Nephrotic syndrome Flashcards

1
Q

What is nephrotic syndrome?

A

Increased filtration of macromolecules across the glomerular capillary due to structural and functional abnormalities of the glomerular podocytes
Hypoalbuminaemia
Oedema
Hypercholesterolaemia and hypertriglycarideaemia

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2
Q

What are glomerulopathies associated with nephrotic syndrome? (bland urine sediments)

A

Primary glomerular disease:
Minimal-change glomerular disease Membranous nephropathy
Focal segmental glomerulosclerosis Congenital nephrotic syndrome
Secondary glomerular disease:
Amyloidosis
Diabetic nephropathy

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3
Q

What are glomerulopathies associated with nephrotic syndrome? (active urine sediments- mixed nephrotic/nephritic)

A

Primary glomerular disease:
Mesangiocapillary glomerulonephritis Mesangial proliferative glomerulonephritis
Secondary glomerular disease:
Systemic lupus erythematosus Cryoglobulinaemic disease Henoch–Schonlein syndrome Idiopathic fibrillary glomerulopathy Immunotactoid glomerulopathy Fibronectin glomerulopathy

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4
Q

What causes membranoproliferazive glomerulonephritis?

A
Chronic infection (abscesses, IE,)
Cfyloglobuminaemia secondary to hep C
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5
Q

What are the clinical features of nephrotic syndrome?

A

Oedema of ankles, genitals and abdominal wall
Periorbital oedema and arms in severe cases
Proteinuria
Hypoalbuminaemia
hyperlipidaemia
Complications- hypertension, thromboembolic disorders, peritonitis

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6
Q

What is nephritic syndrome?

A

When it occurs in glomerulus it’s glomerulonephritis

Kidney disease involving inflammation

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7
Q

What are the clinical features of nephritic syndrome?

A
Hematuria
Proteinuria 
Hypertension 
Blurred vision
Azotemia 
Oliguria
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8
Q

What causes nephritic syndrome?

A

Goodpasture’s
SLE
Rapidly progressive glomerulonephritis
IE
Cryoglobulinaemia (antibodies sensitive to cold)
Membranoproliferazive glomerulonephritis (MPGN)
Henoch-schonlein
Post-streptococcal
Post infectious- (mumps, legionella, hep B/C, schistosomiasis, malaria)

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9
Q

What are the features of rapidly progressive glomerulonephritis?

A
Acute nephritis, crescent shape
GBM breaks 
50's-60's- poor prognosis 
Focal necrosis with or without crescents and rapidly progressive renal failure over weeks to months
Caused by:
Anti-GBM antibody (good pastures)
Immune complexes (SLE, IgA nephropathy)
Idiopathic
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10
Q

What is tubulointerstitial nephritis?

A

Primary injury to the renal tubules and interstitium that results in decreased renal function
Acute- due to allergic drug reaction (penicillin/NSAIDs) and infections
Chronic- analgesic nephropathy, diabetes, toxins (lead)

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11
Q

What are the clinical features of tubulointerstitial nephritis?

A

Acute- fever, eosinophilia and eosinophiluria, AKI

Chronic- Polyuria, proteinuria uraemia

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12
Q

What occurs in minimal change disease?

A
Nephrotic syndrome 
Most common in children 
T cells attack the foot processes of podocytes (effacement), less of charge barrier so albumin can pass through 
Associated with Hodgkin's lymphoma 
No change seen on light microscopy
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13
Q

What is Goodpasture’s syndrome?

A

Autoimmune disease that affects lungs and kidneys
hemoptysis ans hematuria
Environmental factors: infection, smoking, oxidative stress

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14
Q

What are the histological descriptions of glomerular pathology?

A

Global: whole glomerulus is diseased
Segmental: small patches of one glomerulus are damaged
Diffuse: >50% glomeruli
Focal: <50% glomeruli

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15
Q

What are secondary factors causing deposition of antigens causing glomerulonephritis?

A
NSAID HSP
Neoplasm 
SLE 
Amyloid 
Infection 
Diabetes 
Henoch Schonlein Purpura
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16
Q

What is chronic interstitial nephritis pathology?

A

Chronic pyelonephritis, irregular areas of scarring, chronic inflammatory infiltrate
Reflux associated chronic interstitial nephritis: incompetent vesicoureteric valves, predisposing inflammation + scarring. Presents in early adulthood
Obstructive chronic interstitial nephritis: anatomic abnormality leads to recurrent infections (prostate, retroperitoneal fibrosis), stones

17
Q

How can diabetes damage the kidney?

A

Direct glomerular damage: basement membrane thickening, increased permeability of capillary wall + proteinuria, eventual glomerular hyalinisation —> CKD
Ischaemia due to arterial disease: atherosclerosis causes reduced eGFR and glomerular ischaemia
Ascending infection

18
Q

What is nephritic syndrome pathology?

A

TETRAD: haematuria + red cell casts, oliguria, proteinuria, hypertension
Proliferative (increased cell numbers) + damage to basement membrane –> casts form from blood and protein
Primary causes: IgA nephropathy, Goodpastures
Secondary causes: SLE, HSP

19
Q

What are the differences between IgA nephropathy and post-streptococcal glomerulonephritis?

A

IgA- 1-2 days after URTI. post-s- 1-2 weeks
IgA- young males, macroscopic haematuria
Post-s- proteinuria, low complement

20
Q

What is acute tubular necrosis associated with?

A

Granular muddy brown urinary casts

Normal urea:creatinine ratio