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Renal > Nephritic and Nephrotic syndrome, and Glomerulonephritis > Flashcards

Nephritic and Nephrotic syndrome, and Glomerulonephritis Flashcards

1
Q

What is the definition of nephrotic syndrome?

A

Quadrad of:

  • Proteinuria > 3g/24hrs
  • Hypoalbuminaemia - < 30g/L
  • Oedema
  • Hypercholesterolaemia
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2
Q

What are primary renal diseases which can cause nephrotic syndrome?

A
  • Minimal change disease
  • Membranous nephropathy
  • Focal segmental glomerulosclerosis
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3
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease

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4
Q

What are secondary causes of nephrotic syndrome?

A
  • Diabetes mellitus
  • Lupus nephritis
  • Hep B + C
  • HIV
  • Myeloma
  • Amyloidosis
  • Pre-eclampsia
  • Malignancy
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5
Q

What is the pathophysiology of nephrotic syndrome?

A

Proteinuria results from podocyte and glomerular basement membrane pathology - normally have negative charge which prevents passage of protein into the urine.

There is an increase in the size and number of pores, allowing passage of more and larger molecules. Electrical charge is also involved in glomerular permeability.

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6
Q

Why do those with nephrotic syndrome develop hyperlipidaemia?

A

Hyperlipidaemia is the consequence of increased synthesis of lipoproteins (such as apolipoprotein B, C-III lipoprotein (a)), as a direct consequence of a low plasma albumin. There is also a reduced clearance of the principal triglycerides bearing lipoprotein (chylomicrons and VLDL) in direct response to albuminuria.

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7
Q

What is minimal change disease?

A

An altered cell-mediated immunologic response with abnormal secretion of lymphokines by T cells is thought to reduce the production of anions in the glomerular basement membrane, thereby increasing the glomerular permeability to serum albumin through a reduction of electrostatic repulsion. The loss of anionic charges is also thought to favor foot process fusion

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8
Q

What are symptoms that someone with nephrotic syndrome tend to present with?

A
  • Generalised pitting oedema
  • Frothy urine
  • Systemic symptoms if secondary cause - cough, weight loss, night sweats etc.
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9
Q

What are clinical signs seen in nephrotic syndrome?

A
  • Mild/severe pitting oedema - whole body
  • Muehrcke’s lines
  • Xanthelasmata
  • Possible hypertension
  • Normal JVP
  • AScites
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10
Q

What are the different ways in which glomerulonephritis present?

A
  • Isolated haematuria and/or proteinuria
  • Nephrotic syndrome
  • Nephritic syndrome
  • Acute renal failure
  • Chronic renal failure
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11
Q

What might the following child have?

A

Nephrotic syndrome

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12
Q

What would your differential diagnosis be for someone with features of nephrotic syndrome?

A
  • CCF
  • Liver disease
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13
Q

What investigations would you consider doing in someone with features of nephrotic syndrome?

A
  • Bedside - urine dipstick, 24 hour urine collection
  • Bloods - FBC, U+E’s, LFT, BNP, Serum albumin, ANCA, anti-GBM
  • Imaging - Renal imaging, CXR, Dopplers - VTE
  • Other - Throat swab, US guided Renal biospy
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14
Q

What is minimal change disease?

A

In this condition the glomeruli appear normal on light microscopy. The only abnormality seen on electron microscopy is fusion of the foot processes of epithelial cells (podocytes).

Thought to be due to immature differentiating CD34 stem cells rather than mature T lymphocytes

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15
Q

What proportion of nephrotic syndrome in children is caused by minimal change disease?

A

80%

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16
Q

What might you see on microscopy in someone with minimal change disease?

A

Fused podocytes

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17
Q

How would you manage someone with minimal change disease?

A
  • Reduce oedema - Fluid restriction (1L/day), salt restriction
  • High dose Prednisolone - 4-6 weeks
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18
Q

How would you generally manage someone with nephrotic syndrome?

A
  • Treat underlying cause
  • Reduce oedema - Fluid restriction (1L/day), salt restruction
  • Loop diuretics (+/- thiazide if resistant oedema)
  • Consider ACEi/ARB - reduce proteinuria
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19
Q

What are the main non-proliferative glomerulonephritidies?

A
  • Minimal change disease
  • FSGS
  • MGN
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20
Q

What are the main proliferative glomerulonephritidies?

A
  • IgA nephropathy
  • Membranoprolifertive glomerulonephritis
  • Post infectious glomerulonphritis
  • Rapidly progressive glomerulonephritis
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21
Q

What type of GN is minimal change disease; proliferative or non-proliferative?

A

Non-proliferative

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22
Q

What type of GN is FSGS; proliferative or non-proliferative?

A

Non-proliferative

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23
Q

What type of GN is membranous glomerulonephritis?

A

Non-proliferative

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24
Q

What type of GN is IgA nephropathy; proliferative or non-proliferative?

A

Proliferative

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25
Q

What type of GN is Membranoproliferative GN; proliferative or non-proliferative?

A

Proliferative

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26
Q

What type of GN is Rapidly progressive GN; proliferative or non-proliferative?

A

Proliferative

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27
Q

What type of GN is Post infectious GN; proliferative or non-proliferative?

A

Proliferative

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28
Q

What are examples of rapidly progressive (crescentic) GNs?

A
  • Goodpastures syndrome
  • Lupus
  • Vasculitic disorders
    • Wegeners
    • Microscopic polyangitis
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29
Q

What syndrome does minimal change disease present with; nephritic or nephrotic syndrome?

A

Nephrotic syndrome

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30
Q

What syndrome does Focal segmental glomerulosclerosis present with; nephritic or nephrotic syndrome?

A

Nephrotic syndrome

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31
Q

What syndrome does membranoproliferative GN tend present with; nephritic or nephrotic syndrome?

A

Nephritic syndrome

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32
Q

What syndrome does Membranous GN tend present with; nephritic or nephrotic syndrome?

A

Nephrotic syndrome

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33
Q

What is Focal Segmental Glomerulosclerosis?

A

Segmental glomerulosclerosis is seen, which later progresses to global sclerosis. The deep glomeruli at the corticomedullary junction are affected first.

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34
Q

How would you manage someone with FSGS?

A
  • ACEi/ARBs and BP control
  • Corticosteroids - often ineffective
  • Consider calcineurin inhibitors
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35
Q

How would you manage someone with membranous nephropathy?

A
  • ACEI/ARB and BP control in all
  • Consider immunosuppression
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36
Q

What are secondary casues of membranous nephropathy?

A
  • Malignancy - lung, breast, GI, Prostate, haematological
  • Infection - hepatitis B/C, Streptococcus, malaria, schistosomiasis
  • Autoimmune - SLE, RA, sarcoidosis, Sjogren’s
  • Drugs - gold, penicillamine
37
Q

What is membranous glomerulonephritis/nephropathy?

A

MGN is caused by immune complex formation in the glomerulus. The immune complexes are formed by binding of antibodies to antigens in the glomerular basement membrane. The antigens may be part of the basement membrane, or deposited from elsewhere by the systemic circulation.

The immune complex serves as an activator that triggers a response from the C5b - C9 complements, which form a membrane attack complex (MAC) on the glomerular epithelial cells. This damages capillary walls causing them to become “leaky”.

38
Q

What proportion og those with MGN progress to renal failure?

39
Q

What is membranoproliferative glomerulonephritis?

A

Refers to a pattern of glomerular injury based on the following three characteristic histopathologic findings:

  • Proliferation of mesangial and endothelial cells and expansion of the mesangial matrix
  • Thickening of the peripheral capillary walls by subendothelial immune deposits and/or intramembranous dense deposits
  • Mesangial interposition into the capillary wall, giving rise to a double-contour or tram-track appearance on light microscopy
40
Q

What are the histological features of membranous nephropathy?

A

Diffusely thickened GBM, with spikes on silver staining

41
Q

What might you see on histology in someone with membranoproliferative GN?

A

A proliferative glomerulonephritis with electron dense deposits:

  • Thickened basement membrane
  • Thickened mesangium
  • Immunofluorescence - Subendothelial deposition of IgG, Linear pattern
42
Q

How would you manage membranoproliferative GN?

A

Usually progresses to renal failure

  • ACEi and BP control in all
  • Trial immunosuppression
43
Q

What is diabetic nephropathy?

A

Nephropathy secondary to diabetes - thought to be due to a combination of increased growth factos, RAAS activation, oxidative stress and production of glycosylation end products

This leads to increased glomerular capillary pressure, podocyte damage, and endothelial dysfunction

44
Q

How does diabetic nephropathy tend to present; nephrotic or nephritic?

45
Q

What syndrome do those with SLE nephropathy tend to present with; nephrotic or nephritic?

A

Nephrotic or nephritic

46
Q

What syndrome do those with amyloidosis associated nephropathy tend to present; nephrotic or nephritic syndrome?

47
Q

What syndrome do those with myeloma associated nephropathy tend to present with; nephrotic or nephritic syndrome?

48
Q

What nephrotic glomerulonephropathy is most responsive to steroids?

A

Minimal change disease

49
Q

What are complications of nephrotic syndrome?

A
  • VTE
  • Infection
  • Hyperlipidaemia
  • Renal failure
50
Q

Why are those with nephrotic syndrome at increased risk of infection?

A

Urinary losses of immunoglobulins and immune mediators in combination with areas of fluid accumulation (cellulitis, peritonitis, empyema)

51
Q

What is nephritic syndrome?

A

A syndrome which comprises:

  • Haematuria
  • Proteinuria
  • Hypertension
  • Oedema
  • Temporary oliguria
  • Uraemia
52
Q

What are causes of nephritic syndrome?

A
  • Post-streptococcal glomerulonephritis
  • IgA nephropathy
  • Rapidly progressive glomerulonephritis (crescentic glomerulonephritis)
  • Goodpasture’s syndrome
  • Vasculitic disorder – Wegener’s granulomatosis / Microscopic Polyangiitis / Churg Strauss disease
  • Membranoproliferative glomerulonephritis – primary or secondary to SLE / Hepatitis B/C
  • Henoch-Schönlein purpura
53
Q

What type of GN is post-strep GN; proliferative or non-proliferative?

A

Proliferative

54
Q

What type of GN is IgA nephropathy; proliferative or non-proliferative?

A

Proliferative

55
Q

What type of GN is rapidly progressive GN; proliferative or non-proliferative?

A

Proliferative

56
Q

What are signs that someone has nephritic syndrome?

A
  • Micro/macroscopic haematuria
  • Hypertension
  • Oedema
  • Oliguria
  • Proteinuria on disptick
57
Q

Which is the relatively more proteinuric syndrome than the other; nephritic or nephrotic?

58
Q

What is the most common GN in adults?

A

IgA nephropathy

59
Q

How long after a URTI/GI infection does IgA nephropathy occur?

60
Q

What is IgA nephropathy?

A

Disease caused by deposits of immunoglobulin A (IgA) in a granular pattern in the mesangium (by immunofluorescence), a region of the renal glomerulus.

61
Q

What would you find on biopsy in someone with IgA nephropathy?

A

IgA deposition in mesangium

62
Q

How does IgA nephropathy tend to present?

A

Can be asymptomatic, or:

  • Non-visible/episodic visible haematuria (within 12-72 hrs infection)
  • Hypertension
  • Proteinuria
63
Q

How would you manage someone with IgA nephropathy?

A
  • ACEi/ARB - reduce proteinuria
  • Consider corticosteroids - if proteinuria over 1-3g/day
64
Q

What is henoch-schonlein purpura?

A

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

65
Q

How do those with HSP tend to present?

A
  • Purpuric rash on extensor surfaces
  • Flitting polyarthritis
  • Abdominal pain +/- GI bleeding
  • Nephritis
66
Q

How would you diagnose henoch schonlein purpura?

A
  • Usually clinical
  • Can get positive immunoflourescence for IgA and C3 in the skin
67
Q

What is HSP identical to on renal biopsy?

A

IgA nephropathy

68
Q

How long after throat infection can post-strep GN occur?

A

Approximately 2 weeks

69
Q

How does post-strep GN occur?

A

Strep antigen deposits in the glomerulus leading to immune complex formation and inflammation

70
Q

How does post-strep GN present?

A

Haematuria to acute nephritis - haematuria, oedema, HTN, oliguria

71
Q

How would you diagnose post-strep GN?

A
  • Increased ASOT
  • Increased anti-DNAse B
  • Decreased C3
72
Q

What is ASOT?

A

Anti-streptolysin O antibodies - measure of blood plasma levels of antibodies which indicate past streptococcal exposure

73
Q

How would you manage someone with Post-strep GN?

A
  • Supportive
  • Consider Antibiotics
74
Q

What is Anti-GBM disease?

A

Goodpasture’s syndrome

Auto-antibodies produced to type IV collagen which presents in glomerular and alveolar basement membranes

75
Q

How do those with anti-GBM present?

A
  • Renal disease - nephritis/AKI
  • Lung disease - haemoptysis, SOB
76
Q

How long does it take post-infectious GN to resolve?

77
Q

How would you manage someone with Anti-GBM?

A
  • Plasma exchange
  • Corticosteroids
  • Cyclophosphamide
78
Q

What ANCA is most commonly associated with microscopic polyangitis?

79
Q

What ANCA is most commonly associated with Wegener’s?

80
Q

What investigations might you consider in someone presenting with features of nephritic syndrome?

A
  • Bedside - BP, Urine dipstick
  • Bloods - FBC, U+E’s, LFTs, CRP, ANCA screen, Anti-GBM antibody, ASOT, Cryoglobulins, C3, C4, blood culture
  • Imaging - Renal USS, CXR
  • Other - Renal biopsy, 24 hr urine, Urine microscopy, Throat swab,
81
Q

What is generally diagnostic of Rapidly progressive GN on histology?

A

Breaks in GBM allow influx of inflammatory cells so that crescents are seen on renal biopsy

82
Q

How would you generally manage nephritic syndrome?

A
  • Daily weights
  • Fluid restriction - intake and output, salt restriction
  • BP monitoring
  • Diuretics
  • Dialysis (if needed)
  • Consider Antibiotics - post-strep GN
83
Q

What complications are associated with nephritic syndrome?

A
  • Hypertensive encephalopathy
  • Pulmonary oedema
  • Severe uraemia
84
Q

How would you manage wegener’s assocaited nephropathy?

A

Steroids + cyclophosphamide

85
Q

How would you manage diabetic nephroppathy?

A
  • Intensive DM control - prevent microalbuminaemia
  • BP control
  • Sodium restriction
  • Statins
  • ACEi/ARB for CV and renal protection
86
Q

How would you manage Microscopic polyangitis associated nephropathy?

A
  • Long term steroids +/- cyclophosphamide
  • Can use plasmapheresis acutely
87
Q

What would you see on microscopy in Post-strep GN?

A

Light microscopy shows:

  • Proliferation of mesangial cells
  • Neutrophils and monocytes
  • Bowman space is compressed – seen as classical crescentic glomerulonephritis
88
Q

What is cyclophosphamide used as in wegener’s granulomatosis?

A

Steroid sparing agent

Renal (19 decks)

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