Pathology of the urinary system Flashcards
1
Q
Name the features of a nephron
A
- renal corpuscle
- glomerulus with Bowmans capsule
- Tubular system
- prox convoluted tubule
- L of H
- distal convoluted tubule
- collecting duct
- intersititium (conn tissue)
- vasculature
2
Q
What occurs if 1 kidney is lost?
A
- compensatory hypertrophy of other kidney- nephrons increase in size
3
Q
What happens if you lose above 60% of functional nephrons?
A
- start to see signs of renal disease
4
Q
What id the nephron loss is more than 75%?
A
- renal failure
5
Q
What are the most common anomalies of renal development in domestic animals and describe their main features
A
Anomalies in the amount of renal tissue
- Agenesis (unilateral or bilateral) - kidney does not develop
- Renal hypoplasia- does not fully develop (reduced number of nephrons)
Anomalies of position, form and orientation
- malposition = renal ectopia, pevlic or inguinal location
- fusion e.g. horseshoe kidney
- fetal lobulation
Renal dysplasia
Renal cysts
- simple renal cysts
- polycystic kidney disease
- obstructive cysts
6
Q
What anomalie is this?
A
- unilateral renal agenesis
7
Q
What anomalie is this?
A
- horseshoe kidney
- fusion at the cranial poles
- not fatal as long as theres no blockage
8
Q
What anomalie is this?
A
- renal dysplasia
- bilateral asymmetric development
- small size and fibrous tissue strands
- disorganised development of renal parenchyma
- usually congenital
9
Q
What anomalie is this and which species would you expect to find it?
A
- simple renal cysts
- (pig + calves-common)
- no functional problems
10
Q
What anomalie is this and what species does it normally affect?
A
- feline PKD
- Persian cats and Bull terriers
- defects in polycistin gene
- concurrent cysts in liver, pancreas
11
Q
What are the circulatory disturbances of the kidney?
A
- renal hyperaemia
- renal haemorrhages
- renal infarction
- renal cortical necrosis
- renal medullary necrosis
- hydronephrosis
12
Q
What is Infarction?
A
- focal lesions of coagulative necrosis produced by embolic or thrombotic occlusion of the renal artery or one of its branches
- trunk of artery- subtotal infarction
- arcuate a. - wedge of cortex = medulla
- radiate vessel - just a wedge of cortex
13
Q
What is wrong with these kidneys?
A
- infarction
- well defined borders
- cortex not shiny
- lower pic = obstruction at apex
14
Q
Describe the sequelae of events from acute infarction to scarring
A
15
Q
What are Renal cortical necrosis and Acute tubular necrosis usually the result of?
A
- hypoperfusion or shock
- during hypotension
- perfusion of outer cortical nephrons is reduced
- perfusion of the deeper cortical nephrons is maintained
- = intrarenal blood flow is redistributed towards the inner cortex and medulla
16
Q
A
17
Q
Name the glomerular diseases
A
- multifocal/ embolic glomerulonephritis - inflammation of the glomerulus, also implies tubule-interstitial and vascular disease
- glomerulitis- inflammation restricted to the glomerulus
- glomerulopathy - glomerular disease with no inflammatory cell/ unknown aetiology
- diffuse glomerular disease
- membrano-proliferative
- membranous
- glomerulosclerosis - fibrosis of the glomeruli
- glomerular amyloidosis
18
Q
How does embolic/ multifocal glomerulitis occur?
A
- embolic through circulation
- bacteriaemia/ embolism -> lodges in glomeruli -> suppurative inflammation
- often induced directly by agent
- foals and calves
- Pigs - erysepelothrix rhuspathies
- foals - actinobacillae equi
- can cause septicaemia
19
Q
What is this showing?
A
20
Q
What is diffuse glomerulonephritis?
A
- 2 mechanisms:
- IC deposition on GBM - (non-glomerulus IC) - immune response
- Anti -GBM granulonephritis - immune response
- always immune responses in subep area or BM
- activation of the complement system
21
Q
What is membrano-proliferative glomerulonephritis?
A
- most common in dogs
- soluble IC deposit
- subendo
- intramembranous
- attracts leukocytes/ fixes complement
- neutrophils damage glomerulus
- proliferation of mesengial cells, accumulation of inflam cells, hypertrophy of endothelial cells
- thickening of the BM
22
Q
What is membranous glomerulonephritis?
A
- most common in cats
- soluble IC deposite
- subepithelial
- little inflammation
- little prolif of mesengial cells
- thickened BM (wire loop)
23
Q
Name the diseases associated with IC deposition
A
- dogs
- neoplasia
- pyometra
- Leishmania spp
- acute pancreatitis
- SLE
- canine adenovirus
- cats
- SLE
- FeLV
- Horses
- equine infectious anaemia
- streptococcus
- Pigs
- African and classical swine fever
24
Q
What is IC deposition normally associated with?
A
- diseases with prolonged antigenaemia
25
Q
What is glomerulosclerosis?
A
- end result - not revesible
- sequel to chronic glomerular disease
- increase in fibrous tissue
- increase in mesengial matrix
- loss of capillaries
26
Q
What is glomerular amyloidosis?
A
- amyloidosis = deposition of insoluble amyloid fibrils in extracellular spaces, disrupting normal function
- amyloid - from acute phase protein serum amyloid A (SAA)
- from liver (chronic inflam)
- familial disease - Abyssinian cat and Shar Pei dog = excess
- most animals - in glomeruli
- CATS EXCEPTION - in medulla (interstitium, vessel walls, tubular BM)
27
Q
What is this?
A
- Glomerular amyloidosis
- enlarged, pale, firm kidney
- waxy consistency
- prominent glomeruli on cut edge = grains of salt
- small, irregular ‘emd-stage- kidneys if blood supply affected
- can have secondary necrosis
- Lugols iodine and dilure sulfuric acid - red/ brown staining of amyloid
28
Q
What is shown?
A
- Glomerular amyloidosis
- glomeruli are enlarged by amorphous, pale eosinophilic deposits (amyloid)
- acellular
- same material deposited in medulla
- stains orange-red/ peach with Congo red
- apple green birefringence under polarised lught
29
Q
How would you describe this kidney?
A
- end stage
- small
- hard
- irregular
- finely granulated surface
- pale
- lost most of parenchyma
- fibrous tissue
- chronic kidney disease
30
Q
What is proteinuria?
A
- = hallmark of glomerular pathology and increased glomerular permeability (absence of haematuria and inflam)
- low - small proteins
- then damage increases - globulins + albumins
- weight loss, lethargy, decreased muscle mass
31
Q
What is Nephrotic syndrome?
A
- characterised by:
- hypoalbuminaemia
- hypercholestrolaemia
- ascites
- anasarca
- systemic oedema - reflects hypoalbuminaemia and activation of RAAS + independent intrarenal mechanisms (retains Na and water)
- liver responds to hypoalbuminaemia - by producing more protein and also LDLs - large so not lost through leaky glomerulus = hypercholestrolaemia
- animals with this = hypercoagulability
- hypoalbuminaemia promotes sticky platelet aggregation
- antithrombin only 6,500 daltons - so lost
- increased hepatic synthesis of large clotting factors
32
Q
How does renal failure occur from glomerular disease?
A
- decreased glomerular capillary blood flow
- decreased GFR
- decreased formation of ultrafiltrate
- decreased perfusion of peritubular capillaries
- decreased blood suppl to tubules and renal intersitium
- loss of entire nephron
- lead to acute or chronic renal failure
33
Q
What is a difference between toxic and ischaemic injury (ATI)?
A
- toxic - lose an area involving several nephrons
- ischaemic - lose segments (lack of O2)
34
Q
A
35
Q
What are the causes of ischaemic ATI?
A
- prolonged hypotension (shock - haemorrhagic, post-op)
- ischaemia - severe dehydration, heat stroke, anaemia, burns
- necrosis of tubular ep and BM
36
Q
What are the causes of Nephrotoxic ATI?
A
- drugs
- aminoglycosides e.g. gentamycin
- cisplatin
- tetracyclines
- amphotericin
- oxalate
- ethylene glycol
- plants containign oxalate - halogeton, rhubarb
- melamine and cyanuric acid
- plants
- amaranthus
- quercus spp
- lilium
- grapes and raisins
- pigments
- haemoglobin
- myoglobin
- bacterial toxins
- C.perfringens type D
37
Q
What are the mechanisms of action of the toxic renal drugs?
A
- aminoglyocides - direct tubular toxicity and vasoconstriction
- cisplatin - direct tubular damage and RAAS system vasoconstriction
- tetracyclines - direct tubular toxicity
- amphotericin B - direct tubular toxicity
38
Q
What is this?
A
- tetracyclin toxicity, cattle
- tubular necrosis = pink
39
Q
Explain the pathogenesis of aminoglycosides
A
- aminoglycosides filtered by the glomerulus
- stick to the phospholipids in the brush border of proximal convulted tubular ep cells
- enter via pinocytosis
- fuse with lysosomes
- inhibit lysosomal enzymes e.g. phospholipase, sphingomyelinase
- the lysosomal enzymes cannot degrade the phospolipid rich cell membranes (phosphlipidosis)
- membranes accumulate in phagolysosome
- formation of myeloid bodies - lamellar structures that contain undegraded phospholipid)
- lysosomes enlarge and rupture
- enzyme leakafe causes cellular degradation and necrosis
- also inhibit Na-K-ATPase
- influx of Hydrogen and sodium
- influx of water
- cellular swelling
- cell death
40
Q
A
- aminoglyoside toxicity
- accumulation of lamellar bodies which eventually cause necrosis of tubular ep cells
- blue = myelin body
41
Q
Why is ethylene glycol toxic?
A
- antifreeze
- young dogs - 6.6 ml/kg
- cats - 1.5 ml/kg
- cattle
- small amount oxidised by alcohol dehydrogenase in the liver
- glycoaldehyde
- glycolic acid
- glycoxylate
- oxalate binds to Ca - filtered by glomeruli
- as water is reabsorbed by tubules and pH of the filtrate decreases, calcium oxalates precipitate to form crystals
- renal tubular blockage
- degeneration and necrosis
- nephrosis
- hypocalcaemia, uraemia
- renal failure, death
42
Q
What would be seen in ethylene glycol poisoning?
A
- large numbers of crystals in the tubules is nearly pathognomonic for EG
- tubular estasia, renal ep cell degeneration and necrosis , with a PRESERVED tubular BM
- the calcium oxalate crystals - found in the intersitium, tubular ep cells and prox tubule lamina
- light yellow
- arranged in sheaves, rosettes and prisms
43
Q
WHat is seen here?
A
- calcium oxalate crystals sticking to ep membrane
44
Q
What are these?
A
- rhubarb
- halogeton
- contain oxalate at toxic levels
45
Q
What is melamine nephrosis?
A
- melamine - pet food contaminant
- falsely increases protein content
- china, 2007
- used to make plastic, fertilizer, dyes
- it sticks in the tubules
- big brown crystals
- causes massive tubular ep necrosis
- clinical signs in a couple of days
46
Q
What is this?
A
- melamine nephrosis
47
Q
What is this showing? which animal does it effect?
A
- lily toxicity
- cats - very small amounts
- acute tubular necrosis
48
Q
Is nephrotoxicosis reversible?
A
- in absence of renal failure - yes
- proximal convoluted tubule ep cells will regenerate - BM preserved
49
Q
What is haemoglobinuria?
A
- intravascular haemolysis - rupture of erythrocytes
- chronic copper toxicity in sheep
- red maple leaf toxicity
- leptospirosis
- babesiosis
- Haemoglobin binds to haptoglobin - transport (HG = 65)
- it is not secreted in urine if bound to haptoglobin - but if haptoglobin is saturated then it is - haemoglobinuria
- the tubular ep reabsorb some of it and stored as ferritin and haemosiderin
- TOXIC
50
Q
A
51
Q
WHat is this?
A
- foal, haemoglobinuric nephrosis due to Babesia equi
- would also have red urine due to haemoglobin in urine
52
Q
What is this?
A
- myoglobinuria
- rhabomyolysis - rupture of skeletal muscle
- azoturia - monday morning disease - horses
- capture myopathy - exotic/ wild
- direct trauma to muscle
- release of myoglobin from muscles -> go through glomerular filtration system
- passed out in urine
- renal ischaemia secondary to hypovolaemic shock
- (myoglobin increases tubular toxicity)
- myoglobinuric nephrosis
- rhabomyolysis - rupture of skeletal muscle
53
Q
What are the tubulo-interstitial diseases?
A
- interstitial nephritis
- suppurative
- non-suppurative
- pyelonephritis - inflam of renal pelvis
54
Q
What is intersitial nephritis?
A
- accumulation of inflam cells in interstitium
- interference with transport between tubules and capillaries
- can affect resoption
55
Q
WHat is non-suppurative interstitial nephritis?
A
- inflammation against arteries, veins, lymohatics, connective tissue
- usually non-consequential
- non-specific
- granulomatous / lymphoplasmatic
- duration - chronic more common - fibrosis and atrophy
56
Q
What is supurative interstitial nephritis?
A
- haematogenous (embolic)
- ascending from lower urinary tract
57
Q
What is the difference between primary and secondary intersitial nephritis?
A
- primary - specifically target kidneys
- leptospira
- encephalitozoon cuniculi - rabbits
- white spotted kidneys
- secondary (involvement as part of systemic disease)
- feline infectious peritonitis
- embolic nephritis
- larva migrans in dogs (toxocara )
58
Q
What is leptospirosis?
A
- specifically targets kidneys
- septicaemia
- nephritis
- hepatitis
- meningitis
- abortion
- stillbirth
- natural reservoir = proximal convoluted tubules
- dogs
- leptispira interrogans var canicola, icterohaemorrhagiae and others
- pigs/ cattle
- leptospira interrogans var pomona
59
Q
Describe the lesions of leptospirosis?
A
- acute renal injury
- leptospira reaches renal capillaries
- persists to intersitium (interisitial inflam)
- migrates through tubular ep and into lumen
- associates with ep microvilli
- degeneration and necrosis of tubular ep
- septicaemia/ bacteraemia -> haemolysis -> haemoglobinuria
- acute liver disease
- placentitis (pig and cattle) -> abortion
60
Q
What is this?
A
- pig, intersitial nephritis - white flat coalescing spots in cortex
- multifocal white lesions - accumualtion of lymphocytes and plasma cells in interstitium
61
Q
What is this?
A
- dog, chronic intersitial nephritis
- fibrosis
- scarring
- atrophy
- parenchyma lost - end stage
62
Q
What is white spotted kidneys?
A
- best known as non-suppurative interstitial nephritis
- early lesions - suppurative / chronic - non
- incidental finding - calves
- multifactoral - E.coli, salmonella, leptospira, brucella
63
Q
A
- white spotted kidneys
- radial or wedge-shaped inflam infiltrate expands the intersitium
64
Q
What is this showing?
A
- encephalitozoon cuniculi
- obligate, intracellular microsporidiam parasite
- commonly results in latent infection of lab rabbits
- wide range of hosts
- immunosupression - clinical disease - lesions in brain and kidneys
- macrophages cannot clear infection - persistent
65
Q
What would be seen in kidneys and brain with encephalitozoon cuniculi?
A
- kidneys - granulomatous/ nonsuppurative inflam - organisms present in ep and lumina of tubules, glomerular caps, in intersitium
- brain - granulomatous meningoencephalilitis, foci of malacia
66
Q
What is this?
A
- feline infectious peritonitis
- round lesions
- granulomatous inflam
- white coalescing nodules
- differential = renal lymphoma
67
Q
WHat is suppurative intersitial nephritis?
A
- analogous to abscess formation in any organ
- seeding of bacteria in bacteraemia or thromboembolism
- usually start from glomeruli
- agents
- horses
- actinobacillus equuli
- swine
- erysipelothrix rhusiopathiae
- cattle
- trueperella pyogenes
- sheep and goats
- corynebacterium pseudotuberculosis
- horses
68
Q
What is pyelonephritis?
A
- inflam of the renal pelvis and renal parenchyma
- infections ascending from lower urinary tract
- E.coli, strept, staph, enterobacter, proteus, pseudomonas
- mechanism: vesico-ureteral reflux
- during micturition
- manual compression of bladder
- medulla - most susceptible
69
Q
WHat is this?
A
70
Q
What causes renal gout?
A
- result of impaired excretion by kidneys and overproduction of uric acid
- increased plasma conc of uric acid - hyperuricaemia
- precipitation of monosodium urate crystals (tophi) on visceral and articular surfaces
- inflam and fibrosis
- causes of impaired excretion
- severe dehydration
- renal disease
- postrenal obstruction
- nephrotoxic drugs
71
Q
What causes gout in birds?
A
- cold/ damp
- vit A/ B12 def
- type A influenza
- high protein diets
- dehydration
72
Q
What is this?
A
- gout
73
Q
A
- numerous tophi expand the tubular lumen and cause degen and necrosis of the tubular ep
- granulmatous inflam surrounding tophi
74
Q
What is gout?
A
- characterised by urate crystal deposition on articular/ synovial surfaces of joints and serous surfaces of viscera in birds, reptiles, humans
- catabolism of purines (nucleotides and dietary)
- adenine -> inosine -> hypoxanthine -> xanthine -> uric acid -> allantoin
- guanine -> xanthine -> uric acid -> allantoin
- humans and higher apes, birds and reptiles - no uricase (uric acid -> allantoin)
- uric acuid normally eliminated by glomerular filtration, secretion, reabsorption, post-secretory reabsorb
- 8-12% - excreted
- 90% reabsorbed
75
Q
What is renal neoplasia?
A
- renal adenoma - benign
- renal carcinoma - malignant
- nephroblastoma
76
Q
A
