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YEAR 5: HISTOPATH > Histo: Renal Disease > Flashcards

Histo: Renal Disease Flashcards

1
Q

List the major functions of the kidneys.

A
  • Excretion of metabolic waste products and foreign chemicals
  • Regulation of fluid, electrolytes and acid/base balance
  • Regulation of blood pressure (renin)
  • Regulation of calcium and bone metabolism (1,25-dihydroxy vitamin D)
  • Regulation of haematocrit (EPO)
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2
Q

List some key anatomical features of the kidneys.

A
  • Retroperitoneal
  • T12-L3
  • Right kidney lies lower
  • Mean length = 11cm
  • Normal weight = 115-170g
  • 1 million nephrons per kidneys - can lose of lot of nephrons without decrease in funciton
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3
Q

What proportion of cardiac output goes to the kidneys?

A

20%

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4
Q

By what mechanism is blood filtered through the glomerulus?

A
  • High hydrostatic pressure (60 mmHg)
  • Podocytes create a charge-dependent (anionic) and size-dependent barrier
  • Filtration rate = 125 ml/min
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5
Q

Describe the role of the following parts of the nephron:

  1. Proximal convoluted tubule
  2. Loop of Henle
  3. Distal convoluted tubule
  4. Collecting duct
A
  1. Proximal convoluted tubule
    • Actively absorbs sodium
    • Carries out hydrogen exchange to allow carbonate resoprtion
    • Co-transport of amino acids, phosphate and glucose
    • Reabsorption of potassium
  2. Loop of Henle
    • Descending limb and thin ascending limb: permeable to water, impermeable to ions and urea
    • Ascending limb: actively resorbs sodium and chloride
    • This creates a counter-current multiplier that is aligned with the vasa recta
  3. Distal convoluted tubule
    • Impermeable to water
    • Regulates pH by active transport of protons and bicarbonate
    • Regulates sodium and potassium by active transport (aldosterone)
    • Regulates calcium (PTH, 1,25-dihydroxy vit D)
  4. Collecting duct
    • Reabsorb water (principal cells, ADH)
    • Regulates pH (intercalated cells, proton excretion)
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6
Q

Describe how immune complex deposition can lead to renal disease.

A

Complex deposition in the glomerulus results in complement and inflammatory cell activation resulting in damage to the kidney

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7
Q

List some signs and symptoms of renal disease.

A
  • Haematuria
  • Proteinuria
  • Uraemia
  • Hypertension
  • Oliguria/anuria
  • Polyuria
  • Oedema
  • Colic
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8
Q

List some genitourinary malformations of the kidney.

A
  • Agenesis
  • Renal fusion - e.g. horseshoe
  • Ectopic kidney
  • Renal dysplasia
  • PUJ obstruction
  • Posterior urethral valve
  • Vesicoureteric reflux
  • Ureteral duplication

congenital

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9
Q

Outline the presentation of polycystic kidney disease.

A
  • Hypertension
  • Haematuria
  • Flank pain
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10
Q

What is the inheritance pattern of polycystic kidney disease and which genes are implicated?

A

Autosomal dominant (most of the time)

Genes: PKD1 and PKD2

NOTE: PKD is associated with an increased risk of berry aneurysms (and subarachnoid haemorrhage)

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11
Q

In which group of renal patients do renal cysts often develop?

A

Patients with end-stage renal disease who are on dialysis

Cysts are often:
multiple
bilateral
cortical and medullary

NOTE: cystic disease is associated with increased risk of malignancy (papillary renal cell carcinoma)

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12
Q

List the renal syndromes

A
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13
Q

List some causes of acute renal failure.

A
  • Pre-renal = failure of perfusion (shock, heart failure)
  • Renal = ATN, acute glomerulonephritis, thrombotic microangiopathy
  • Post-renal = obstruction (enlarged prostate, stones)
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14
Q

What is the most common cause of acute renal failure?

A

Acute tubular injury

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15
Q

List some causes of acute tubular injury.

A

Tubular epithelial cells damaged by:

Ischaemia

Toxins (contrast, haemoglobin, myoglobin, ethylene glycol)

Drugs

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16
Q

Which commonly used class of drugs predisposes to acute tubular injury?

A

NSAIDs - inhibits vasodilatory prostaglandins which predisposes to ATN

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17
Q

How does acute tubular injury lead to reduced GFR?

A
  • Blockage of tubules by casts (dead cells)
  • Leakage from tubules into interstitial space
  • Secondary haemodynamic changes (due to the blockage/leakage)

dramatic decrease, but potentially reversible + no scarring

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18
Q

What is acute tubulo-interstitial nephritis?

A

Immune injury to tubules and interstitium

Can be caused by infection (TB) and **drugs **(NSAIDs, antibiotics, diuretics, allopurinol, PPIs)

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19
Q

what drugs cause actue tubulo-interstitial nephritis

A
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20
Q

Describe the histological appearance of acute tubulo-interstital nephritis.

A

Heavy interstitial infiltration with eosinophil and granulomas

Consider TB and sarcoid, but most common is drugs

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21
Q

What causes crescents to appear in acute glomerulonephritis?

A

Occurs in severe glomerulonephritis due to proliferation of cells within Bowman’s capsule

22
Q

List some causes of acute crescentic glomerulonephritis.

A
  • Immune complex deposition e..g IgA nephropathy)
  • Anti-GBM disease (Goodpasture’s) - renal emergency
  • Pauci-immune (ANCA)

NOTE: these can rapidly lead to irreversible renal failure –> urgent needs diagnosis + treatment

23
Q

List some causes of immune complex-associated crescentic glomerulonephritis.

A
  • SLE
  • IgA nephropathy
  • Post-infectious glomerulonephritis
24
Q

What techniques can be used to visualise immune complexes in these diseases?

A

Immunohistochemistry

Electron microscopy

25
Q

What are the antibodies directed against in anti-GBM disease?

A

Against the C-terminal domain of type IV collagen

NOTE: these antibodies can cross-react with the alveolar basement membrane leading to pulmonary haemorrhage and haemoptysis

26
Q

Describe the immunohistochemistry picture produced in anti-GBM disease,

A

Linear deposition of IgG on the glomerular basement membrane

Also can detect antibody on serology

27
Q

What are the main features of pauci-immune crescentic glomerulonephritis?

A
  • Scanty glomerular immunoglobulin depositis
  • Usually associated with ANCA
  • Triggers neutrophil activation and glomerular necrosis
  • Vasculitis elsewhere
28
Q

What is thrombotic microangiopathy?

A
  • Damage to the endothelium in glomeruli, arterioles and arteries resulting in thrombosis
  • Red cells can be damaged by fibrin causing MAHA or HUS
29
Q

List some causes of thrombotic microangiopathy.

A
  • Diarrhoea-associated: E. coli - toxins can target the renal epithelium
  • Non-diarrhoea associated: defects in complement regulation, deficiency of ADAMTS13, drugs (calcineurin inhibitors - post transplant), radiation, hypertension, scleroderma, antiphospholipid syndrome
30
Q

What are the characteristic features of nephrotic syndrome?

A
  • Proteinuria (>3,5 g/day or >300mg/mmol PCR)
  • Hypoalbuminaemia
  • Oedema
  • Hyperlipidaemia
31
Q

List some causes of nephrotic syndrome.

A
  • Primary glomerular disease (non-immune complex mediated)
    • Minimal change disease
    • Focal segmental glomerulosclerosis
  • Primary renal disease (immune complex mediated)
    • Membranous glomerulonephritis
  • Systemic disease
    • SLE
    • Amyloidosis
    • Diabetes mellitus
32
Q

What is minimal change disease?

A
  • most common cause of nephrotic syndrome in children
  • Glomeruli look normal on light microscopy, but electron microscopy shows loss of foot processes
  • Generally responds well to steroids and immunosuppression
33
Q

Describe the histological appearance of focal segmental glomerulosclerosis.

A

Some glomeruli are partially scarred, some are intact

NOTE: this responds less well to immunosuppression

this is a diagnosis, not descriptive term

34
Q

What is membranous glomerulonephritis?

A
  • Common cause of nephrotic syndrome in adults
  • Characterised by immune deposits outside the glomerular basement membrane (subepithelial)
  • Primary disease is autoimmune
  • It can occur secondary to epithelial malignancy, SLE, drugs and infections

remember to exclude malignancy as a cause

35
Q

Which antibodies are often found in primary membranous glomerulonephritis?

A

Antibodies against phospholipase A2 type M receptor (PLA2R)

36
Q

Describe the typical progression of diabetic nephropathy.

A

Typically begins with microalbuminuria

Progresses to proteinuria and, eventually, nephrotic syndrome

37
Q

List and describe the stages of diabetic nephropathy.

A
  • Stage 1: thickening of the basement membrane on electron microscopy
  • Stage 2: increase in mesangial matrix, without nodules
  • Stage 3: nodular lesions/Kimmelstein-Wilson nodules
  • Stage 4: advanced glomerulosclerosis
38
Q

What is amyloidosis?

A

Deposition of extracellular proteinaceous material exhibiting beta-pleated sheet structure

39
Q

What are the two types of amyloidosis?

A
  • AA - derived from serum amyloid protein and associated with chronic inflammatory disease
  • AL - derived from immunoglobulin light chains usually as a result of multiple myeloma
40
Q

Name two causes of isolated microscopy haematuria.

A
  • Thin basement membrane
  • IgA nephropathy
41
Q

what is the staining for amyloidosis

A

congo red

normal light - salmon pink
polarised light - apple green

42
Q

How can the cause of asymptomatic proteinuria be confirmed?

A

Renal biopsy (could be caused by several abnormalities)

43
Q

What is thin basement membrane disease and what causes it?

A
  • Basement membrane <250 nm thickness
  • Caused by a hereditary defect in type IV collagen synthesis
  • Microscopic haematuria is the only consequence in most cases

Can be caused by Alport syndrome

44
Q

What is Alport syndrome?

A
  • X-linked disease caused by a mutation in the alpha-5 subunit of type IV collagen (some forms affect alpha-3 and alpha-4)
  • Leads to progressive damage resulting in renal failure in middle-age
  • Often accompanied by deafness and ocular disease
45
Q

What is IgA nephropathy?

A
  • Most common cause of glomerulonephritis
  • Caused by mesangial IgA immune complex deposition
  • 30% will progress to end-stage renal failure

NOTE: Henoch-Schonlein purpura is a type of IgA nephropathy

46
Q

List some causes of chronic kidney disease and state which is most common.

A
  • Diabetes mellitus
  • Glomerulonephritis
  • Polycystic kidney disease
  • Pyelonephritis
  • Hypertension
  • Renal vascular disease
  • Unknown

Unknown is most common
Of the known causes most common is diabetes

46
Q

How is IgA nephropathy scored

A

Oxford classication

MEST-C

best prognosis if 0 in all categories

47
Q

What are some diseases associated with chronic kidney disease?

A
  • Ischaemic heart disease
  • Calcium and phosphate derangement (due to resulting hyperparathyroidism, osteomalacia and osteoporosis)
48
Q

What are consequences of hypertensive nephropathy?

A
  • Shrunken kidneys with granular cortices
  • Nephrosclerosis on histology (arterial hyalinosis, arterial intimal thickening, ischaemic glomerular changes, segmental and global glomerulosclerosis)
49
Q

What system is used to classify lupus nephritis?

A

ISI/RPS classification

50
Q

How does SLE affect kidneys

A

deposition of immune complexes in kidneys (along with in skin, joints, heart, CNS)

anti-dsDNA, anti-nuclear antibodies

has a very variable effect on kidneys

patient can present with - actue renal failure, nephrotic syndrome, isolated urinary abnormality, CKD

YEAR 5: HISTOPATH (20 decks)

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