Glomerulonephritis Flashcards

1
Q

What does the combination of haematuria and proteinuria usually mean?

A

An underlying glomerulonephritis
(Can also happen if BP is very high)

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2
Q

What does glycosuria indicate?

A

Diabetes (which can cause a glomerulonephritis)
Pregnancy

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3
Q

What would you see on a dipstix in a UTI?

A

Leucocyturia and Nitrituria
Can also cause a little bit of haematuria (but will be accompanied by nitrituria)

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4
Q

What does urobilinogenuria indicate?

A

Haemolysis
Hepatitis, cirrhosis, liver disease

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5
Q

What are the anatomical parts of the kidney?

A

Cortex
Medulla - pyramids
Arterial and venous system

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6
Q

What is the functional unit of the kidney?

A

Glomerulus
- afferent arteriole
- efferent arteriole
- descending loop of Henle
- ascending loop of Henle
- collecting duct
- vasa recta (responsible for mainiting osmotic gradient in kidney (countercurrent mechanism))

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7
Q

What does the filtration barrier consist of?

A

Endothelium - fenestrated to allow small solutes through
Basement membrane - allows small, positively charged molecules through
Podocyte - maintains structural conformation of glomerular tuft and basement membrane components - keeps albumin etc. inside capillary system

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8
Q

What would you see on urine microscopy in glomerulnephritis

A

Red cell casts - rapidly progressive nephritic GM
White cell casts - inflammation - acute interstitial nephritis
Granular cast - acute tubular necrosis
Broad cast - nonspecific
Hyaline cast - nonspecific
Epithelial cell casts - nonspecific

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9
Q

Diagnostic approach in glomerulonephritis

A

History -> Examination -> dipstix -> microscopy -> renal function + FBC + CXR -> albumin, lipid profile, UPCR -> serology -> renal USS -> kidney biopsy

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10
Q

What do the findings on serology mean?

A

ASOT/Anti-DNAse B - post infectious GN
ANA/ds-DNA - lupus nephritis
c3/c4 - differentiates between types of nephritis
ANCAs - vasculitis
anti-GBM Ab - GBM disease

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11
Q

What is nephrotic syndrome?
What does it look like clinically?
Give the main causes

A

Injury to the filtration barrier (podocytes) -> leakage of protein

Usually slowly progressing
- Oedema, ascites, and facial swelling
- Frothy urine (proteinuria (>0.3g/24hrs), low albumin, high cholesterol)
- Hypercoagulable
- Increased propensity for infection

Causes:
Minimal change nephropathy
Focal segmental glomerular sclerosis (e.g., HIVAN)
Membranous nephropathy
Diabetic nephropathy
Amyloidosis

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12
Q

What is nephritic syndrome?
Give the main causes

A

Inflammation inside glomerulus -> breaks filtration barrier -> inflammatory cell and blood cell leakage

Causes:
Anti-GBM disease
Small vessel vasculitis (e.g., ANCA vasculitis)
Post-streptococcal glomerulonephritis

Mild proteinuria, haematuria, hypertension, oliguria, rising U and Cr

Mesangial capillary glomerulonephritis/ membranoproliferative glomerulonephritis (mix of nephrotic and nephritic)

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13
Q

Causes of proteinuria

A

Physiological:
- Fever
- Trauma
- Surgery
- Exercise
- Burns
- Conservative management

Nephrotic syndrome:
- FSGS
- Minimal change
- Diabetes
- Membranous
- Amyloidosis
- Biopsy!

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14
Q

Why are people with nephrotic syndrome at risk of infections?

A

There is podocyte fusion -> charged barrier lost -> albumin, immunoglobulins and complement lost in the urine

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15
Q

Why do people with nephrotic syndrome get oedema?

A

Primary:
Proteinuria -> hypoalbuminaemia -> low capillary colloid oncotic pressure -> decreased circulatory volume -> underfill -> compensatory Na+ and water reabsorption -> oedema

Interstitial inflammation:
Proteinuria -> Na+ and water retention -> overfill -> expanded circulatory volume -> oedema

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16
Q

Why do people with nephrotic syndrome get hypercholersterolaemia?

A

Proteinuria -> loss of constituents of cholesterol backbone -> unregulation of cholesterol synthesis in liver

17
Q

Why are people with nephrotic syndrome hypercoagulable?

A

Coagulation cascade proteins leak -> unregulated synthesis of factors -> hypercoagulability

18
Q

What is different about HIVAN?

A

Doesn’t present with classic nephrotic syndrome
Usually involves tubules -> salt and water wastage -> no significant oedema