show?

A

1) IgA nephropathy.
2) HTN and proteinuria usually <1g.
3) IgA deposition in mesangium.

64
Q

Describe the basic management of IgA nephropathy.

A

ACEi/ARB to reduce proteinuria and protect renal function. Corticosteroids and fish oil if there is persistent proteinuria >1g despite 3-6 months of ACEi/ARB + a GFR >50.

65
Q

Give 2 factors associated with post streptococcal GN.

A

1) Deposition of immune complexes (streptococcal antigens) forming sub epithelial humps.
2) Presence of anti streptococcal antibodies int he blood.

66
Q

Describe the clinical presentation of post-streptococcal GN.

A

Can occur about 2 weeks after a throat infection or 3-6 weeks after a skin infection with presentation varying from haematuria to acute nephritis.

67
Q

Name 4 signs or symptoms of post-streptococcal GN.

A

1) HTN
2) Haematuria
3) Oedema
4) Oliguria

68
Q

Give 4 diagnostic indicators of post-streptococcal GN.

A

1) Evidence of streptococcal infection
2) Increased anti-streptolysin O titre
3) Increased anti-DNAse B
4) Decreased C3.

69
Q

Describe the basic treatment for post-streptococcal GN.

A

Supportive. Antibiotics to clear nehpritogenic bacteria.

70
Q

State 2 distinguishing features of lupus nephritis.

A

1) Presence of ANA
2) Full house immunofluorescence staining (IgG, IgM, IgA, C3, C1q)

**may also be anti-dsDNA antibodies

71
Q

1) How can kidney damage as a result of lupus nephritis present?
2) In lupus nephritis, where is immune complex deposition seen?

A

1) As nephritis or nephrosis.

2) In the mesangium, subendothelium and subepithelium.

72
Q

Describe 5 clinical features which may be present if a patient were to present with lupus nephritis.

A

1) Rash
2) Photosensitivity
3) Ulcers
4) Arthritis
5) Serositis
6) CNS effects
7) Cytopenias
8) Renal disease

73
Q

Describe the basic treatment for stage I/II lupus nephritis.

A

ACEi/ARB for renal protection and hydroxychloroquine for extra renal disease.

74
Q

Describe basic treatment for stage III/IV/V lupus nephritis.

A

Immunosuppression required; mycophenolate, glucocorticoids, cyclophosphamide, rituximab.

75
Q

Describe membranoproliferative glomerulonephritis.

A

Not a disease in itself but a pattern of disease/ injury seen in GN and in nephrotic syndrome. Can have both nephrotic and nephritic pictures.

76
Q

How is membranoproliferative GN diagnosed and what are 3 distinguishing factors?

A

Diagnosed based on biopsy with renal histopathology showing:

1) mesangial cell expansion
2) GBM thickening
3) ‘Tramtrack’ findings with double contour on the GBM.

77
Q

1) What are the 2 types of membranoproliferative GN?

2) State the sub -classifications of these types.

A

1) Immune complex mediated and complement mediated.
2) Immune complex mediated = primary (idiopathic) or secondary (due to infection, autoimmune disease or paraproteinaemia). Complement mediated = primary (idiopathic) or genetic (complement dysregulation).

78
Q

1) In immune complex mediated membranoproliferative GN, how does complement activation occur?
2) In complement mediated membranoproliferative GN, how does complement activation occur?

A

1) Complement activation occurs by the classical pathway which promotes the inflammatory response.
2) Direct activation of the alternate pathway which promotes the inflammatory response.

79
Q

Describe the difference in laboratory findings between immune complex mediated and complement mediated membranoproliferative glomerulonephritis.

A

1) Immune complex mediated = normal or mildly decreased C3 and low serum C4
2) Complement mediated = low serum C3 and normal C4 due to activation of alternate pathway.

80
Q

What is Henoch-Schönlein Purpura?

A

Small vessel vasculitis and systemic variant of IgA nephropathy with IgA deposition in skin, joints and gut in addition to in the kidney.

81
Q

Give 4 possible features of the clinical presentation of Henoch-Schönlein Purpura.

A

1) Purpuric rash on extensor surfaces.
2) Flitting polyarthritis
3) Abdominal pain (GI bleeding)
4) Nephritis

82
Q

Describe how Henoch-Schönlein Purpura can be diagnosed.

A

Diagnosis is usually clinical. Confirmed with positive immunofluorescence for IgA and C3 in the skin. Renal biopsy is identical to IgA nephropathy (mesangial and glomerular capiallary IgA deposits).

83
Q

Describe the basic management for Henoch-Schönlein Purpura.

A

Renal disease is managed as IgA nephropathy (ACEi/ARB to reduce proteinuria and protect renal function, then corticosteroids and fish oils if persistent proteinuria >1g despite ACEi/ARB).

Steroids may be used for gut involvement.

84
Q

What causes Alport syndrome?

A

X-linked recessive gene mutation causing abnormalities in type IV collagen which prevents the kidneys from properly filtering blood.

85
Q

Why can aport syndrome also cause sensorineural hearing loss and vision abnormalities?

A

Because type IV collagen is also important in the organ of corti and for lens and retina shape in the eye.

86
Q

Name 6 signs and symptoms that could be features of the clinical presentation of Aport syndrome.

A

1) Haematuria
2) Proteinuria
3) Oedema
4) Osteodystrophy
5) Sensorineural hearing loss
6) Vision abnormalities (anterior lenticonus)

87
Q

Describe the basic management for those with Aport syndrome.

A

For most it can lead to ESRF, so a renal transplant will be required (this can run the risk of anti-GBM disease as graft type IV collagen may be recognised as foreign).

88
Q

What can the use of nephrotoxic drugs cause?

A

Use of nephrotoxic drugs can potentially precipitate an AKI or can worsen existing CKD.

89
Q

What causes the afferent arteriole to normally have a widen lumen than the efferent arteriole?

A

Prostaglandin mediated vasodilation of the afferent arteriole and angiotensin-II mediated vasoconstriction of the efferent arteriole.

**This creates a pressure gradient across the glomerulus.

90
Q

What will happen if there is decreased blood flow through the afferent arteriole?

A

The efferent arteriole will need to vasoconstrict in order to compensate for the pressure difference.

91
Q

How can ACE inhibitors and angiotensin receptor blockers cause a decrease in GFR?

A

They block angiotensin-II (main mediator of EA vasoconstriction) > dilated afferent arteriole > decreased resistance > increased outflow of blood > reduced pressure gradient > reduced GFR.

92
Q

Describe the effect of NSAIDs on the kidney.

A

Use of NSAIDs reduce the production of prostaglandins, leading to vasoconstriction of the afferent arteriole and a reduced GFR.

In order to maintain the GFR, the efferent arteriole then needs to vasoconstriction to maintain the pressure gradient.

93
Q

List the drugs which should be stopped or adjusted in the case of an AKI or CKD.

A

D - diuretics
A - ACEis/ARBs
M - Metformin
N - NSAIDs

94
Q

Name 3 diseases of renal vasculature.

A

Renal artery stenosis
Renal artery aneurysm
Atheroembolic renal disease

95
Q

Why does HTN occur secondary to diseases of renal vasculature?

A

HTN occurs secondary to these diseases due to renal hypoperfusion causing activation of the RAAS.

96
Q

How can renal vascular disease lead to glomerulosclerosis?

A

RAAS activation > HTN > atherosclerosis > narrow lumen > reduced kidney perfusion > macrophage recruitment to the area > increased TGF-B1 > Mesangial cell regression > depletion of extracellular matrix > glomerulosclerosis.

Block 34 - Metabolic (18 decks)

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