11.2 Glomerulonephritis Flashcards

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1
Q

What is glomerulonephritis (and the more appropriate term)? Is it acute or chronic?

A
  • Glomerulonephritis is usually regarded as inflammation of the glomeruli in the kidneys
  • However, not all GN are inflammatory in histological nature - “glomerulopathy” may be more appropriate
  • It can be either acute or chronic
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2
Q

Describe the clinical features of glomerulonephritis

A
  • Haematuria
  • Proteinuria
  • Oedema
  • Nausea/vomiting
  • Oliguria
  • Fatigue
  • Decreased GFR
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3
Q

Describe some causes (and corresponding treatments) for glomerulonephritis

A
  • Infection (give antibiotics)
  • Autoimmune disease (such as lupus nephritis or goodpasture’s disease)
  • Generalised vasculitis
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4
Q

Is proteinuria worse in nephritic or nephrotic syndromes? What is the threshold of the answer to the previous question in terms of daily protein loss?

A

Nephrotic (remember Matt Arnold)

Nephrotic threshold is 3.5g/day

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5
Q

Why might there be high levels of triglycerides and cholesterol in the blood during nephrotic syndrome?

A

Because the liver tries to compensate for massive proteinuria, but if it can’t make enough replacement albumin (despite hypoalbuminaemia), it spits out TAGs instead.

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6
Q

Nephritic vs nephrotic syndrome

A

Nephritic: haematuria, proteinuria (less than nephrotic), hypertension

Nephrotic: massive proteinuria (>=3.5g/day), oedema, hypoalbuminaemia, hypercoagulability

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7
Q

What is the relationship between glomerulonephritis and nephrotic/nephritic syndrome? Are they categories of one another? The same thing? Explain.

A
  • Glomerulonephritis refers to inflammation of the glomerulus within the kidney
  • Nephrotic/nephritic syndromes are exactly that; syndromes. They refer to specific collections of symptoms. Glomerulonephritis can cause these syndromes, but the syndromes themselves are not comparable to GN. They are in different categories.
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8
Q

What symptoms make up nephritic syndrome

A
  • Haematuria
  • Mild proteinuria
  • Oliguria
  • Oedema
  • Hypertension
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9
Q

What symptoms make up nephrotic syndrome

A
  • Heavy proteinuria
  • Subsequent hypoalbuminuria
  • Heavy oedema (since there is nothing holding the fluid in)
  • Hyperlipidaemia (why?)
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10
Q

What is rapidly progressive GN?

A

Acute severe drop in GFR associated with glomerulonephritis.

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11
Q

Macro vs microscopic haematuria

A

Macroscopic: visible to the naked eye
Microscopic: visible only on dipstick/microscopy

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12
Q

How do we detect glomerulonephritis?

A
  • Not difficult: do a urine dipstick test
  • Looking for blood and protein in urine, both of which are leaked into urine following inflammation of the glomerulus
  • Also, urine microscopy shows dysmorphic RBCs with cytoplasmic blebs (acanthocytes; acanthos = thorny flower)
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13
Q

Why is it a bad idea to use creatinine to detect glomerulonephritis?

A
  • Inversely exponential relationship
  • By the time creatinine is above normal range, over half of GFR is lost
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14
Q

How do we diagnose the cause of glomerulonephritis?

A
  • Renal biopsy (we have no blood test at the moment)
  • Some aetiologies have diagnostic blood tests
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15
Q

What are glomerular crescents? What do they indicate on histology?

A
  • They are proliferation of bowmans capsule endothelium, forming an abnormal crescent-like structure alongside the glomerulus
  • They indicate severe glomerulonephritis
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16
Q

The world’s most common primary glomerulonephritis is…

A

IgA glomerulonephritis

17
Q

What is synpharyngitic haematuria? What condition is it known to occur in?

A
  • Haematuria close in time to the development of URTI or GI infection
  • Thought to occur in IgA nephropathy
18
Q

Explain the pathophysiological mechanism of IgA nephropathy

A
  • Abnormal IgA produced, which the body attacks with other Abs, forming immune complexes
  • These immune complexes deposit in the mesangial cells of the glomerulus, causing localised inflammation and permanent kidney damage
19
Q

Clinical features of IgA nephropathy

A
  • Synpharyngitic haematuria
  • Proteinuria
  • Oedema (typically in face and legs)
  • Hypertension
  • Decreased GFR
20
Q

Pathological findings of IgA nephropathy

A

Mesangial proliferation and signs of IgA deposition in mesangial areas (such as on immunofluorescense staining)

21
Q

Anti-GBM glomerulonephritis/goodpastures pathophys and clinical features

A
  • Loss of tolerance of type IV collagen, which is found in GBM and lungs, leading to autoantibody mediated attack
  • Often leads to haemoptysis from lungs
  • In terms of kidneys, patients always present with rapidly progressing glomerulonephritis, loss of GFR, proteinuria, and haematuria
22
Q

Pathological findings in goodpasture’s

A
  • IgG autoantibody deposition in GBM

(G for Goodpasture’s)

23
Q

Clinical features of post-strep glomerulonephritis

A
  • Smoky-dark urine (strep = s = smoky)
  • Haematuria
  • Mild peripheral oedema
  • Hypertension
  • Hypocomplementaemia
  • Varying ARF
24
Q

Pathologgical findings of post-strep glomerulonephritis

A

Positive antibodies for DNAaseB, streptolysin-O, and hylauronidase