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PATHOLOGY > renal pathology > Flashcards

renal pathology Flashcards

1
Q

what are the major kidney functions

A
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2
Q

macro anatomy of the kidney

A
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3
Q

what allows the blood to be filtered at the glomerulus

A

High hydrostatic pressure (60mmHg)

Podocytes create charge-dependent (anionic ie –ve charge) helps retain protein and size-dependent barrier

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4
Q

what is the volume of filtrate

A

125ml/min

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5
Q

what makes up the tubules

A

Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Collecting tubule
Collecting Duct

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6
Q

role of PCT

A
  • actively resorbs sodium
  • Hydrogen exchange to allow carbonate resorption
  • Co-transport of amino acids, phosphate, glucose
  • Potassium reabsorbed
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7
Q

role and structure of loop of henle

A

it doubles back on itself

  • Descending / thin ascending limb permeable to water but not ions or urea;
  • ascending limb actively resorbs sodium and chloride
  • Countercurrent Multiplier allow concentrate urine; aligned with vasa recta
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8
Q

role of the distal convoluting tubule

A

impermeable to water
* regulates pH by active trasnport (proton/bicarb)
* Regulates sodium, potassium via active transport (aldosterone)
* Regulates calcium (parathyroid hormone, 1,25 dihydroxycholecalciferol

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9
Q

role of the collecting duct

A

resorbs water - principle cells, ADH

regulates pH - intercalated cells, proton excretion

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10
Q
A

Low power view of cortex

Renal corpuscles

Between them you see tubules

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11
Q
A

EM

Podocytes – form foot processes tat interdigitate that form barrier

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12
Q
A

Podocytes on outside of loop
Between are the filtration spaces

Fenestrated endothelial cells – spaces between

Endothelial are on outside where blood is

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13
Q

effect of immune complexes in kidney

A

Latticework of antibody and antigen
May be endogenous or exogenous antigens

May deposit in the glomerulus ->
* Inflammatory response
* Complement activation
* Stimulation of inflammatory cells

May deposit at different rates
May deposits at different sites – depend where deposits on the manifestation

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14
Q
A

Basement membrane v thick
No podocytes – effaced
Normal loop of endothelial cells
Blotches in BM = electron dense deposits towards podocyte aspect ie subendothelial

Immuoflurence shows what it is IgG – fits with membranous glomerulonephritis depending on clinical picture

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15
Q

signs and sx in any renal disease

A

Haematuria
Proteinuria
Uraemia
Hypertension
Oliguria / Anuria
Polyuria
Oedema
Colic

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16
Q

what are some congenital diseases of kidney

A

Agenesis
Renal Fusion (e.g. horse-shoe)
Ectopic Kidney
Renal Dysplasia (hasn’t grown properly)
Pelvi-ureteric Junction Obstruction
Ureteral Duplication
Vesicoureteral Reflux
Posterior urethral Valves

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17
Q
A

horse-shoe kidney ie renal fusion

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18
Q

what is autosomal dominant polycystic kidney disease

A

common
10% of end-stage renal failure
Presents in adulthood with
* hypertension,
* flank pain
* haematuria because of the size

mutations: PKD1, PKD2
-> Berry aneurysm -> SAH

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19
Q

who gets cysts in the kidney and consequences

A

end stage renal disease who are on dialysis = acquired cystic disease
* Multiple
* Bilateral
* Cortical and Medullary

->

Increased risk of malignancy
7% risk at 10 years
Papillary renal cell carcinoma from from cells of prox convoluted tubule

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20
Q

what is AKI

A

Rapid deterioration in renal function (hours, days)

common

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21
Q

causes of AKI

A

Pre-Renal:
* Failure of perfusion (normally get 20% perfusion)

Renal:
* Acute tubular injury,
* acute glomerulonephritis,
* thrombotic microangiopathy

Post-Renal:
* Obstruction (stones/prostatism)

22
Q

summarise acute tubular injury

A

Commonest cause of acute renal failure

Tubular epithelial cells damaged by:
* Ischaemia
* Toxins (contrast, haemoglobin, myoglobin, ethylene glycol)
* Drugs

Common in critical illness

Drugs that inhibit vasodilatory prostaglandins predispose eg NSAIDs

23
Q

changes in acute tubular injury

A

Changes in order of time:

  1. Loss of brush border
  2. Loss of integrin
  3. Degradation of ATPase
  4. Apoptosis of cells -> fall into lumen/necrotic
  5. Cells that have survived spread out and try and de-differentiate -> flatterned appearance
  6. Proliferation and differentiation and back to polarised state hopefully
24
Q

consequence of acute tubular injury

A

Failure of Glomerular Filtration because:

  • Blockage of tubules by casts ->
  • Leakage of tubules to interstitial space ->
  • Secondary haemodynamic changes - knock on effect on GFR
25
Q

summarise acute tubulo-interstitial nephritis

A

Immune injury to tubules and interstitium

Can also be due to infection and drugs
* NSAIDs
* Antibiotics
* Diuretics
* Allopurinol
* Proton Pump Inhibitors

Heavy interstitial inflammatory infiltrate with tubular injury
* Can see eosinophils, granulomas – drugs are the most common cause

26
Q

what is acute glomerulonephritis

A

**Acute inflammation of glomeruli**

Presents with
* oliguria
* **urine casts containing erythrocytes and leucocytes** – because of inflammation in glomeruli

When sufficient to cause acute renal failure, there are almost always **crescents** - **Proliferation of cells within Bowman’s space**

27
Q

what is acute cresenteric glomerulonephritis

A

when most glomeruli have cresents

caused by:
* Immune Complex
* Anti Glomerular Basement Membrane Disease
* Pauci-immune (anti-neutrophil cytoplasm antibodies) – means could be some immune complex deposition eg in ANCA vasculitis

Leads rapidly to irreversible renal failure
Correct diagnosis and treatment are urgent

28
Q

summarise immune complex associated glomerulonephritis

A

caused by:
* SLE
* IgA nephropathy
* Post-Infectious Glomerulonephritis

Immune complexes can be identified and localised with immunohistochemistry and electron microscopy
Final diagnosis depends on specific findings interpreted within the appropriate clinical context.

29
Q

summarise anti-GBM disease

A

Rare and severe disease

antibodies directed against the glomerular basement membrane

Ab against C-terminal domain of Type IV collagen

May cross-react with alveolar basement membrane -> pulmonary haemorrhage

Antibody may be detected with serology

Linear deposition of IgG demonstrable on glomerular basement membrane
silver stain

30
Q

summarise pauci-immune cresenteric glomerulonephritis

A

Only scanty glomerular immunoglobulin deposits

Usually ANCA-associated

Trigger neutrophil activation and glomerular necrosis

Vasculitis elsewhere

Cresental necrosis

31
Q

pathology of thrombotic microangiopathy

A

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

Loops are full of thrombus
Arterioles are blocked with cellular material and thrombin

Red cells may be damaged by fibrin ->
* Microangiopathic haemolytic anaemia
* Haemolytic Uremic Syndrome

32
Q

causes of thrombotic microangiopathy

A

Diarrhoea associated
* Bacterial gut infection such as with E. coli
* Toxins released that target renal endothelium

Non-Diarrhoea associated
* Defects in regulation of complement
* Deficiency in ADAMTS13
* Drugs (calcineurin inhibitors)
* Radiation
* Hypertension
* Scleroderma
* Antiphospholipid Antibody Syndrome (+/- SLE)

33
Q

definition of nephrotic syndrome

A

Breakdown in selectivity of glomerular filtration barrier leading to protein leak

Proteinuria (>3.5g/day)
Hypoalbuminemia
Oedema
Hyperlipidaemia

34
Q

causes of nephrotic syndrome

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

35
Q

features of minimal change disease

A
  • Glomeruli look normal by light microscopy
  • Effacement of foot processes on electron microscopy
  • Common cause of nephrotic syndrome in children
  • Generally responds to immunosuppression
36
Q

what is focal segmental glomerulonephritis

A

def: Some glomeruli are partially scarred

Less likely to respond to immunosuppression – once have scarring it is less likely to go away

No immune complexes

Must exclude possible other diseases that can produce a similar appearance
* These tend not to be nephrotic
* IgA nephropathy
* Lupus

37
Q

summarise membranous glomerulonephritis

A

Associated with immune deposits (IgG and C3) on outside of glomerular basement membrane
Subepithelial -> impair function of podocytes

Common cause of nephrotic syndrome in adults

Primary disease is autoimmune
* Antibody against phospholipase A2 type M receptor (PLA2R) in 75% of cases

Need to exclude secondary disease
* Epithelial malignancy,
* drugs,
* infections,
* SLE

Interpret findings in clinical and serological context

38
Q

cause and epi of diabetic nephropathy

A

30-40% of diabetics
High glucose levels thought to be directly injurious
Typically starts as microalbuminuria -> proteinuria -> nephrotic syndrome

39
Q

stages of diabetic neuropathy

A

Nodular Glomerulosclerosis
* 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

40
Q

how does amyloidosis effect the kidney

A

Abnormally folded protein material

Deposition of extracellular proteinaceous material exhibiting β-sheet structure

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 immunoglobin light chains; 80% of patients have multiple myeloma

41
Q

what are the isolated urinary abnormalities

A

Microscopic Haematuria
* Thin basement membranes
* IgA Nephropathy

Asymptomatic Proteinuria
* May be associated with a broad range of glomerular structural abnormalities or immune complex deposition
* Diagnosis often requires renal biopsy for histology, immunohistochemistry and electron microscopy

42
Q

summarise thin basement membrane

A

Hereditary defect in Type IV collagen synthesis

Basement membrane less than 250nm thickness

Haematuria is only consequence in most cases

43
Q

summarise Alport syndrome

A

X-linked dominant mutations affecting ⍺5 subunit
Forms exist in which mutation affects ⍺3 or ⍺4 subunit
Typically progressive, renal failure in middle age
Often have deafness, ocular disease
Show normal or thickened BM – but look like branching tissue

44
Q

what is IgA nephropathy

A

Commonest glomerulonephritis
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)

30% develop end stage renal failure

45
Q

classification of IgA nephropathy

A

Oxford Classification (MEST-C) – scoring in any of these = worse px – higher = more likely end stage renal failure

  • M – how many cells in mesangium – 1 = too much, 0 = right amount
  • E – endocapillary proliferation
  • S – segmental scarring
  • T – tubular atrophy less than 25% 25-50% >50%
  • C – cresents – yes in some, yes in a lot, no
46
Q

what is CKD associated with

A

ischaemic heart disease
* Hypertension,
* hyperlipidaemia,
* calcification of blood vessels

Association with calcium and phosphate metabolic derangement
* Hyperparathyroidism
* osteomalacia
* osteoporosis

Not always clear which is the driver and what is the cause

47
Q

stages of CKD

A
48
Q

causes of CKD

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%

49
Q

summarise hypertensive nephropathy

A

Pathophysiology is not fully understood

Narrowing of arteries and arterioles -> scarring and ischaemia of glomeruli

Hypertension in glomeruli -> altered haemodynamic environment, stress and segmental scarring

Shrunken kidneys with granular cortices

Histopathology may show “nephrosclerosis”
* Arteriolar hyalinosis,
* arterial intimal thickening,
* ischaemic glomerular changes,
* segmental and global glomerulosclerosis

50
Q

summarise SLE

A
  • SLE is a systemic autoimmune disease
  • Affects the kidney, skin, joints, heart, serosal surfaces and the central nervous system
  • common
  • > women
  • Deposition of immune complexes in the kidney is common
  • Anti-nuclear and Anti-dsDNA antibodies are typical
51
Q

classification of SLE in kidney

A
52
Q

effect of SLE on kidney

A

Highly variable disease

Depending on site, speed and intensity of immune complex deposition, may present as:
* Acute Renal Failure
* Nephrotic Syndrome
* Isolated Urinary Abnormality
* Chronic Kidney Disease

PATHOLOGY (94 decks)

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