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Pathology of the urinary system Flashcards

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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
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2
Q

What occurs if 1 kidney is lost?

A
  • compensatory hypertrophy of other kidney- nephrons increase in size
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3
Q

What happens if you lose above 60% of functional nephrons?

A
  • start to see signs of renal disease
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4
Q

What id the nephron loss is more than 75%?

A
  • renal failure
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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
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6
Q

What anomalie is this?

A
  • unilateral renal agenesis
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7
Q

What anomalie is this?

A
  • horseshoe kidney
  • fusion at the cranial poles
  • not fatal as long as theres no blockage
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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
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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
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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
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11
Q

What are the circulatory disturbances of the kidney?

A
  • renal hyperaemia
  • renal haemorrhages
  • renal infarction
  • renal cortical necrosis
  • renal medullary necrosis
  • hydronephrosis
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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
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13
Q

What is wrong with these kidneys?

A
  • infarction
    • well defined borders
    • cortex not shiny
    • lower pic = obstruction at apex
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14
Q

Describe the sequelae of events from acute infarction to scarring

A
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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
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16
Q
A
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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
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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
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19
Q

What is this showing?

A
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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
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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
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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)
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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
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24
Q

What is IC deposition normally associated with?

A
  • diseases with prolonged antigenaemia
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25
What is glomerulosclerosis?
* end result - not revesible * sequel to chronic glomerular disease * increase in fibrous tissue * increase in mesengial matrix * loss of capillaries
26
What is glomerular amyloidosis?
* 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
What is this?
* 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
What is shown?
* 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
How would you describe this kidney?
* end stage * small * hard * irregular * finely granulated surface * pale * lost most of parenchyma * fibrous tissue * chronic kidney disease
30
What is proteinuria?
* = 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
What is Nephrotic syndrome?
* 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
How does renal failure occur from glomerular disease?
* 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
What is a difference between toxic and ischaemic injury (ATI)?
* toxic - lose an area involving several nephrons * ischaemic - lose segments (lack of O2)
34
35
What are the causes of ischaemic ATI?
* prolonged hypotension (shock - haemorrhagic, post-op) * ischaemia - severe dehydration, heat stroke, anaemia, burns * necrosis of tubular ep and BM
36
What are the causes of Nephrotoxic ATI?
* 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
What are the mechanisms of action of the toxic renal drugs?
* aminoglyocides - direct tubular toxicity and vasoconstriction * cisplatin - direct tubular damage and RAAS system vasoconstriction * tetracyclines - direct tubular toxicity * amphotericin B - direct tubular toxicity
38
What is this?
* tetracyclin toxicity, cattle * tubular necrosis = pink
39
Explain the pathogenesis of aminoglycosides
* 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
* aminoglyoside toxicity * accumulation of lamellar bodies which eventually cause necrosis of tubular ep cells * blue = myelin body
41
Why is ethylene glycol toxic?
* 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
What would be seen in ethylene glycol poisoning?
* 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
WHat is seen here?
* calcium oxalate crystals sticking to ep membrane
44
What are these?
* rhubarb * halogeton * contain oxalate at toxic levels
45
What is melamine nephrosis?
* 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
What is this?
* melamine nephrosis
47
What is this showing? which animal does it effect?
* lily toxicity * cats - very small amounts * acute tubular necrosis
48
Is nephrotoxicosis reversible?
* in absence of renal failure - yes * proximal convoluted tubule ep cells will regenerate - BM preserved
49
What is haemoglobinuria?
* 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
51
WHat is this?
* foal, haemoglobinuric nephrosis due to Babesia equi * would also have red urine due to haemoglobin in urine
52
What is this?
* 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
53
What are the tubulo-interstitial diseases?
* interstitial nephritis * suppurative * non-suppurative * pyelonephritis - inflam of renal pelvis
54
What is intersitial nephritis?
* accumulation of inflam cells in interstitium * interference with transport between tubules and capillaries * can affect resoption
55
WHat is non-suppurative interstitial nephritis?
* inflammation against arteries, veins, lymohatics, connective tissue * usually non-consequential * non-specific * granulomatous / lymphoplasmatic * duration - chronic more common - fibrosis and atrophy
56
What is supurative interstitial nephritis?
* haematogenous (embolic) * ascending from lower urinary tract
57
What is the difference between primary and secondary intersitial nephritis?
* 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
What is leptospirosis?
* 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
Describe the lesions of leptospirosis?
* 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
What is this?
* pig, intersitial nephritis - white flat coalescing spots in cortex * multifocal white lesions - accumualtion of lymphocytes and plasma cells in interstitium
61
What is this?
* dog, chronic intersitial nephritis * fibrosis * scarring * atrophy * parenchyma lost - end stage
62
What is white spotted kidneys?
* best known as non-suppurative interstitial nephritis * early lesions - suppurative / chronic - non * incidental finding - calves * multifactoral - E.coli, salmonella, leptospira, brucella
63
* white spotted kidneys * radial or wedge-shaped inflam infiltrate expands the intersitium
64
What is this showing?
* 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
What would be seen in kidneys and brain with encephalitozoon cuniculi?
* kidneys - granulomatous/ nonsuppurative inflam - organisms present in ep and lumina of tubules, glomerular caps, in intersitium * brain - granulomatous meningoencephalilitis, foci of malacia
66
What is this?
* feline infectious peritonitis * round lesions * granulomatous inflam * white coalescing nodules * differential = renal lymphoma
67
WHat is suppurative intersitial nephritis?
* 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
68
What is pyelonephritis?
* 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
WHat is this?
70
What causes renal gout?
* 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
What causes gout in birds?
* cold/ damp * vit A/ B12 def * type A influenza * high protein diets * dehydration
72
What is this?
* gout
73
* numerous tophi expand the tubular lumen and cause degen and necrosis of the tubular ep * granulmatous inflam surrounding tophi
74
What is gout?
* 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
What is renal neoplasia?
* renal adenoma - benign * renal carcinoma - malignant * nephroblastoma
76

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