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YR5 Histopathology > Crash course: Renal > Flashcards

Crash course: Renal Flashcards

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1
Q

What is AKI? What is it measured by?

A

acute decline in renal function, leading to fall in urine output

Measured by rise in creatinine + urea

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2
Q

What is CKD? How is it measured?

A

Decline in renal function due to progressive damage present for >3 months

Measured via decline in eGFR

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3
Q

What are the stages of CKD based on eGFR?

A

1: >90
2: 60-89
3a: 45-59
3b: 30-44
4: 15-29
5: <15 = end stage, dialysis

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4
Q

What are the caveats of stage 1 and 2 CKD grades?

A

If stage 1/2 based on eGFR but NO Sx, NOT CKD

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5
Q

What are the 2 most common causes of CKD?

A

Diabetes
HTN

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6
Q

Give 2 less common causes of CKD

A

Autosomal dominant polycystic kidney disease

Untreated AKI (Pyelonephritis, ATN, obstruction)

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7
Q

What are the 3 broad causes of AKI?

A

PRE-renal: decrease in flow to the kidneys.

RENAL: direct damage to nephrons

POST-renal: ‘Surgical causes”- physical outflow obstruction

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8
Q

From most to least common, what are the broad causes of AKI

A

Pre-renal
Post-renal
Renal

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9
Q

Give 5 causes of pre-renal AKI

A

Hypovolaemia
Sepsis
CCF
Renal artery stenosis
ACE inhibitors

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10
Q

Give 6 causes of renal AKI

A

Ischaemia
Nephrotoxins
Glomerulonephritis
Interstitial nephritis
Hepatorenal syndrome
HUS / TTP

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11
Q

Give 4 causes of post-renal AKI

A

Stone
Tumour
Prostate
Blocked catheter

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12
Q

Which 3 structures can be damaged to result in renal causes of AKI?

A

Glomerulus: Nephrotic + Nephritic syndrome

Blood vessels: HUS + TTP

Tubules: ATN + acute interstitial nephritis

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13
Q

Give 4 causes of nephrotic syndrome

A

Minimal change
Membranous
FSGS
Secondary causes

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14
Q

What triad characterises Nephrotic syndrome?

A

Peripheral oedema

Proteinuria (3g/day or PCR >300mg)

Low serum albumin

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15
Q

Give 2 other features of nephrotic syndrome

A

Increased cholesterol

Increased clotting tendency- Antithrombin III is lost

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16
Q

What is the pathophysiology in all causes of nephrotic syndrome?

A

Breakdown of PODOCYTES (filtration barrier)

Large molecules e.g. Protein not filtered out - lost in urine

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17
Q

What is the broad management of nephrotic syndrome?

A

Steroids

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18
Q

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

A

Minimal change disease

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19
Q

What is seen on histology in minimal change disease?

A

Light microscopy: Nothing

Electron microscopy: Loss of podocyte foot processes

Immunofluorescence: Nothing

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20
Q

What is the prognosis for minimal change disease?

A

Majority respond to Prednisolone ~(90%)

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21
Q

In which population is membranous glomerulonephropathy seen?

A

Adults

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22
Q

What do immunofluorescence microscopes detect?

A

Immune complexes

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23
Q

What is seen on histology in membranous glomerulonephropathy?

A

Light microscopy: Diffuse basement membrane thickening

Electron microscopy: Spikey immune complex deposits

Immunofluorescence: Immune complexes across all of basement membrane

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24
Q

How does membranous glomerulonephropathy respond to steroids?

A

Poor response

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25
Give 2 associations to Membranous glomerulonephropathy
SLE Anti-phospholipase A2 antibodies
26
What is focal segmental glomerulonephritis? (FSGS)
Focal = Only some glomeruli are damaged (vs diffuse) Segmental = Only some regions of each individual glomerulus damaged
27
Which population is affected by focal segmental glomerulonephritis?
Adults
28
What is seen on histology in Focal segmental glomerulonephritis?
Light microscopy: Focal + segmental scarring Electron microscopy: Loss of foot processes Immunofluorescence: Nothing
29
How does focal segmental glomerulonephritis respond to steroids?
Not great (better than membranous glomerulonephropathy)
30
Give 2 secondary causes of nephrotic syndrome. What is seen on histology?
Diabetes: Kimmelstiel Wilson nodules Amyloidosis: apple green birefringence on Congo red stain
31
What are the 2 types of amyloidosis? What causes each?
AA: chronic inflammation (e.g RA, SLE) AL: Light chains (MM): plasma cells produce Abs, Abs clog up kidneys + cause damage
32
Give 5 causes of nephritic syndrome
IgA Post streptococcal Rapidly progressive (crescentic) Alport's syndrome (hereditary) Benign familial
33
What triad characterises nephritic syndrome?
HTN Haematuria Peripheral oedema
34
What is seen in the urine in nephritic syndrome?
Red cell casts- "Cola-coloured"
35
What is seen on bloods in nephritic syndrome?
Deranged U+Es
36
What is the pathophysiology of nephritic syndrome?
Big proteins + complexes damage delicate blood vessels + cause inflammation
37
Give 3 features of IgA nephropathy?
Commonest cause of nephritic syndrome worldwide After group A Streptococcal infection (1-2 days remember: IgA = Acute) Deposition of IgA immune complexes within glomeruli
38
What is seen on immunofluorescence in IgA nephropathy?
IgA immune deposits in mesangium
39
What is the prognosis for IgA nephropathy?
1/3 get better 1/3 get CKD 1/3 need dialysis
40
Give 2 features of post-streptococcal glomerulonephritis
After group A strep infection (1-3w) Thought to be due to antigen mimicry + immune complex deposition
41
What is seen on bloods in post-streptococcal glomerulonephritis?
Raised Anti-streptolysin-O titre Reduced C3 (as immune complex mediated)
42
What is seen on immunofluorescence in post-streptococcal glomerulonephritis?
Granular IgG deposits in basement membrane
43
What is management in post-streptococcal glomerulonephritis?
Supportive
44
What is Rapid progressive nephritic syndrome? (crescentic)
Most aggressive type of glomerulonephritis causing renal failure in weeks. Characterised by severity + presence of crescents (macrophages in Bowman’s space)
45
Name 3 causes of rapidly progressive nephritic syndrome
Goodpasture's Immune complex mediated Pauci-immune (ANCA associated)
46
What is Goodpasture's characterised by?
Presence of Anti-glomerular basement membrane antibodies Causes glomerulonephritis + pulmonary haemorrhages
47
What is the antigen targeted in goodpastures disease?
Alpha-3 subunit of type IV collagen found in the basement membrane of the lungs + kidneys.
48
What is seen on histology in Goodpasture's?
Light microscopy: Crescents Immunofluorescence: LINEAR deposition of IgG in GBM
49
Give 4 causes of immune complex mediated rapidly progressive nephritic syndrome
SLE IgA nephropathy Post-infectious HSP
50
Describe histology in immune complex mediated rapidly progressive nephritic syndrome
Light microscopy: Crescents Immunofluorescence: BUMPY deposition of immune complexes in GBM or mesangium
51
What are the subtypes of Pauci-immune rapidly progressive nephritic syndrome?
cANCA: granulomatosis with polyangiitis (GPA) pANCA: microscopic polyangitis (MPA), eosinophilic granulomatosis with polyangiitis (eGPA)
52
What is seen on histology in Pauci-immune rapidly progressive nephritic syndrome?
Light microscopy: Crescents Immunofluorescence: No/ scanty immune complexes
53
What other features may be seen in Pauci-immune rapidly progressive nephritic syndrome?
Vasculitis: Skin rash, pulmonary haemorrhage
54
What causes Alport's syndrome?
X-linked abnormalities in type IV collagen
55
What triad is seen in Alport's syndrome?
Nephritic syndrome Bilateral sensorineural deafness Lens dislocation
56
What is the prognosis of Alport's syndrome?
Progressive, causes end stage renal failure in early adulthood
57
What causes benign familial haematuria?
Autosomal dominant abnormality in type IV collagen aka. thin basement membrane disease
58
What are the symptoms of benign familial haematuria?
Asymptomatic haematuria No other issues generally
59
What is the most common renal cause of AKI?
Acute tubular necrosis
60
What is acute tubular necrosis?
Damage to tubules Tubule cells die + shed leading to presence of brown casts in urine
61
Give 2 causes of acute tubular necrosis
**Hypovolaemia** **Toxins:** * Aminoglycoside abx: gentamicin * Myoglobin (rhabdomyolysis) * IV contrast
62
What should you think of in acute interstitial nephritis? What occurs?
Think of allergic reaction to medications Interstitial infiltrate + eosinophils excreted as white cell casts or white cells in urine with no infection (sterile pyuria) +/- rash +/- fever
63
Give 3 drugs that may precipitate acute interstitial nephritis?
Penicillins Allopurinol NSAIDs
64
What causes chronic interstitial nephritis?
Long term paracetamol/ NSAID use
65
What is haemolytic uraemia syndrome?
Microangiopathy characterised by: * Progressive renal failure (AKI) * Microangiopathic haemolytic anaemia (MAHA) * Thrombocytopenia
66
What is the most common cause of HUS?
E. coli O157:H7 (shiga toxin-producing E. coli or STEC)
67
Describe the pathophysiology of HUS
1. Gastroenteritis (E.coli 90%) → toxin 2. Endothelial damage 3. Thrombosis, platelet consumption + fibrin strand deposition → ↓ Platelets 4. Destruction of RBCs: schistocytes, ↓ Hb
68
Where are micro thrombi in HUS?
Microthrombi confined to kidneys
69
What pentad of features characterises Thrombotic thrombocytopenic purpura?
Haemolytic anaemia Uraemia Thrombocytopenia Fever Neurological Sx: seizures, hemiparesis, impaired consciousness, impaired vision
70
What is the mortality in TTP if untreated?
90%
71
Give 6 causes of TTP
Post-infection e.g. UTI, GI Pregnancy Drugs: ciclosporin, OCP, penicillin, clopidogrel, aciclovir Tumours SLE HIV
72
What is the pathophysiology of TTP?
1. Deficiency in protease ADAMTS13 that cleaves vWF 2. Large vWF multimers form 3. Platelet aggregation + fibrin deposition 4. Microthrombi
73
Where do microthrombi occur in TTP?
Everywhere, esp. CNS
74
What is the aetiology of polycystic kidney disease? What does this cause?
Autosomal Dominant Due to mutation in PKD gene encoding polycystin Causes haematuria + kidney failure
75
Give 2 extra renal manifestations of PKD
Liver cysts (common) Berry aneurysms (leading to SAH)
76
What is the aetiology of lupus nephritis? What is seen?
Damage due to immune complex deposition, See wire loop capillaries + lumpy immune complex deposition
77
What are the 2 extremes of lupus nephritis?
Early stage (stage 1): only mesangial disease- not affecting kidney function Advanced (stage 6): >90% sclerosis = end stage
78
A 25M is involved in an RTA. On arrival his BP is 65/40 mmHg but he is quickly resuscitated and stabilised in ITU. 2 days later the SHO notices that over the past 6h, his catheter urine output has only been 50ml. What is the cause of his renal dysfunction?
Acute tubular necrosis Often get a pre-renal AKI, rehydrate them, become stable, but then renal function continues to decline- because you cant reverse necrosis (he has progressed from pre-renal to ATN)

YR5 Histopathology (27 decks)

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