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a path 3 > HISTO: Renal pathology > Flashcards

HISTO: Renal pathology Flashcards

1
Q

What are the major functions of the kidney?

A
  • Excretion of metabolic waste products and foreign chemicals (including drugs)
  • Regulation of fluid, electrolyte and acid/base balance
  • Regulation of blood pressure - renin
  • Regulation of haematocrit - erythropoietin
  • Regulation of calcium and bone metabolism – via 1,25 Dihydroxycholecalciferol
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2
Q

Where is the kidney located? What is its size? What % of cardiac output does it receive?

A

Location: retroperitoneal; T12 to L3 on left; right is lower

Size: Mean length 11cm, normal weight 125-170g (male), 115-155g (female)

Cardiac output: Receive around 20% of cardiac output

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3
Q

What is the basic unit of the kidney and what does it consist of?

A
  • Glomerulus
  • Afferent and efferent arterioles
  • Tubules
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4
Q

What is the pressure at the glomerulus? How much blood is filtered per min? Which cells are vital in its function?

A
  • High hydrostatic pressure (60mmHg)
  • 125 mL/min

Podocytes create charge-dependent (anionic) and size-dependent barrier

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5
Q

What is the function of the proximal convoluted tubule?

A
  • Actively resorbs sodium
  • Potassium is also reabsorbed
  • Hydrogen exchange to allow carbonate resorption
  • Co-transport of amino acids, phosphate, glucose
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6
Q

What is the function of the Loop of Henle?

A
  • Descending / thin ascending limb permeable to water but not ions or urea;
  • Ascending limb actively resorbs sodium and chloride
  • Countercurrent multiplier; aligned with vasa recta
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7
Q

What is the function of the distal convoluted tubule?

A
  • Impermeable to water
  • Regulates pH via active transport (proton / bicarbonate)
  • Regulates sodium, potassium via active transport (aldosterone)
  • Regulates calcium (parathyroid hormone, 1,25 dihydroxycholecalciferol
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8
Q

What is the function of the collecting duct?

A
  • Resorbs water (principal cells,ADH)
  • Regulates pH (intercalated cells, proton excretion)
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9
Q

Which part of the nephron has these functions?

  • actively resorbs sodium
  • is a countercurrent multiplier, aligned with vasa recta
  • regulates pH
  • regulates calcium
  • resorbs water
A
  • Sodium active resorption - PCT, LoH (ascending),
  • Regulates pH - DCT, CD
  • Countercurrent multiplier - LoH
  • Calcium regulation - DCT
  • Resorbs water- CD (but LoH ascending is permeable to water, whereas DCT is impermeable)
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10
Q

What is RC?

A

renal corpuscle

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11
Q

What is M? A?

A

M - Mesangium

A - afferent arteriole

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12
Q

What is labelled FS?

A

Fenestration between podocytes of the glomerulus

Below:

  • Endothelial cells (inside)
  • GBM
  • Podocytes outside with fenestrations
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13
Q

What are the signs and symptoms of renal disease/

A
  • Haematuria
  • Proteinuria
  • Uraemia
  • Hypertension
  • Oliguria / Anuria
  • Polyuria
  • Oedema
  • Colic
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14
Q

List 3 renal ‘syndromes’.

A
  1. Acute renal failure/AKI
  2. nephrotic syndrome
  3. microscopic haematuria

ie. constellations of symptoms

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15
Q

List 5 genitourinary/kidney malformations.

A
  • Agenesis
  • Renal Fusion (e.g. horse-shoe)
  • Ectopic Kidney
  • Renal Dysplasia
  • Pelvi-ureteric Junction Obstruction
  • Ureteral Duplication
  • Vesicoureteral Reflux
  • Posterior urethral Valves
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16
Q

What is the inheritance pattern of polycystic kidney disease? How common is it? What is a common consequence?

A

AD

1 in 500

Cause 10% of all end-stage renal failure

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17
Q

What genetic mutations are implicated in polycystic kidney disease?

A

PKD1, PKD2.. etc

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18
Q

What extra-renal manifestations may occur in PKD?

A

Berry aneurysm

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19
Q

What is an iatrogenic cause of kidney cysts? Are they dangerous?

A

Cysts commonly develop in patients with end stage renal disease who are on dialysis. These can be multiple, bilateral, cortical and medullary

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20
Q

What type of renal malignancy can occur due to cystic disease of the kidney?

A

Papillary renal cell carcinoma

7% risk at 10 years

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21
Q

Define acute renal failure/AKI.

A

Rapid deterioration in renal function (hours, days)

Common, often in the setting of pre-existing disease

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22
Q

What are some causes of acute renal failure? What is the commonest cause?

A
  • Pre-Renal: Failure of perfusion
  • Renal: Acute tubular injury, acute glomerulonephritis, thrombotic microangiopathy
  • Post-Renal: Obstruction

Acute tubular injury/ATN is most common.

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23
Q

What can cause acute tubular injury?

A
  • Ischaemia
  • Toxins (contrast, Hb, myoglobin, ethylene glycol)
  • Drugs esp. PG inhibitors like NSAIDs
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24
Q

Describe the pathophysiology of ATN.

A
  1. Loss of brush border and degradation of cells
  2. Apoptosis of epithelial cells and sloughing into the lumen which may cause luminal obstruction
  3. Cells which survive spread out
  4. In recovery, there should be proliferation, differentiation and re-polarisation of these cells again.
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25
Q

What is Acute Tubulo-Interstitial Nephritis? What are the causes of ATIN?

A

Immune injury to tubules and interstitium

Caused by immune injury but can also be due to infection and drugs such as:

  • NSAIDs
  • Antibiotics
  • Diuretics
  • Allopurinol
  • Proton Pump Inhibitors
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26
Q

Describe the infiltrate seen in ATIN.

A
  • Heavy interstitial inflammatory infiltrate with tubular injury
  • Can see eosinophils, granulomas
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27
Q

What is acute glomerulonephritis? How does it usually present?

A

AGN = Acute inflammation of glomeruli

Presents with oliguria with urine casts containing erythrocytes and leucocytes

When sufficient to cause AKI, there are almost always _crescents_ (proliferation of cells within Bowman’s space) as shown.

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28
Q

List three types of acute ‘crescentic’ glomerulonephritis.

A
  1. Immune Complex Complex Associated Crescentic Glomerulonephritis
  2. Anti Glomerular Basement Membrane Disease
  3. Pauci-immune Crescentic Glomerulonephritis (NB: ANCA positive i.e. anti-neutrophil cytoplasm antibodies)
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29
Q

What are the aetiologies of immune complex associated crescentic glomerulonephritis?

A
  • SLE,
  • IgA nephropathy
  • Post-Infectious Glomerulonephritis
30
Q

What is anti-GBM disease? What specific antibody is found in anti-GBM disease?

A

Rare and severe disease caused by Ab directed against the GBM

Ab directed at C-terminal domain of Type IV collagen - may be detected with serology

31
Q

What is an extra-renal complication of anti-GBM disease?

A

Lung injury - this occurs because antibodies in anti-GBM may cross-react with alveolar basement membrane leading to pulmonary haemorrhage

32
Q

What is seen on histology/immunofluorescence in anti-GBM disease?

A

Linear deposition of IgG demonstrable on glomerular basement membrane

33
Q

What are the characteristic features of is Pauci-immune crescenteric glomerulonephritis?

A

Only scanty glomerular immunoglobulin deposits

Usually ANCA-associated - trigger neutrophil activation and glomerular necrosis

Vasculitis elsewhere

34
Q

What is the patter of Ig glomerular deposition in Pauci-immune crescenteric glomerulonephritis?

A

scanty glomerular immunoglobulin deposits

35
Q

What is the pathophysiology of thrombotic microangiopathy? What can happen to RBCs in this condition?

A

Damage to endothelium in glomeruli, arterioles, arteries leading to thrombosis

Red cells may be damaged by fibrin –> MAHA/ HUS

36
Q

What are the aetiologies of thrombotic microangiopathy(TMA)?

A

Divided into diarrhoea and non-diarrhoea associated.

Diarrhoea associated - e.g. E. coli, toxins released that target renal endothelium

Non-Diarrhoea associated

  • Hypertension
  • Scleroderma
  • Antiphospholipid Antibody Syndrome (+/- SLE)
  • Defects in regulation of complement
  • Drugs (calcineurin inhibitors)
  • Radiation
  • Deficiency in ADAMTS13
37
Q

Name the four main diagnostic features of nephrotic syndrome.

A

Breakdown in selectivity of glomerular filtration barrier leading to protein leak

  • Proteinuria (>3.5g/day)
  • Hypoalbuminemia
  • Oedema
  • Hyperlipidaemia
38
Q

How are the causes of nephrotic syndrome grouped? Give an example of each.

A

Primary Glomerular Disease, Non-Immune Complex Related =

  • Minimal Change Disease
  • Focal Segmental Glomerulosclerosis

Primary Renal Disease, Immune Complex Mediated =

  • Membranous Glomerulonephritis

Systemic Disease =

  • Diabetes mellitus
  • Amyloidosis
  • SLE
39
Q

What is the characteristic/diagnostic feature of MCD?

A
  • Glomeruli look normal by light microscopy
  • Effacement of foot processes on EM
  • More common in children
40
Q

What is the prognosis with MCD vs FSGN?

A

MCD = generally responds to immunosuppression

FSGN = less likely to respond to immunosuppression

41
Q

Define focal segmental glomerulonephritis.

A
  • Focal = means <50% of glomeruli
  • Segmental = only part of the glomeruli
  • Sclerosis = scarred

Therefore: some partially scarred glomeruli

42
Q

Where do immune complexes deposit (IgG and C3) in membranous glomerulonephritis?

A

Associated with immune deposits on outside of glomerular basement membrane i.e. subepithelial

Most common cause of NEPHROTIC syndrome in adults

43
Q

What is the antibody directed against in primary MGN?

A

Primary disease –> antibody against phospholipase A2 type M receptor (PLA2R) in 75% of cases

44
Q

What are some secondary causes of MGN?

A

Need to exclude possibility of a secondary disease e.g.

  • Epithelial malignancy,
  • drugs,
  • infections,
  • SLE
45
Q

How common is diabetic nephropathy?

True or false: High glucose levels thought to be directly injurious in diabetic nephropathy.

A

Affects 30-40% of diabetics

True

46
Q

What are the stages of diabetic nephropathy?

A

Typically starts as microalbuminuria –> proteinuria –> nephrotic syndrome

Nodular Glomerulosclerosis (shown below, left to right)

  • Stage 1 – Thickening of basement membrane on EM
  • Stage 2 – Increase in mesangial matrix, without nodules
  • Stage 3 – Nodular lesions / Kimmelstiel-Wilson
  • Stage 4 – Advanced glomerulosclerosis
47
Q

What is amyloidosis? What structure does it tend to deposit in?

A

Amyloidosis - Deposition of extracellular proteinaceous material exhibiting β-sheet structure

48
Q

What are the commonest forms of amyloidosis in the kidney? What condition is each associated with?

A

Commonest forms in kidney are

  • AA - derived from serum amyloid associated protein (SAA), an acute phase protein; patients tend to have a chronic inflammatory state
  • AL - derived from Ig light chains; 80% of patients have multiple myeloma
49
Q

What stain is used in amyloidosis? Describe its appearance under normal light and polarised light.

A

Congo red

  • Normal light – salmon pink appearance*
  • Polarised – apple green appearance (birefringence)*
50
Q

What are two causes of microscopic haematuria?

A
  • Thin basement membranes
  • IgA Nephropathy
51
Q

What are some causes of asymptomatic proteinuria? What investigations would need to be done?

A

Broad range of glomerular structural abnormalities or immune complex deposition

Diagnosis often requires:

  • renal biopsy for histology
  • immunohistochemistry
  • EM
52
Q

What is the pathophysiology of thin BM? How is thin defined here? How does it present?

A
  • Hereditary defect in Type IV collagen synthesis
  • Basement membrane <250nm thickness

Presentation: haematuria is only consequence in most cases

53
Q

What genetic condition causes thin basement membranes? What is the prognosis?

A

Alport’s Syndrome

X-linked dominant - mutations affecting ⍺5 subunit (but forms exist in which mutation affects ⍺3 or ⍺4 subunit)

Prognosis: typically progressive, renal failure in middle age

Other features: deafness, ocular disease

54
Q

What is the most common glomerulonephritis?

A

IgA nephropathy

55
Q

What is the aetiology of IgA nephropathy? What condition can it be associated with?

A

–> IgA-predominant mesangial immune complex deposition

Aetiology:

  • Not well understood in primary form
  • Secondary forms observed in liver, bowel and skin disease
  • Can be seen with small-vessel vasculitis (Henoch-Schönlein Purpura)
56
Q

What classification system is used for IgA nephropathy?

A

Oxford classification (MEST-C)

57
Q

What are the stages of CKD?

A
58
Q

Define end stage renal failure. What stage of CKD is this?

A

eGFR <15

Stage 5 of CKD

59
Q

What is the most common cause of CKD requiring RRT? NB: unknown/uncertain in a lot of cases

A
  • Diabetes – 27.5%
  • Glomerulonephritis – 14.1%
  • Polycystic Kidney Disease – 7.4%
  • Pyelonephritis – 6.5%
  • Hypertension – 6.8%
  • Renal Vascular Disease – 5.9%
  • Other / Uncertain – 31.7%
60
Q

What is the pathophysiology of hypertensive nephropathy?

A

Not fully understood

Narrowing of arteries and arterioles–> to scarring and ischaemia of glomeruli

HTN in glomeruli –> altered haemodynamic environment, stress and segmental scarring

61
Q

What are the histological features of hypertensive nephropathy?

A

Gross: shrunken kidneys with granular cortices

Histopathology may show:

  • “nephrosclerosis”
  • arteriolar hyalinosis
  • arterial intimal thickening
  • ischaemic glomerular changes
  • segmental and global glomerulosclerosis
62
Q

How does SLE affect the kidney? Which antibodies are commonly found in the kidney in SLE?

A

–> deposition of immune complexes

Antibodies directed at a broad range of intracellular and extracellular antigens e.g. anti-nuclear and anti-dsDNA antibodies are typical

63
Q

What classification system is used for renal SLE?

A

ISN/RPS Classification

64
Q

How is renal SLE classified?

A
  1. Class 1 – near normal on light microscopy, minimal mesangial disease
  2. Class 2- mesangial deposits, not past BM
  3. Class 3- focal (i.e. <50%) disease, subendothelial deposits
  4. Class 4 – diffuse (>50%) disease, diffuse deposits
  5. Class 5 – membranous pattern, subepithelial depoists
  6. Class 6 – advanced sclerosis (>90%)

NB: Patients can move between classes; it is not necessarily progressive.

65
Q

Which classes of renal SLE are associated with these types of disease:

  • Mesangial ?
  • Endothelial ?
  • Epithelial ?
A
  • Mesangial - class II
  • Endothelial - class III and IV
  • Epithelial - class V
66
Q

List 4 ways in which renal SLE can present.

A
  1. Acute Renal Failure/AKI
  2. Nephrotic Syndrome
  3. Isolated Urinary Abnormality
  4. Chronic Kidney Disease
67
Q
A

1

  • LKM 1 and LKM 2 – AI hepatitis and chronic hepatitis respectively*
  • Desmoglein 1 and 2 – pemphigus and cardiac disease respectively*
68
Q
A

2

69
Q
A

1

  • Oil Red O – fat detection*
  • Sirius Red – scarring and fibrosis detection*
70
Q
A

2

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